Archive for the ‘CABG’ Category

A Fantastic Vessel-Clearing Innovation on The vessel-clearing device, U.S. Patent No. 8,663,209

This article is a Contribution to this Open Access Online Scientific Journal and to our BioMed e-Series on 2/29/2016 by William Harrison Zurn, member of our Team, holder of multiple US Patents in the Medical Devices field.


This article will be REPUBLISHED with permission in a forthcoming e-Book by Leaders in Pharmaceutical Business Intelligence in our BioMed e-Series


Series E: Patient-centered Medicine

Content Consultant: Larry H Bernstein, MD, FCAP

Volume 1: 

The VOICES of Patients, HealthCare Providers, Care Givers and Families: Personal Experience with Critical Care and Invasive Medical Procedures – Work-in-Progress



This article first appeared in the February 2016 issue of Inventors Digest magazine. Published by permission.

Permission SOURCE to re-publish

From: Cama McNamara <cama@inventorsdigest.com

Date: 2/26/2016 08:39 (GMT-08:00) 

To: William Zurn <wilzur@msn.com

Subject: Re: Re-Publish Article 


Cardiac Patient’s Comment to the article:

Re-published with permission

Permission SOURCE to re-publish

On Feb 28, 2016, at 8:19 PM, William Zurn <wilzur@msn.com> wrote:

 Aviva, the person with the reply gave his permission.

Please removed all his contact information.


It’s from a heart patient, who underwent a triple bypass in his 40s, and Dr. Mehmet Oz performed the surgery.

Received on LinkedIn on 02/19/2016: 

“Hello, My name is XXXXX  and I am a cardiovascular disease patient. I am a retired NY police officer and I read about your great work in Inventors Digest. I was 44yrs of age when I suffered a heart attack and had triple bypass surgery at Colunbia Prebyterian Hospital in NYC.Dr.Mehmet Oz was my surgeon. I am very active in a gym and exercise daily.I am now 64 yrs of age and God willing I will continue to be healthy. I was so interested in your work I had to write to you. God Bless you for your brilliant mind and the work you are doing. Please keep me in mind if in the future you get to a stage that heart arteries can actually me cleaned of any arterial plaque. I would be happy to undergo this procedure when you have perfected this.

Thank you….


[Name, Phone Number and e-mail address was omitted to maintain Patient’s Privacy.]


How the 1960s-era Science-Fiction Movie Fantastic Voyage Is Becoming a Reality

By Clifford Thornton


In 1966, the science-fiction movie Fantastic Voyage was far ahead of its time in special effects, technology and cinematography. What is most remarkable, though, is the foresight of the film’s creators and directors to capture an almost unimaginable concept at the time: nano technology and micro-electro mechanical systems, which are coming very close to reality today.

Previous science-fiction movies focused on intergalactic travel, but Fantastic Voyage delved into another kind of space—“inner space”—space inside the human body. In this case, the body is explored by a successful brain surgeon, scientists and other specialists aboard the customized submarine Proteus, which is designed to navigate through the human vascular system after it is shrunk to microscopic size, placed in a syringe and injected into the bloodstream.

The team’s mission is to save the life of the scientist who holds the secrets of the miniaturization technology. He suffers from a life-threatening blood clot in his brain, which has left him in a coma.

Once miniaturized, the submarine and its crew are inserted into the scientist’s carotid artery, where it begins its arduous journey. The nuclear-powered vessel’s location is tracked through the isotopes it emits, and the vessel’s status is monitored by control-and-command center personnel, who use radio to communicate with the crew.

To determine the shortest route through the scientist’s vessels to the clot, the team uses diagrams of the human anatomy as navigation charts. Once the submarine reaches the clot, the scientists aboard use a laser beam to pry the clot from the blocked vessel. The journey is quite exciting, as the crew can see what no human has previously seen: the wonders and workings of the inner human body at the microscopic level—in close proximity and vivid detail.


Lasers and MRIs

What do miniature submarines, a dying scientist and a surgical laser beam have to do with nanotechnology and MEMS? This imagined medical surgical capability, as far-fetched as it seemed at the time, is extremely close to becoming a reality. Inventor William Zurn has exercised his decades-long experience in technology development and engineering to design a now-patented vessel-clearing system that will accomplish, in a very similar fashion, what Proteus and its crew set out to do—eliminate blood clots—but in a more modern and realistic way.

Clotting of the blood, such as when an injury occurs and the bleeding stops, is a normal occurrence in the body. However, clotting can also cause irreparable bodily damage, or even death. Clots that pose a risk or threat to a patient can occur in the heart, veins or arteries.

Zurn was inspired to develop a patentable stent after researching the causes and effects of aneurysms. This led to a system of controlling, guiding and placing medical-implant modules within the principles of nuclear magnetic resonance. The vessel-clearing device is a huge leap in medical technology, transcending present methods of clearing atherosclerotic plaque and clots from human vessels and arteries. The vessel-clearing system will enable complete mapping of the cardiovascular system via magnetic resonance imaging, and precise locating and targeting of the occlusion.

Additionally, computer-assisted surgical methods of clearing clots and atherosclerotic plaque will be employed. The system computes the circulatory system path algorithm, which, in turn, allows for navigation to, around and from the source of the blockage. Finally, an algorithm for removing the blockage, which is programmed into the master computer, directs the motion of a biocompatible module apparatus, constructed by nanotechnology and/or semiconductor material, which then utilizes laser energy to remove the blockage. This is a much more effective, safe and efficient method than a traditional angioplasty procedure, which uses a balloon to compress the blockage or plaque against the artery walls. Recent studies have shown that after a few years, many patients must have an additional angioplasty procedure.

Nanotechnology Is a Giant Step

What exactly is the vessel-clearing system and how does it work? We can compare Proteus and its imagined capabilities to the vessel-clearing system. Within the system, a biocompatible module composed of multiple subsections, referred to as “pods,” are constructed by a combination of nanotechnology and integrated circuit technology. The size of these injectable pods is approximately 100 nanometers by 50 nanometers (a nanometer is equal to one-billionth of a meter). These pods are analogous to Proteus, and just as Proteus was introduced to the scientist’s body through a syringe and needle, the BCMs, or pods, will be inserted into patients in the same fashion.

In the same way that Proteus had radio communication between its crew and the control center, the vessel-clearing system will allow for similar communication between the pods and the control console, which is operated by a surgeon. As such, the pods have a communications unit, a radio frequency receiving and conversion section, and a laser-transmission section. The laser functions as the tool to untether and fragment the clot. The remaining residue is processed by the kidneys. Just as Proteus’ location in the scientist’s body was tracked by the control center via nuclear emissions, the vessel-clearing pods will be transmitted and closely and accurately tracked by nuclear resonance imaging. The collected information will be displayed on the control console.

In the film, Proteus and its crew have a certain time frame—60 minutes—in which the miniaturized state will remain active. Past that time, everyone and everything involved return to normal size. Zurn’s vessel-clearing system will not experience this problem. The vessel-clearing system and related procedure will be carried out in an efficient and timely manner with a focus on patient safety. Once, it is determined that all applicable and dangerous blockages have been cleared, the BCMs will be collected and extracted from the patient’s body in the same way in which they were introduced, via a syringe and needle.

If this sounds like another fantastic voyage, think again. The vessel-clearing device, U.S. Patent No. 8,663, 209, will be making its inaugural journey soon.


Clifford M. Thornton is a Certified Cardiovascular Technologist and a registered Diagnostic Cardiac Sonographer. He is also a journalist in the medical device field, particularly in the fields of cardiology and nanotechnology.






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A Patient’s Perspective: On Open Heart Surgery from Diagnosis and Intervention to Recovery – A New Day, a New Lease and Unfolding Questions!

Guest Author: Ferez S. Nallaseth, Ph.D.

Life Sciences Institute of New Jersey, Belle Mead, NJ 08502; Complex Biological Systems Alliance, Boston, MA; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ 08901.

Contact information:

Email Addresses: ferez.nallaseth@cbsaimtt.com


Tel: 646 283 5163 (M)
908 431 5069 (CBSA)
Skype Address: ferez.nallaseth
Websites:Life Sciences Institute of New Jersey, Belle Mead, NJ.
Member – Complex Biological Systems Alliance
Ferez S. Nallaseth, Ph.D. (Google Scholar)
Ferez S. Nallaseth, Ph.D. (Google Sites)
Ferez’nSquashDocs (website and blog)

This article will be published in 

Series E: Patient-Centered Medicine 

Volume One: The Patient’s Voice: Personal Experience with Invasive Medical Procedures

All subsequent excerpt submissions for publications elsewhere MUST include the following sentence:


I, Ferez Nallaseth, PhD was commissioned (at no exchange of any financial rewards) by Dr. Aviva Lev-Ari, PhD, RN, the Editor-in-Chief of the Open Access Online Scientific Journal 


on 2/14/2015 to write an original article representing “The Voice of the Cardiovascular Diseased Patient who underwent an invasive procedure, i.e. CABG, aka, Open Heart Surgery.”

Date: Sat, Feb 14, 2015 at 5:37 AM

Subject: Invitation to write one article about your experience: From Diagnosis to Recovary

To: Ferez Nallaseth <ferez.nallaseth@gmail.com>

Cc: Aviva Lev-Ari <AvivaLev-Ari@alum.berkeley.edu>

We are publishers of a BioMed e-Books e-Series

Please go to


Click on

BioMed e-Series

1. Please click on Series A: Cardiovascular Diseases

Volume 1,2,3,4,5,6

2. Please Click on Series E: Patient-Centered Medicine

Volume One: The Patient Voice – Experience with Invasive Surgery


Please reply if interested.

I am looking forward to your reply.

Aviva Lev-Ari, PhD, RN

Editor-in-Chief BioMed Series

  • This article was edited by Stephen J Wiiliams, PhD, Senior Editor at Leaders in Pharmaceutical Business Intelligence (LPBI) as part of the publishing process of the article in the Journal.

This article was published in the Journal on May 10, 2015. This article will appear in the forthcoming ebook, Titled, 

 This is Volume One in Series E: Patient-centered Medicine, in the BioMed e-Series will be published by LPBI on Amazon.com

The URL for the original article is listed, below:



  • All References to the article as a Reference source, should cite the link, above

HOWEVER, since this article has been included already in Volume One of Series E AND Volume One is WORK-IN-PROGRESS, not yet on Amazon.com as a published e-Book THEN 

  • for all cases of using an excerpt versus citing the article in its entirety for ANY OTHER PUBLISHER, i.e. Squash Report, it needs to add a footnote with the QUOTE, above

A Patient’s Perspective: On Open Heart Surgery from Diagnosis and Intervention to Recovery – A New Day, a New Lease and Unfolding Questions!

Ferez S. Nallaseth, Ph.D.

Life Sciences Institute of New Jersey, Belle Mead, NJ 08502; Complex Biological Systems Alliance, Boston, MA; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ 08901.


A minor cardiac event last Christmas revealed how seriously my life was threatened. It was averted by the amazing efforts of the, Biomedical Community, Family, Friends and Colleagues all pulling together and from around the Globe. The brush with ‘eternity and infinity’ left me aware that the ‘just war’ in which I had been engaged for close to 4 decades had left too much not done and too many, neglected in too many ways and too far removed from the core of my being! At least part of the consequences of that trauma on the 25th of December was the initiation of a thought process (or the lack of it) in filling this void! And yet remaining mindful of history and those in it, even ordinary ones, to whom we owe so much, precisely because they made the right and hard, choices that I am faced with today!


This is the perspective of a Life Scientist who underwent a Heart Attack and triple Bypass Surgery. Because this is a retrospective experience with little data to support it and I am neither a Cardiologist nor a Cardiac Surgeon, this exercise is of necessity, a largely subjective delivery of the process that saved my life. It is one in which I was merely the beneficiary of the highest form of dedicated professionalism! It is in part an expression of my deepest gratitude to my family, friends, some even emerging from long neglect, and medical professionals who leapt to my rescue! As well as addressing a need for more systematized studies to address the true frequencies of the events that I underwent. A gratitude that usually dawns when one has had a brush with ‘eternity and infinity’ and effectively becomes bedridden – if only transiently so! Considering the technical complexity of the undertaking by (a) Dr. Andrew Shanahan, my Cardiologist, in detecting the block by catheterization and angiography and (b) Dr. George Batsides, my Cardiac Surgeon and (c) their respective teams in intervening with the triple bypass surgery, all with a 98% success rate, it is nothing short of amazing!

However, the scientific and medical literature and my Cardiologist’s and Cardiac Surgeon’s observations also supports the interpretation, although not experimentally verifiable, that competitive Squash and training for it in India delayed Coronary Artery Disease and kept me alive till Dr. Shanahan and Dr. Batsides had time to intervene! It probably saved my life in 3 important ways. Firstly, as 1 of about 20 high intensity sports (METs of 6 -13) it is likely to have significantly lowered the risk of Coronary Disease (22 – 40%), thus secondly, delaying the massive blockage (95% – 99%) of 5 major Coronary Arteries by Coronary Artery Disease (CAD) that was recorded. Lastly Squash, and training for it, likely preconditioned (Ischemic Preconditioning or IPC) my cardiomyocytes, making them resistant to hypoxia and so ensured their predominant survival (96 – 98%) when the inevitable Heart Attack (Myocardial Infarction or MI) predicted by several Risk Factors, occurred. However, the ~2% of cardiomyocytes which did succumb to cell death could not have been resistant to total Oxygen (O2) deprivation (anoxia) as is expected e.g.from observations in Sudden Cardiac Arrest (SCA). Conversely, the hypoxia resistance of my cardiomyocytes may have contributed to the inability to stress them with O2 deprivation in Stress Tests as was revealed by Electrocardiograms, Transthoracic Echocardiography and Electroradiographic monitoring. This may have, despite chest spasms, led to the inability to detect the disease over 10 years. Only catheterization and angiography, justified by the elevation of circulating levels of the biomarker Troponin T and done by Dr. Shanahan could confirm this dire Coronary Artery Disease diagnosis.

Although an attempt has been made to include, (1) useful information recommended by all the Medical Personnel involved who have previewed an outline of this article, (2) select scientific and medical literature relevant to it have been added to each of the contributing dimensions that were considered (but are restricted to Supplementary Information Boxes (SIB)), (3) those lifelong events, activities and habits (including the assault on my professional work and personal life) that either contributed to or ameliorated known Risk Factors for the Heart Attack which on hindsight was inevitable! At the very least the combination of my decades long cardiac and sports experience, the scientific literature and the findings of Dr. Shanahan and Dr. Batsides after I finally had a Heart Attack, as well as the experience of others in the Cardiac Physiotherapy Program that I attend, strongly suggest a need for a systematic screening for these symptoms. Of necessity preceded by a re-evaluation of the methods for detection of all types of silent diseases affecting the Cardiac system.  For example development of various Tomography approaches e.g. Multi Spectral Optoacoustic Tomography (MSOT) (97,98).

I’ve also made an attempt to come to terms with perhaps an insidious process that is still underway – somewhere in the back of my mind. It may mimic the ‘know thyself’ of Delphos, and what I like to think of as the nebulous, amorphous and often contradictory aspects of being human. This includes the many communities in any life – family, friends, medical, professional and social networks. Those who were either at one with me or dropped everything in their own lives to leap to my rescue, and also included onlookers and even outright adversaries who seemed to be genuinely concerned! Possibly transfixed by the specter of mortality?

Work unfinished due to unavoidable circumstances that were alluded to earlier and the transience of life were the compelling, if sub conscious, forces over the past 40 years or so and although now dampened by these events, they have not disappeared. And in some unclear ways may perhaps even have been heightened in my sub-conscious by the potential extent of the waste of my life if things had ended less favorably. Not only of the terminated future, but also of the long span of the past which had been dedicated to the body of unpublished Scientific work, which would have been discarded instead of being in the literature where it serves a more useful purpose!

However, the true nature and impact of the recent events on my life and their effects go beyond the Operating (Surgical) Theater and are still evolving! Included are a revision of the cavalier considerations of activities and habits contributing to cardiac Risk Factors with ‘you only live once’ which have now been tempered by that brush! A temperance into both, a reticence that is almost Pavlovian as well as one of a sense of responsibility to those whose graciousness, generosity, sacrifice and hard work rescued me from near certain death! In addition to those Physicians and Surgeons who played the most active roles in saving my life, all those unbelievably dedicated Biomedical Support Personnel who assiduously contributed to the diagnosis, intervention and recovery of a relative stranger who had undergone a Heart Attack and required Critical Care are included here. They are implicitly or explicitly noted in the acknowledgements (link). This event and the period spanning it will remain a watershed that has unleashed many ongoing developments in my life.


Last Christmas morning (25th December 2014) would become a Watershed Day in my life! Although I had, what was subsequently confirmed as, only a minor Heart Attack (Myocardial Infarction), it unleashed a progression of events that culminated in Open Heart Surgery. They continue to alter my perspectives radically, and in ways, with which I am still coming to terms. For a start it conclusively resolved the “Will-O’–the-Wisp” of Chest Pains and Diagnoses’ that ‘ruled out’ Cardiac malfunctions over the last 10 years. There were other ways in which it does so but this followed more (bad but good) news that was yet to come. When I was brought in by the Emergency Medical Services the Biomedical teams in the Emergency Room of the University Medical Center of Princeton in Plainfield, led by Chief Emergency Physician Dr. Eileen Daly, the Attending Physician Dr. Ying-Kei Hui and the Cardiologist Dr. Banu Mahalingam immediately concentrated on stabilizing my condition, the seriousness of which I alone was not fully aware! And more on this effort was to follow. I looked on all this as an inconvenience and planned on getting back to my keyboard – sooner than later. It would be nearly a month before I had finally managed to have done so – and likely would not have been writing this if I had been allowed to have my way! Since this is meant to address the concerns of those Patients who will follow in my experience I think it would be useful to define an outline of this article that the Editor of BioMed Online (Cancer, Cardiology, and Cardiology Devices) Dr. Aviva Lev-Ari had asked me to write. First of all the simple question arises as to why, as a Scientist who depends on controlled experiments, I would even agree to write something that is so subjective an experience? The short, if incomplete answer, is gratitude! For those who kept me alive medically and my family members and friends who dropped everything in their lives to either appear by my side or write and some even reappear in my life! And of equal importance these events convey a need that has been identified by others like myself – for a systematic and controlled study to address the gaps in a system that is otherwise remarkably fail safe!

But to address this and other questions meaningfully, it would be useful to deliver this narrative in (1) a chronological order, (2) while making necessary diversions with supplemental information boxes (SIB) included for short informative discussions on the, (a) literature on e.g., Risk Factors and rudimentary Cardiology and Cardiac Surgery, (b) definitions and analyses such as, (c) vital signs that may have made revelations about the process and why cause and effect as scientific and medical conclusions are unknowable in my case, (d) pain from Open Heart Surgery, (e) compassion, warmth, concern and yet skill, dedication and professionalism of all the Biomedical personnel involved, (3) summary of the relevant literature on contemporary methods of (a) establishing Risk Factors, (b) the energetics and physiology behind the cardio-pulmonary system, (c) the molecular, cellular and developmental biology of the cardiac system, its protection from genotoxic shock and disease states, (d) the contribution of specific processes to Risk Factors as well as their amelioration, (e) Sports Physiology and the role of Sports with an emphasis on Squash in the reduction of cardiac Risk Factors, (4) a summary on elements of the literature and the observations of my Cardiologist and Cardiac Surgeon that are consistent with the explanations for the events – first slowing down plaque buildup and then protecting my cardiomyocytes and allowing survival from the Myocardial Infarction (MI) or Heart Attack, (5) acknowledgement of those who either saved or eased my life, (6) reference list, (7) a more detailed review of this article focused on Sports Physiology and Cardiac Risk Factors to be oriented and submitted to a Sports or Clinical Sports Journal (1).

(8) (a) To begin with, it is only appropriate to thank my Cardiologist Dr. Andrew Shanahan and my Cardio -Thoracic Surgeon Dr. George Batsides. Dr. Batsides’ highly encouraging message to my query for permission to publish an event that involved his work, his team as well as his Editorial assistance:

“Ferez, I’m very glad to hear that you are doing well.  Thank you for your very kind words.  Our team would be honored to be included.  We are all very happy that this has not only helped you physically but has also impacted you in such a positive manner.  Cardiovascular disease is still the great killer and one’s experience and perspective throughout the diagnosis, intervention, and recovery can be very valuable to others.  This can save lives by informing others on what to look for, how to seek help, and to not completely fear the process. Thank you for undertaking this project.  Please feel free to contact us for any help.  

All the best,

George B.  “

(8)(b) this article has additional input, (i) from concerned, highly skilled, dedicated, kind and professional, Biomedical Staff, Physicians and Surgeons at both the University Medical Center of Princeton (UMCP) in Plainsboro as well as at the Robert Wood Johnson University Hospital (RWJUH) in New Brunswick, (ii) my Family, and Friends, including my brother Attorney Cyrus Nallaseth who flew in from Bombay, (Mumbai) India on a moment’s notice, family, friends spanning generations such as Dr. Adil Mulla, an Anesthesiologist and his daughter Dr. Simone Mulla, who either appeared by my side or called regularly, at a vanishingly short notice, (iii) a long list of the most warm, kind, supportive and encouraging friends, fellow Squash Players, Scientists, fellow LinkedIn Members, fellow ResearchGate Members, Teachers at Princeton High School and others from around the World who responded via email to my ‘Late New Year’s Greetings’ and postings of the news, with nothing but the most supportive words that were re-invigorating in ways that I could not even have imagined! They are all listed in the acknowledgements link! In addition the article attempts to recognize as many contributors as were identifiable (with apologies included for any inadvertent omissions). This narrative will of necessity require covering the Risk Factors for Cardiac Disease that were both imposed or unavoidable and inevitably led to the cardiac event of the 25th of December 2014. As well as the ones that were those that I had either exacerbated or ameliorated. This will follow after introducing a few events in chronological order.


     1. Pre Heart Attack symptoms.

Over the last 10 years or so, prior to the Heart Attack, I had fleeting spasms in different locations of my chest and even while at rest. Depending on the circumstances e.g. acute stress, I had always had digestive and neurophysiological symptoms that are recognized as stress and environment related. They could either mask or promote cardiac pathologies. Approximately 35% of the US population displays all or some of these and other related symptoms (2). Furthermore, my colleague Peter Shimon of the Darwinian Evolutionary Medicine Group on LinkedIn identified a publication noting that Historians had recorded that these stress related symptoms, although near incapacitating, were overcome by those associated with the creative characteristics common to many artists, scientists and others, including Charles Darwin (3a,b)! In fact Darwin continued working, while having to solely depend on the ineffective therapies of his time, such as cold compresses applied to the spine. He wrote a whole chapter in the ‘Descent of Man’ while immersed in ice water to relieve the grip of nausea and migraine! (3a). It was, what we call, ‘Mind over Biology’ in the World of Sports!

As far as the spasms in my chest went, initially I did not think much of them but from around 2004 onwards, consulted Cardiologists and had gone through several Stress and other tests which were negative for cardiac malfunction that they had administered over that period. So it was hard to diagnose the cause of those chest spasms and my Primary Care Physician Dr. Perry Pong reminded me to remain wary of pulsating pains in the area of the sternum but not to worry too much about the other areas. Advice that was to save my life!

     2. Did Overtraining in my competitive Squash playing days lower the Risk Factors for Heart Disease through Ischemic Preconditioning (IPC)?

I had trained hard (in Sports Physiology this is termed over-training) in India 38 years ago (up to 1976 when I left for the US) for competitive Squash, an intense sport (~ 20 of 100 sports with a near maximal Metabolic Equivalent Task (METs) of 6 to 12). From results in national level tournaments, I was in the top 10 and remained in good shape even after decades of detraining an example of the training regimen I used was posted for the Rutgers University Squash Racquets Club (and this will matter as we will see later) (4). In the United States, after I had lived for 13 years in small University towns, which due to a lack of competition, essentially resulted in detraining, my game had ceased to exist and conditioning had dropped irreversibly to a fraction of the level in India along with my performance on the court. This happens to the best of Racquet Athletes who detrain relatively early in their careers e.g. Wimbledon and multiple (near) Grand Slam Tennis Champion Bjorn Borg! However, I still regained some of this conditioning, on subsequent retraining, with new literature referenced and to be discussed in this article, providing a molecular and cellular mechanistic basis for this observation – one which has always been well known to Athletes.

After moving up to the New York area in 1989 my game was partially recovered and I was nationally ranked in the USA in 1992 as a 40 year old (top 20 in the 5.5 level and higher in other age group divisions, by US Squash). Even in 2006/2007 long after my prime when I was 54/55 the residual game and conditioning retained were still sufficient to secure semi-final and final level performances in Open tournaments in New York (at 5.0 or Ltd A levels – 3 levels down from the highest 6.0 level)! As well as a 3 -2 win over a top ranked (by US Squash) Amateur/Pro (6.0 level) level competitor, Shane Doyle in a tough 90 minute interclub match. I was playing for the Rutgers USRC against Francis Odeh’s Valkyrie Club. Shane was an All American Surf Boarder and one of the toughest players in this semi-contact sport whom I have ever played in the United States! This may mean that 30 years after ceasing high intensity training, I still retained some of the conditioning developed in India. Squash, has been rated as having the highest Exercise Intensity (METs = 6 -12 cals/kg/hr), Health Benefit to Injury Ratios (517 Calories per 30 minutes of a game to Injury Score of 2) and Healthiest Sport with a total score of 22.5 of 10 sports as measured by Sports Physiologists, Athletes and Coaches (5, 6). And so a lifetime of conditioning in Squash, was likely to have contributed to my cardiac conditioning and saved my life (as will be shown later). However, after 2006/2007, I was again professionally pre-occupied and despite perfunctory workouts in the local gym my game and conditioning deteriorated further to low levels. This is dealt with in greater detail in the final segment.

     3. Did I have a Heart Attack in April 2010 long before the one on December 2014 that could not be detected by all the tests for cardiac malfunction that were administered?

At some time in April 2010, while on the court, I had a prolonged (1- 2 minute) chest spasm of medium intensity. Dr. Pong and I decided it was time to have it thoroughly examined by a Cardiologist. The Cardiologist whom we consulted was Dr.Tak Kwan. He was methodical, dedicated, reassuring, skilled and professional! I was subjected to 4 tests that were considered to constitute a thorough analyses of cardiac malfunctions. They were:

  • Electrocardiogram
  • Transthoracic Echocardiography (without 2D, color flow Doppler Echocardiography)
  • Transthoracic Echocardiography (with 2D, color flow Doppler Echocardiography)
  • Exercise Myocardial Perfusion Imaging with Dual Isotopes SPECT (Gated Tomography) or Electroradiographic monitoring for 24 hours

Based on the results of these 4 tests Dr. Kwan excluded cardiac mal-function with a 95% confidence interval. He felt that the Health Insurance Provider would not authorize any further more definitive tests such as catheterization and angiography. And subsequent events on the 25th of December 2014 confirmed the elusive nature of detecting even an ongoing Myocardial infarction (Heart Attack) which supported his conclusion.

As I was not a Cardiologist, there was little more that I could do and since I did not want to become a hypochondriac, I stopped thinking about this problem and did what we are trained to do in our time as athletes! That is work our way through ‘Pain Barriers’ as defined by the Multiple British Open Squash Champion, Jonah Barrington, in the 1970s (7). Although to be honest this level of pain would qualify for discomfort – at best!

That is till about 8.00 am on Christmas morning of 2014. I was on the computer keyboard – probably checking the Online News when things began to happen! The circumstances became reminiscent of my father’s passing from the second and fatal of two Ventricular Fibrillations that he suffered which was far more traumatic than my Heart Attack.


(I) My apartment on Christmas day of 2014:

(i) On holidays I made a conscious effort to try and forget the ‘Elephant in the Room’ (‘EitR’ to be explained). Since one of its latest consequences was a lack of a job and funds for the past 8 (and often in the last 35) years my entertainment was restricted to consumption and TV at home. On that day this included Appetizers, Breads, Liquors, Prime Rib, Vegetables, Mashed Potatoes, and Christmas Plum Pudding with Plum Sauce! It was a good meal and sampling began on Christmas Eve (12/24/2014) although its leftovers were anticipated to last through the holidays – and well past New Year’s day!

The lipids and calories associated with this meal when either consumed in excess or regularly are classified as Risk Factors by the American Heart Association, the National Heart, Lung and Blood Institute of the national Institutes of Health and the Centers for Disease Control (CDC), the New York State Department Of Health and the Mayo Clinic Health System] as representing significant Risk Factors for Coronary Heart Disease (CHD), Coronary Artery Disease (CAD) and Coronary Vein Disease (8 – 26). The multifactorial nature (gene, environment, etc..) of heart disease(s) has always made it difficult for Cardiologists to identify and evaluate the impact of Risk Factors. However, contemporary genetic and statistical methods which are far more comprehensive as well as of higher resolution are accepted as reliably identifying and quantifying the Risk Factors associated with cardiac diseases (SIB-1, 7A to 7D). Included are the Risk Factors that my life style clearly incurred and those that it ameliorated.

The above meal was a Risk Factor! However it was a needed the distraction, could not be afforded often enough for it to amount to a dangerous Risk Factor, there were routinely included counteractive measures (workouts, statins, diet, etc..) and after all one only lived once! As we will see shortly, this led to an enforced leave of absence for 3 weeks in the Hospital, I ended up giving away, returning or discarding all the ‘good stuff’ – and may have not lived long enough to write this article!

(narrative interrupted).

Supplemental Information Box: SIB- 1:

Why do we have Heart Attacks, Cardiac Arrests and Ischemia/Strokes? To appreciate the reasons behind these pathological conditions requires some understanding of the basic biology of the (a) the 2 specialized organs the heart and the brain and their functional cells, called cardiomyocytes and neurons, which function through their generation of an electrical output? Addressed in: (26, 27, 28, 29, 31, 32, and 33), (b) How do they function to produce an electrical discharge/current (depolarization/repolarization) which induces cardiac contraction, in a process that includes the heart generating its own electrical discharge? Addressed in: (20, 23, 25 – 34), (c) What are their requirements for the source of their energy (ATP molecules) synthesized in the cellular power plants of all cells called Mitochondria? Addressed in: (32, 33), (d) Why is O2 critical for their function as well as their survival? Addressed In: (20, 23, 25 – 34), (e) What happens when the blood supply and so the O2 it transports to the heart via red blood cells is reduced or cutoff? Addressed In: (20, 23, 25 – 34), (f) How much work is done and what is the volume of blood pumped by a heart in the lifetime of an individual? Addressed In: (26, 30, 34, 35).

(a) The physiological functions of the heart and brain, are similarly dependent on electrical output, generated by cells carrying out the functions characteristic of these 2 organs called cardiomyocytes and neurons (26 – 34). Although in other ways cardiomyocytes and neurons are distinct, because of their high energetic demands, they are both hypersensitive to O2 deprivation, compared to e.g. muscle cells (myocytes) which can survive anaerobically through glycolysis. Energetic and reducing equivalents (biochemical molecules called ATP and NADH) required for the functions of all cells including cardiomyocytes and neurons are generated in mitochondria (26 – 34). The energy vehicle ATP is a molecule with a high energy chemical bond which when it is cleaved releases the energy necessary for executing most of the biochemical processes in most forms of life (26 – 34).

(b) Cardiomyocytes and neurons depend on ATP and NADH to drive the ion channels and pumps required for creating the electrical gradients across their cell membranes. This gradient is required for their functions of electrical discharge or depolarization (electrical waves) by pumping Na+ and K+ ions out and Cl ions into cardiac cells through special channels and pumps (that require ATP) causing their beating (26 – 34).

(c) ATP and NADH are generated on mitochondrial membranes by a controlled ‘slow burn’ of molecules derived from food, which unlike rapid combustion (flame), allows the harnessing of released energy as high energy chemical bonds of ATP molecules. Food is digested and biochemically degraded (catabolism) by specific biochemical pathways (glycolysis and the TCA cycle) preceding the products being ‘fed’ into the Mitochondrial Electron Transport system. The electrons from the (‘burnt’) molecules of food are sequentially passed down a series of membrane bound complexes, called the electron transport chain which represent increasingly oxidized (‘burnt’) molecules (oxidation states). The passage of electrons is harnessed with the synthesis of ATP by pumping electrons and H+ through another complex known as the F1/F0 complex which traverses the mitochondrial membrane. The process of ATP synthesis is called Oxidative Phosphorylation and is chemically and enzymatically coupled with Electron Transport. The final complex in the electron transport chain donates electrons to O2 as the final (terminal) acceptor molecule of electrons and H+ (protons) producing H2O as a reduction product. When e.g. arteries are either partially or completely blocked, O2 levels drop, electrically specialized and sensitive cells like cardiomyocytes and neurons not only cannot function but also die e.g. usually by a process called programmed cell death or apoptosis, which cleaves the cell while packaging is contents to prevent spillover of immunogenic components (27, 36, 37, 47, 50, 51).

(d) In ischemia/hypoxia-reperfusion studies products of genes such as HIF1, EPAS1, Akt, Bcl2, VEGF, CD-29, p38 Kinase, JAK-STAT, p29, and NOX2 and the hormone Estrogen attenuate injury by ROS to cardiac tissue through a multitude of mechanisms which will be covered in the section on the molecular, cellular and developmental biology of the cardiac system (36 – 51).

(e) the beating (contraction/relaxation) of the cells in the Heart is initiated from 3 electrical centers (called nodes) of cardiomyocytes that discharge coordinated electrical impulses. These impulses are known as depolarization and repolarization waves and basically represent an inversion and restoration of electrical charge and voltage across cell membranes which is known as membrane potential. These nodes are the Sinoatrial (SA) node located in the upper right Atrial chamber which releases the first discharge. The depolarization wave (current) then migrates down to the Atrioventricular (AV) node located at the junction of the 2 chambers causing it to discharge. There is a third system lining the walls of the Ventricle called the His-Prurkinje (H-P) system which therefore also discharges. Illustrating the extreme coordination underlying the contractions of the heart. Contraction is ATP dependent and mechanically mediated by intracellular (cardiomyocyte) filaments of motor molecules of Actin, Myosin and Troponin that are anchored to cell membranes. They have specific structural arrangements similar to anchored fibers and ratchets that facilitate contraction and relaxation of the cardiomyocyte. The electrochemical basis of the discharge is positively charged ions like Ca++, Na+ and K+ and negatively charged ions like Cl which can only cross cell membranes through specific specialized ‘pores’ called ion channels and require ATP to do so. When there is an influx of Ca++ ions into the cardiomyocytes it precipitates the passage of Na+/K+ , depolarization (inversion of electrical gradients across the cell membrane) occurs and there is a generation of an electrical voltage and current. All of which also require energy supplied by ATP. The beating of cardiomyocytes is synchronized in and between the various chambers of the Heart (Auricles (Atrial chambers) and Ventricles) to allow it to pump blood throughout the body – including to all the extremities and over a lifetime. Some indicators of the amount of work done and the volumes pumped by the Heart (29, 30):

  • The average adult heart beats 72 times a minute; 100,000 times a day;3,600,000 times a year; and 2.5 billion times during a lifetime.f
  • Though weighing only 11 ounces on average, a healthy heart pumps 2,000 gallons of blood through 60,000 miles of blood vessels each day.c
  • A kitchen faucet would need to be turned on all the way for at least 45 years to equal the amount of blood pumped by the heart in an average lifetime.a
  • The volume of blood pumped by the heart can vary over a wide range, from five to 30 liters per minute.e
  • Every day, the heart creates enough energy to drive a truck 20 miles. In a lifetime, that is equivalent to driving to the moon and back.a
  • Because the heart has its own electrical impulse, and can continue to beat even when separated from the body, as long as it has an adequate supply of oxygen.c

(See ref: 34, 35 for more data and examples).

Finally there are multiple Risk Factors for Coronary Heart Disease (CHD), Coronary Arterial Disease (CAD), and Sudden Cardiac Arrest or Sudden Death (SCA, SD) that have been established in many different ways by many organizations. Some have counteracting positive behaviors (8 – 27, 34, 35).

(A) Risk factors from the website of the National Heart, Lung and Blood Institutes, National Institutes of Health (NHLB, NIH) (11):

Risk factors are conditions or habits that make a person more likely to develop a disease. They can also increase the chances that an existing disease will get worse. Important risk factors for heart disease that you can do something about are:`

  • High blood pressure
  • High blood cholesterol
  • Diabetes and prediabetes
  • Smoking
  • Being overweight or obese
  • Being physically inactive
  • Having a family history of early heart disease
  • Having a history of preeclampsia during pregnancy
  • Unhealthy diet
  • Age (55 or older for women)

(B) Additional risk factors (National Health Services, UK) (18)

Additional Risk Factors identified by the National Health Services of the United Kingdom are:

  • diabetes
  • ethnic background

Also from the NHS, UK other factors that affect your risk of developing CVD include:

  • sex – men are more likely to develop CVD at an earlier age than women
  • age – your risk of developing CVD increases with age

Results in several new and ongoing areas of research in cardiac molecular, cellular and developmental biology illustrate the unfolding appreciation of the complexity of the Heart in Development and the many points at which its subversion could lead to the accumulation of risk factors! They are discussed in detail in the section (SIB-7C to 7E).

(d) partial interruption of blood flow and thus Oxygen supplies, called hypoxia, which results from plaques of lipid deposits and atherosclerosis causes the milder Heart Attack (Myocardial infarction). While the complete interruption of O2 supplies (anoxia) for 5 minutes due to cardiac electrical malfunction results in the more severe and often lethal Sudden Death (SD) or Sudden Cardiac Arrest (SCA). SCA unrectified for 10 minutes is always lethal. Neurons are irreversibly dead after 4 – 5 minutes of cutoff of O2 in Ischemia/Stroke. However in the case of mammalian (rodent) cardiomyocytes there is such a thing as physiological or ischemic preconditioning (IPC), wherein 20 minutes of hypoxia, elevates the level of resistance of the cardiomyocyte to subsequent challenges of hypoxia administered after even 48 – 72 hours. In the case of Sudden Cardiac Arrest the autonomous electrical supply of the heart initiated by the Sinoatrial Node is no longer coordinated within and between groups of cardiomyocytes in the Auricular and Ventricular chambers leading to their uncoordinated spasmodic contractions or fluttering and Ventricular or Atrial Fibrillation. The O2 supply to both neurons and cardiomyocytes is completely cutoff and the time for a successful resuscitation is a maximum of 5 minutes. It requires restoration of the supply of blood and O2 for rescuing cardiomyocytes with an Automated External Defibrillators (AED) before the patient, as the term suggests goes into irreversible Cardiac Arrest! Atrial Fibrillations (AF) are categorized as those which can (Paroxysmal AF and Persistent AF ) and those which cannot (Permanent AF) be corrected with therapy (23, 24, 25, 27).

(e) diet – a high-fat diet can cause fatty deposits to build up inside your arteries, leading to high blood cholesterol levels and high blood pressure

  • alcohol – excessive alcohol consumption can also increase your cholesterol and blood pressure
  • stress – not taking measures to reduce stress is thought to increase your risk of developing CVD

(C) Other risk factors (WebMD) (19)

Another Risk Factor obesity is now shown to require additional reinforcing factors to manifest their effects in the question: “Could it be genetics, specific dietary intake, physical lifestyle, emotional health or even the microbes that live in the gut? We need more studies to try to understand why obesity causes specific diseases in some people but not in others” (54).

Some risk factors, such as age and family history of early heart disease cannot be changed. Risk factors are multi-factorial and act synergistically.

Although complex the establishment of Risk Factors for CHD, CAD, CVD and Sudden Cardiac Arrest or Sudden Death (SCA, SD) has been made more reliable by contemporary methods such as Genome Wide Association Studies (GWAS) with up to 1,622,114 SNPs, various levels of Metabolic Equivalent Tasks (METs) as indices (METS = 6-16 calories/kilogram body weight/hour), large Cohorts of 6000 to 215,413 individuals, controlled applications of physiological stress (athletics, weights, graded Squash Specific Tests (ST) as opposed to Tread Mill Tests (TT), etc..) alone and strong Personal Record Keeping (high correlation with METs of 0.6.  These methods and Risk Factors will be discussed in detail along with the Risk to Benefit Factor Ratios of exercise e.g. Squash (SIB-7F).

(narrative resumed).

(ii) How many of the Risk Factors identified in SIB-1 were exacerbated and how many were ameliorated by my life style? The answer is mixed. Although as many as 5 of 10 Risk Factors listed by the NHLB, NIH, including moderately high cholesterol, decreased level of physical activity, being a little (20lbs/9kg) overweight, a history of a somewhat unhealthy diet (fast foods for 20 years, but home cooked for the most recent 15 years), and family history of heart disease and even early death from it (all 4 of us in the immediate and others in the extended family) apparently applied but were qualified. However, both family history and physical inactivity were ameliorated by overriding non-genetic factors and somewhat regular workouts. At least 3 more Risk Factors, gender, stress and uncontrolled anger (for good reason) being drawn from the list assembled by the NHS (UK) and WebMD applied to some degree. However determining the Risk Factors contributing to my MI or Heart Attack cannot go far without first addressing the ‘Elephant in the Room,’ (EitR), that had to have contributed heavily to the events under discussion! This is only alluded to once in this article, if for no other reason than to restore attention to those whom it belongs – the Biomedical Community, my family, friends and colleagues from all walks, who in different ways, either set aside all their concerns or preoccupations or focused their occupations, and leapt to save my life!

To understand the magnitude of the pressures from my professional life that had to have been a major contributor to stress as a Risk Factor, events spanning the last 35 years, and still ongoing, require being sketched. To protect something that was well established in Evolutionary Genetics and which led to discoveries of a fundamental Scientific importance and so to the Public Interest, (56, 57), I had to endure a multi-dimensional assault for largely venal reasons! First on our work and then, when an honest editor Dr. Walter Fitch finally published it, on me personally! Our work was first misunderstood by those who should have been more familiar with the literature, then eagerly sought by those at top labs and universities. The assault was coordinated from the highest levels of science by someone at the very pinnacle of scientific authority who was then at a major Research Institution/University in Boston, and had invited me to give a seminar on my work. From hindsight it was clearly with the intent of handing our work over to the designated ‘chosen’ in the field – a long term habit for which all the Principal Investigators involved in this process were infamous! This Investigator was proven to be one of the most unethical and ruthless Scientists in History by a US Congressman, by the National Institute of Health’s Office of Research Integrity (ORI) as well as by the President of an Ivy League University who Chaired a separate Committee Ruling on the events and reported that what had been documented was “only the most visible” of events. All this until a reversal was forced under pressure from the HHS!

In the spectrum of hostile actions taken against us the willing participation, of colleagues and even bystanders from the scientific community, who should have been more trustworthy, was secured! Yes, given the nature of the threat (combined with the prods of incitement and ingratiation!) there were consequences for refusing to participate, but let us just say that the actions of these scientists did not quite amount to upholding the Public Interest. Let alone, amounting to the resistance of, Dr. Robert Oppenheimer to the House Committee on Un-American Activities, or of Dr. Albert Einstein to the Nazis, or of Dr. Andrei Sakharov to the Soviet Politburo and its KGB. And most of all of Dr.Nikolai Vavilov (and his students) who endowed Humankind with Agricultural Biodiversity as well as with their own lives in their resistance to Trofim Lysenko, Lavrenty Beria, Joseph Stalin’s NKVD or the Nazis (during the Siege of Leningrad)!

The only way for me to have protected the Public Interest in our work and yet to have dealt with the ‘EitR’ was to become single minded, developed a thick skin, innovated, resisted attempts at cooption and continued grinding. As can be imagined, that meant losing many things large and small which took a toll finally even including my health! I had obviously concluded that this work was of large enough importance to persevere, if only reluctantly so, and to incur their wrath! However, unfolding results and events clearly supported this conclusion (56, 57)! And so it was always on the back of if my mind including on that morning of the 25th of December 2014.

Although, given its magnitude, prevalence and duration, it is of critical importance, the literature makes it unlikely that this assault on my scientific career and my person was the sole Risk Factor in the Coronary Event of 12/25/2014. As will be clear from the literature these Risk Factors were also likely to have been ameliorated by my having competed and trained hard (overtraining) for the high intensity (METs index of 6 to 12 cals/kg/hr) sport of Squash Rackets. The literature shows that this activity probably resulted in my cardiomyocytes being preconditioned to hypoxia resistance by a process known as ischemic preconditioning (IPC). This IPC can either last or be restored even after long periods of detraining. It also probably lowered the Risk Factors for Coronary Artery Disease (CAD) by 22 – 40% and so slowed down the buildup of plaque from CAD that was underway until the inevitable accumulation of plaques attained 95 – 99% blockage in 5 major coronary arteries as will be documented later. Together with the afore mentioned pressures this CAD inevitably led to the Heart Attack (Myocardial Infarction or MI) on the 25th of December 2014. But again, probably at a much later point in my life, and when it did occur, the MI was minor as ~98% of the (IPC) preconditioned cardiomyocytes survived. Only ~2% of the cardiomyocytes succumbed, as determined by Dr. Andrew Shanahan (using angiography and acoustic methods) and they probably succumbed to anoxia. This preconditioning induced hypoxia tolerance of cardiomyocytes also explains the inability of Cardiologists to detect cardiac malfunctions in Stress Tests over 10 years and so detect the developing CAD probably underlying my chest spasms. It is based on the proven retention of overtraining derived hypoxia tolerance even after a prolonged period of detraining (67). Another factor is the number of new cardiomyocytes born in periods of low or no training calculated from Retrospective Birth Dating (RBD) studies of Dr. Jonas Frisén and his colleagues (58, 59). RBD could have resulted in the maximal replacement of ~4.4% of cardiomyocytes leaving them susceptible hypoxia in the event that IPC was not transferred. However, an alternative explanation is also possible. Those ~2% of cardiomyocytes which succumbed could have done so because they were resident in a cardiac segment that lacked any blood and Oxygen (O2) supply and so were completely anoxic which results in lethality within 5 minutes.

(iii) After my second cup of coffee on Christmas morning, things started going South – but it was still nothing to cause panic! They were all routine digestive and neurophysiological symptoms that were handled before! For example by appropriate titrations of doses of medications and foods – or so I thought!

(iv) I started feeling nauseous, broke out in a cold sweat, vomited, became lightheaded and thought I was passing out, but lay down and recovered. And most differently of all, shortly before 8.00 am, now felt the pulsating beat below the sternum that Dr. Pong had warned me about staying alert. Somewhere along the way I realized that the Emergency Medical Services (EMS) of Princeton might be needed and so dialed: 911. As it turned out this decision ‘not to tough it’ was another one that probably saved my life!

(v) The Princeton EMS personnel were at my apartment in next to no time (about 8.15 – 8.20 am). I had recovered by then, and so could let them in. The Heart Attack, as would be confirmed later, from the time of detection of the Troponin T marker, had probably occurred in this time frame. They checked my vital signs (blood pressure, pulse, heart rate, temperature, etc..) and decided that I had to go into the Emergency Room – they suggested the University Medical Center of Princeton at Plainsboro (UMCP). It turned out to be a very good choice! The EMS personnel kept a close watch, and constantly engaged me in conversation while checking for the vital signs, every 1- 2 miles as we went north up highway US 206 which I knew well! I felt fine – but realized it was time to find a different less destructive distraction to the ‘EitR’!


(i)     We arrived around 8.50 am and by 9.00 am I was in the Emergency Room! With the Nurses and Dr. Shivani Sharma taking my recent and family History for the Charts, a technologist recorded my Electro Cardio Gram (ECG), and vital signs, a technologist drawing blood for the Pathology Lab for the quantification of Lipid Panels, Enzyme and Troponin T markers testing whether a Heart Attack had occurred. My charts show that I was placed on the usual combinations of Blood Thinners, Nitroglycerin paste, Protonix, Aspirin, Statins, etc.. to stabilize the condition resulting from a Heart Attack.

(ii)     Troponin T is a marker which is accepted as 100% diagnostic for a Heart Attack (Myocardial Infarction). Blood drawn at ~ 9.00 am did not show an elevation of this marker. This is not surprising as it takes 2 – 4 hours after onset of Chest Pains to be elevated to detectable levels in the bloodstream and then can lasts at elevated levels for 7 days (15, 18).

(narrative interrupted).

Supplemental Information Box: SIB – 2.

Reasons for the acceptance of Troponin T as a marker for Heart Attacks (Myocardial Infarctions) with near 100% confidence (15, 18).

(narrative resumed).

(iii)     The Electrocardiogram (ECG) traced at 10.40 am confirmed an irregularity. X-rays were taken. The Attending Physician listed on the charts was Dr. Ying – Kei Hui and the Head Physician of the Emergency Room was Dr. Eileen Daly. I was in good hands and most of my early interactions on the 25th of December were with Dr. Shivani, Dr. Daly and their supporting Nurses and Staff.

(iv)     The cell phone rang – my cousin Carl Engineer from San Francisco and his family, wife Dina, son Jehan, daughter Nisha and Son-in-Law (to be shortly), Chris Johnson, broke out in a Christmas Carol! Most of us are not religious, although I was raised in a Jesuit School and our family includes members from a multitude of religions, persuasions and nations, but we do know, as is obvious, a good time! And Christmas brought it whether we were in Bombay or London or New York or San Francisco! And I was not about to let on and ruin it – gaining the Nurses silence during the call! Particularly since over the last 10 years chest pains and stress tests had all turned out to be negative for cardiac mal-function ! By this point my thoughts had drifted back to the keyboard – TV worked as a distraction for about 10 minutes!

(v)     At 2.00 pm the batteries of Tests were administered again. This would soon become an hourly fixture and if anything multiplied in numbers and varieties over the next 3 weeks. The Troponin T level was now detectable at 0.11 ng/ml! Thus ending the ‘Willo-the-Wisp’ of the last 10 years and confirming that a Heart Attack had occurred! Based on the time of appearance of Troponin T, the MI may have been those pulsating spasms below the Sternum that occurred between 8.00 am and 9.00 am when I was still in the apartment! This result changed my life irreversibly! Dr. Daly came in and exclaimed ‘you see there is a method to our madness’ – obviously referring to the wait showing that the Troponin T finally rose to detectable levels as well as to my question about the period of time I would have to stay in the hospital.

(vi)     I was now moved up to the 3rd Floor in the Telemetry Wing for patients requiring either Cardiac Care or Intensive Care Units, fitted with a mobile Heart Rate Monitor which transmits signals that are recorded in a Central Station. The Monitor of the Central Station reports any loss of signal (e.g. wires coming loose from the patient or worse) and a Nurse corrects the problem immediately. The rigor was impressive!

(vii)     Dr. Daly came back took one look and said ‘look at you – cool as a cucumber’! What she could not have known, was that although I am not known to be slow, when it comes to these large, if not monumental events, I tend not to react, as there is not much to do that can change things! An example of a monumental event was represented by the time when I lived with my brother’s family 2 blocks away from the World Trade Center on 9/11 and we heard the first Plane [via Brooklyn fly over and into the North Tower, then waited, kept watch with those who had loved ones in the North Tower, until it collapsed and we had to run from the rush of debris!]. Also by this point, (and Dr. Daly could not have possibly known), my thoughts had positively drifted back to the keyboard – little did I know what lay ahead!

(viii)     Blood drawn at 9.00 pm showed that the Troponin T level further risen to 0.19 ng/ml which is considered high. On 12/27/2014 it had spiked at 0.47 ng/ml before gradually returning to 0.19 ng/ml and then to basal levels in responding to treatment.

(ix)     The Nurses were all in smart uniforms and I thought this was a Christmas Day informal uniform free day – until told with a smile, that it was a regular uniform! Through the night my vital signs were monitored, blood was drawn, medications administered and electronic records updated – like clockwork!

(x)     The next morning I had the pleasure of meeting Dr. Hui and Dr. Mahalingam who went about their usual responsibilities but were warm and empathetic while remaining professional. However, as soon as I asked Dr. Mahalingam about going home I was read the ‘Riot Act’ seemingly reserved for Coronary Patients – she might have been primed. Basically she explained how quickly even a mild Heart Attack, which is what I seem to have had, can turn into one like that which left a current occupant of the ICU hanging by a thread. And we were soon to find out exactly how right she was!

(xi)     It had been decided that a catheterization and angiography was now justifiable as it would reveal more information about the condition of the Heart and its Coronary blood vessels. Dr. Andrew Shanahan who was Dr. Mahalingam’s colleague at the Hospital and at Cardiology Associates of Princeton was the Cardiologist who would perform them at the facilities available at the Robert Wood Johnson University Hospital (RWJUH) Catheter Lab. I had the pleasure of meeting Dr. Shanahan on Saturday the 27th of December and we decided on being transferred (by Ambulance) to the RWJUH on the 29th of December for the procedure..


At this point we were still thinking in terms of a couple of Stents being inserted to relieve a couple of blocked coronary arteries. On the 29 th of December I had neither informed anyone in the family nor any of my friends of the impending tests. And expected to have the stents inserted, to recuperate at home and to inform them when it was safe to do so – long after recovery! The reasons for this will become clear soon! But things were about to change drastically – and although I am on the mend physically the progression of changes in perceptions, relationships and the future continues to evolve.

  1. Catheterization and angiography reveals a problem that is far more serious than we realized :

(i)     Transfer: I was transferred from the UMC Princeton to the core-2 facility in RWJUH in New Brunswick on the 29th of December 2015. The mobile Heart Rate Monitors were switched on and the transporting EMS personnel and ambulance from South Jersey used ‘Ambulance Humor’ because they thought it was needed, while the vital signs were constantly monitored even though they stayed stable! At the core-2 facility in RWJUH New Brunswick I was met by a very capable team of Nurses who carried out the standard procedures. They made me comfortable in every way, had me repeat my name, medical history, contacts, etc.., (to ensure that I was alert), recorded my vital signs, replaced the Intravenous (IV) connection in my arm with a new one, etc..

(ii)     What is cardiac catheterization followed by coronary angiography? In the cardiac catheterization procedure a catheter is inserted into the groin or arm and guided along the blood vessels of the torso to the heart and into the Coronary Arteries (21, 22). In the subsequent coronary angiography X-ray opaque dye is released from the terminus of the catheter and X-rays of the arteries and the heart are taken. The distribution of the dye reveals where blockages have occurred in the arteries (21, 22). Needless to say this requires expertise – manual skills and knowledge in Cardiology, both of which Dr. Shanahan was to reveal in spades.

(narrative interrupted).

Supplementary information box:(SIB-3) incorporated with (SIB-4)

Reasons for (a) relying on catheterization (angiography) in the diagnosis of the condition of the heart and as a cause of Heart Attacks (Myocardial Infarctions) (b) Angioplasty and (c) choice of ByPass Surgery versus Stent Insertion (Section on ByPass Surgery.

(narrative resumed).

(iii)     Catheterization and angiography: On the same evening, of the 29th of December 2015, I was prepared for catheterization and angiography by Dr. Shanahan’s Colleagues and a team. I was wheeled in on a gurney into a holding room until it was time. After depilation the Electro Cardio Gram (ECG) leads could be attached, sterility ensured and contact made.

(iv)     Catheter Lab: The team was waiting for me in the ‘Catheter Lab’ as it is known. Once again as the two most recent Operating Theaters that I had been in, tended to be packed with equipment, this lab was the opposite of the ones I remembered. Either from the last time I was in one around 40 years ago in Bombay or those from Hollywood. It was brightly lit, but sparse (due to miniaturization of electronics and to ensure sterility concerns?) with a high wattage overhead light and a camera/screen and a computer console next to the operating table. The room was really cold and they covered me with blankets that felt like they had just emerged from an oven (sterility considerations?). The areas for insertion of the catheter were further rinsed and shaved to ensure sterility.

(v)     Shanahan and his team: arrived and I was anesthetized!

(vi)     Shanahan finds a high level of blockage by CAD but a negligible level of cardiomyocyte cell death: I woke up groggily to find Dr. Shanahan pointing to the screen and explaining the extent of the mess! He pointed out that 5 major coronary arteries were massively blocked 95% – 99% with lipid plaque (but only ~2% cardiomyocytes had succumbed to cell death)! I was shocked – not realizing at the time that it could be a number of Risk Factors, rather than my behavior alone, that led to this condition. This was much worse than we had anticipated, with too many arteries involved for the safe insertion of stents. Furthermore, the potential for the deterioration of stents was much higher with greater numbers of stents. The alternative approach of ByPass Surgery was required and he had called the Surgeon for the confirmation of this judgement. It was to be a new Ball Game – called Open Heart Surgery, and I began preparing myself for it! They considered the situation ‘dangerous’ enough as per Dr. Shanahan, to warrant doing the ByPass as soon as the basic information (X-rays, MRIs, Sonograms, Blood work, etc…) could be collected and preparations (for the Operating Theater) completed. All the preparations and preliminary tests were immediately begun.

(vii)     Family notifications? At this point my main concern was whether I should keep this new development from my family. My brother Cyrus Nallaseth who lives in Mumbai, India, has serious health issues of his own, which makes travel hazardous to say the least! He also has primary responsibilities to a young family to consider – his wife and his sons! But should I inform him, I knew all this would not stop him from getting on the first available flight to New York any more than it did from New York to Mumbai when our mother was in the Intensive Care Unit after having had a massive Heart Attack.

(viii)      Dr. Shanahan makes the call: It was finally decided for me when Dr. Shanahan asked whether he could call any family members to let them know. I called my cousin in California (Carl Engineer) and then Cyrus to inform them and still got an earful! Never mind that Cardiologists over the last 10 years, could not have predicted this and until the catheterization and angiography results came in nobody could! And so he was on his way! In fact he had our good friend Mr. Mo Noori immediately drive up from Springfield, Virginia for Moral Support!! Mo, who had been a Radiologist, found me in the corridors while I was waiting to be wheeled into the X-ray suite.

(ix)     Pre Surgery Tests: Throughout the next few days I would go through batteries of tests, procedures and therapies in preparation for Surgery. Blood was drawn for various Pathology Lab Procedures (Lipid Panel, Blood Count, etc…), Doppler Sonograms, ECG, X rays, vital signs repeatedly and regularly taken. There were panels of medications and blood thinners that had to be administered regularly in addition to medications already in use prior to hospitalization and records to be entered. Again as at UMC Princeton, all the Residents, Physicians, Physicians Assistants, Nurses, Nurses Assistants, Technologists and Orderlies were thoroughly empathetic, skilled, dedicated and yet professional at whatever time of day or night that they interacted with me. They are all listed in the acknowledgements at the end of this article.

(x)      Dr. Shanahan met with me: was extremely generous with his time in explaining what was involved in ByPass Surgery and that it had a 98% success rate. We will see why this is an astounding success rate later!

(xi)     Dr. Michael Carlucci the Internal Medicine Practitioner: who assists Dr. George Batsides, the Cardiac Surgeon who would be carrying out the procedure, next stopped by several times to explain his role and procedures and tests that had to be completed before surgery.

2.     Open Heart Surgery – Preparations and Necessary Delays; Being Enveloped with the Healing Support of Care Givers, Family and Friends:

(i)     Dr. George Batsides and his Team stop by: On the 31st of December Dr. George Batsides and his team came to my room to meet me and explain the procedure, and re-confirmed that ByPass Surgery had a 98% success rate. The prediction is that the patient emerges from the Operating Theater, is held in the Intensive Care Unit (ICU) for 1 day and then in the general cardiac unit (core-2) of the wards for 5 days before being discharged. In fact because of variations in the vital signs (which may have been expected) it took a total of 9 days to be discharged on the 10th of January 2015 followed by a return after 1 day as a precautionary measure against significant variations of vital signs!

(ii)     The Handbook by Cardiac Coordinators & Nurses Rhonda Sabel and Jen Gopez (60): was extremely useful and outlined Pre and Post Operative Events, Precautions and Preparations in detail for the patient.

(iii)     Dr, Andrew Shanahan and Dr. George Batsides: Perhaps the most important and tangible source of strength and support came from the calm assured manner and concern of both Dr. Shanahan and Dr. Batsides that endured throughout the turmoil that was to follow. As a professional scientist this worked wonders for me!

(iv)     Warmth – circle of Family and Friends: Perhaps another of those most important if intangible sources of strength and support came from the very ones whom I had taken for granted over the years. It is something that as scientists, at least some of us forget, as it is not quantifiable. The presence of Family and Friends – it emanated a glow of warmth! Now I understood another reason beyond precaution, why Dr. Shanahan had asked to notify them. By this time phone calls, emails, cards and appearances from Family members and Life Long Friends (LLF) and/or Long Lost Friends (LLF) from all over the Planet had started pouring in! I had not had a chance to inform most of my colleagues and did not want any of them to feel excluded – or worse unaware of silent cardiac risks that we had uncovered and something of which they may have to be made aware! Although they were always on my mind there were those who had to persevere with penetrating the shell into which I had been placed by my work! Most were confused and shocked to hear the news! I was a good athlete and so they felt I should not have this happening while still others were consumed with worry about Open Heart Surgery as they may not have known of that 98% success rate that Dr. Batsides and Dr. Shanahan had shared. I’ve listed all of them because they all revived me! I had been transported from necessary isolation (and often outright alienation!) for good reason, into a state of warmth, inclusion and belonging! There were many! They were my (1) Nephews Soli Nallaseth, Zahan Nallaseth and my Sister-In-Law Simi Nallaseth, her Mother Sarla Gulati and (2) my cousin Dr. Zenobia Mehta from Bombay (Mumbai) India and daughter of Dr. Meherji P. Mehta, (3) my cousin Anita Jal from Mahableshwar, India (via Melbourne Australia and London, England), (4) my many Cousins and Aunts from London, including Mayerlene Engineer, who is very ill herself, Jessie Dhondy, Perin Martin and Laila and Martin Simpson, Rohin Jal and my cousins Firoza and Farida Cooper and my Aunt Zarine Cooper (whose husband Dr. Rusi Cooper (passed) and Ambassador/Solicitor Nanabhoy ‘Nani’ Palkhivala successfully challenged an stayed a decision by the Prime Minister thus upholding the Indian Constitution in the Supreme Court), and (5) all the Engineers, my cousin Susan and her husband Scott Sherman from California and (6) my Uncle Sarosh Dhondy and Fanny Lopera from Miami FL, (7) and of course Dr.Tehmi Mulla who along with her husband Dr. Dadi Mulla (who has passed) attended Medical School with my father Dr. Soli P. Nallaseth (the first of 3 generations of our family connections) and was deeply concerned! And her son Dr. Adil Mulla my Anesthesiologist/Medical Expert/Life Long Friend (LLF)/Fierce Competitor on the Courts, in the Pools and on the Velodrome or the Road/School Mate, from Warren and Danbury, Connecticut and his daughter Dr. Simone Mulla (JD) of Rutgers University in Newark along with (8) Professor Charles Heckscher my colleague from Rutgers, Squash partner, Coach of the Rutgers Squash Club and neighbor from Princeton and (9) Dr. Rustam Sethna and who came with his wife Katrin Glode-Sethna from Clinton, NJ and my brother’s LLF and my fast friends Mo Noori and Emma Dudang, from Springfield Virginia, (10) Anil Nayar from Miami, FL, a LLF and Squash Mentor and Partner, (11) Libby Case who with her husband both who are also LLF, Squash Students and team mates from Columbia SC from my student days at the University of South Carolina – Libby actually flew up to “bring a glass of water!”, (12) Professor Nawin Mishra who had served as the Chairman of my Dissertation Committee at the University of South Carolina and his wife Punam, called and spoke several times, (13) Cyrus’s Law firm partners Stanley and Maria Wallenstein (Stanley who is not well himself), Piraan Choga and Anil Jethmalani, whom I had got to know over the decades or years, either came or called, (14 )of course decades long friend Sheroy Ranji drove down from Manhatten, NY (15) and finally, Dr. Jeff Ceci with whom I was in Graduate School at USC, Columbia on the phone.

Many of them had emerged instantly and some emerged to recover relationships that had seen years of neglect! I was nestled in a warm glow for once – and not awaiting the Stiletto or the Whisper – with the impending Open Heart Surgery far removed from my thoughts!! It was tonic! I was already grateful, if not for being out of the woods, then certainly for the communion at which I had arrived with those who meant so much to me, and of whom, I had been able to think or think so little over the decades!

(v)     Scientific colleagues, Squash community, Social groups on LinkedIn, Twitter, ResearchGate, and other circles.: I still had to reach out to them! The thought being that disappearing from the Face of the Earth (although unlikely) without reaching out was impolite to say the least – regardless of the background! I had yet to deal with the thought of how easily a struggle to preserve a lifetime of work (again in the Public Interest), could have ended in the garbage if that minor Heart Attack had turned into an irretrievable one either leaving me incapacitated or worse. I had seen a colleague have a Stroke while – we were speaking – as well as the devastation of the after effects and so considered myself fortunate!

(vi)     Adil who is an Anesthesiologist trained at Yale University: had been through a similar life threatening medical situation a few years ago. Professionally he has seen many Open Heart Surgeries and had already inquired about my frame of mind. When I mentioned, that based on my experience (with the effects of the rubbing of enervated trabeculae between the metatarsal and tarsal of the big toe joint in my foot and resection surgery for a pilonidal sinus) I was steeled for the consequences of a motorized surgical saw splitting my sternum, he pointed out that things had changed! The new mesh/net sutures (and superimposed glue) would hold and immobilize the two halves of the sternum and drop the levels of pain that would otherwise come from the ‘rubbing’ of the edges of the enervated trabeculae. Along with the effect of the pain killers and advice by the Nurse’s to hold a pillow firmly to my chest when the inevitable coughing (from fluid filled lungs) or the retching (possibly due to a hyperactive Vagal Plexus (?) began, this turned out to be invaluable and prescient advice!

(vii)     My brother Cyrus Nallaseth was himself: and made me very glad that he had caught that flight to New York despite my exertions! He made sure that the Management at my apartment complex got things, that had been neglected, finally done, made arrangements for a, wonderful Helper at Home, Iris Amaya Castro whom I have got to depend on, arranged for a Visiting Nurse Service, a Rehab Clinic for me after discharge, worked on Health Insurance Extensions, Social Security and other Disability Benefits and generally waited on me hand and foot before and after surgery. I do not think I was ever so glad to see him as shortly after having emerged from Surgery in the Operating Theater and regained consciousness. I found myself in the Intensive Care Unit (ICU) lying on a low slung Gurney craving for a drink of water but unable to speak due to the effects of the anesthesia (60 – 62). I understand that he sent out Daily Bulletins on my condition to our Global Family and Friends.

(viii)     Libby, a LLF arrived from Columbia, SC: after I was moved to the Cardiac Rehab Clinic Libby arrived at a perfect time and spent a few days easing Cyrus’s load both at my apartment and at the Clinic. Libby was being Libby and also waited on me hand and foot! It was good to catch up! While here she called the Social Security Department, worked on Health and Apartment Benefits and set things up so as soon as I came out of the Rehab I could pick up the thread and fill in all the forms on and offline! As of submission the Wheels of Government and Nature are still turning!

(ix)     Mo Noori and Emma Dudang family friends – and a Nurse: who had also helped with my Aunt Firoza Jacobsen when she was in terminal stages of lung cancer in Miami, must have driven up from Springfield, Virginia after work, at least half a dozen times! They kept my brother and I company – as well as running many errands.

(x)     Surgery: Originally, due to the urgency of the situation, surgery was scheduled for the 31st of December. The exact length of time for the procedure itself would depend on the time taken to complete work on complications and the patient ahead of me in the Operating Theater but the total length of each surgery was estimated at 4 – 5 hours.

(xi)     Unforseen Barriers: However a series of complications in my health arose and surgery had to be postponed several times. It speaks to the professionalism of all the teams involved in leading up to to the Open Heart Surgical procedure that they worked with each other seamlessly! Despite the urgency of the situation, specifically in my thorax, all forward motion to surgery seized when a problem that would complicate the outcome, was detected and only resumed when it was solved! The Cardio-Thoracic Surgical Team stepped back and the appropriate replacement team e.g. Hematologists or Gastroenterologists required to solve the problem stepped up with all the teams working seamlessly with each other. The new team evaluated, quantified, analyzed and solved or classified the problem as non-disruptive, decisions were made and forward progress towards surgery resumed. Although they monitored me closely the urgency for surgery did not induce the slightest panic or rush to action in the Cardiac Team! And although I fully appreciated that the possible consequences of a misstep, might have been my life, this professionalism on their part was not only admirable but also deeply reassuring to me as the patient with a background in science!

(xii)     Problem 1: Enlarged liver and elevated liver enzyme activities. The function of the liver is to de-toxify the bloodstream. To clear persistent toenail fungus I had been on anti-fungizones (Fluconazole, Terbinafine) for around 18 months. These drugs are known to be filtered by the liver which therefore is affected, may have elevated its enzyme activities and size. This enlargement could possibly impede the flow rate of blood through the liver and to the heart creating problems during surgery. The alternative cause for enlargement, of alcohol consumption (less than 1 glass wine/day) was less likely and half a glass of wine per day is actually recommended by the American Heart Association. Half a glass of wine (30 gm) or less actually increases survival of CABG patients by 9% according to the AHA (25). Ultrasound measurements and Doppler Acoustic Sonography of the abdomen showed that the flow rate through the liver was not significantly impeded. We could now move forward. Dr. Pong had known and worried about this problem, we were trying to solve it before the Myocardial Infarction.

(xiii)     Problem 2: I was told that my complexion had become yellowish – did I have jaundice? The bilirubin levels were high. Again this was associated with the malfunctioning liver or gall bladder. However, ultrasound measurements and Doppler Acoustic Sonography of the abdomen showed that the flow rate of blood through the liver was not significantly impeded. It was concluded that a long past infection of Hepatitis B could have spontaneously raised and sustained the levels of bilirubin but it was not an impediment to surgery. We could now move forward.

(xiv)     Problem 3: Hemoglobin and the blood count was low. I was given 2 units of blood, the count was restored and we could now move forward.

(xv)     Problem 4: I had always had routine outbreaks of gout caused by crystals of uric acid deposited in joints, possibly breaking loose spontaneously and causing inflammation. Often, as on that occasion, for no apparent reason. Loose crystals could complicate surgery! A quick determination of uric acid levels showed only ~15% elevation. We could now move ahead.

(xvi)     Problem 5: the vital signs (blood pressure, heart rate and temperature) fluctuated fairly widely. It was decided that this was either a consequence of the Heart Attack or not serious enough to hold an urgent procedure where they would be stabilized manually and we could now move forward.

(xvii)     Still more preparation: involved identifying potential veins in the leg which were mapped for Endoscopy Vein Harvesting for CABG in the Endoscopy Lab (60 – 64).

(xviii)     Finally I was wheeled into the Pre Operating Theater: on the morning of the 2nd of January the Orderly wheeled the Gurney I was on into the Pre surgery Preparation Room. Along the way he lightened up the atmosphere by informing me that I had a high bar to match. Someone had gone through Open Heart Surgery and run a marathon only 10 days later!! Well I am not sure what to say – and neither could Dr. Shanahan! Although the whole ByPass Surgical experience was much less painful, if much more weakening than I anticipated (10 days after surgery I could barely sustain a conversation for 10 minutes without getting winded) I cannot imagine having walked let alone running a marathon 10 days after surgery!

3.     Open Heart Surgery – Pre Operating Theater Preparations and the Operating Theater on 01/02/2015:

(i)     In going through the insurance forms and Hospital charges the broad categories of procedures in the Operating Theater were identified and led to the list presented below (SIB -4). They are listed below in the narrative resumed in the Operating Theater

(There were approximately 25 Pre- and Post- Surgery Pathology Tests for Markers, in addition to Electrocardiographs (ECG), Sonograms, X-rays, Doppler and other tests resulting in the conclusion of “ACUTE MI SUBNNOCARDIAL INFARCT INIT EDC” and “RECOVERY” many of them given/measured multiple times/24 hour period. They reflected the extreme care given to me as the patient).

(ii)     The various types of Heart Surgery are well documented by NIH and by RWJUH (60 – 64). I was to be subjected to Pump Assisted Coronary Artery Bypass Grafting (CABG) pronounced like the vegetable or ‘cabbage’, i.e. the Heart is replaced by an artificial pump. As I would be unconscious during the procedure and so unaware of the steps, this is the description of CABG from NHLBI (NIH) website:

(narrative interrupted).

Supplementary information box (SIB) – 4:

(from the National Heart Lung Blood (National Institutes of Health) NHLB (NIH) website) (11, 60 – 62) :

What Is Coronary Artery Bypass Grafting?

Coronary artery bypass grafting (CABG) is a type of surgery that improves blood flow to the heart. Surgeons use CABG to treat people who have severe coronary heart disease (CHD).

CHD is a disease in which a waxy substance called plaque (plak) builds up inside the coronary arteries. These arteries supply oxygen-rich blood to your heart.

Over time, plaque can harden or rupture (break open). Hardened plaque narrows the coronary arteries and reduces the flow of oxygen-rich blood to the heart. This can cause chest pain or discomfort called angina (an-JI-nuh or AN-juh-nuh).

If the plaque ruptures, a blood clot can form on its surface. A large blood clot can mostly or completely block blood flow through a coronary artery. This is the most common cause of a heart attack. Over time, ruptured plaque also hardens and narrows the coronary arteries.

CABG is one treatment for CHD. During CABG, a healthy artery or vein from the body is connected, or grafted, to the blocked coronary artery. The grafted artery or vein bypasses (that is, goes around) the blocked portion of the coronary artery. This creates a new path for oxygen-rich blood to flow to the heart muscle.

Surgeons can bypass multiple coronary arteries during one surgery.

Coronary Artery Bypass Grafting


Figure 1. Coronary Artery Bypass Grafting. Figure A shows the location of the heart. Figure B shows how vein and artery bypass grafts are attached to the heart. Note: Arrows in Figure B show the direction of blood flow.


CABG is the most common type of open-heart surgery in the United States. Doctors called cardiothoracic (KAR-de-o-tho-RAS-ik) surgeons do this surgery.

However, CABG isn’t the only treatment for CHD. Other treatment options include lifestyle changes, medicines, and a procedure called coronary angioplasty (AN-jee-oh-plas-tee).

Angioplasty is a nonsurgical procedure that opens blocked or narrow coronary arteries. During angioplasty, a stent might be placed in a coronary artery to help keep it open. A stent is a small mesh tube that supports the inner artery wall.

CABG or angioplasty may be options if you have severe blockages in your large coronary arteries, especially if your heart’s pumping action has already grown weak.

CABG also may be an option if you have blockages in the heart that can’t be treated with angioplasty. In this situation, CABG may work better than other types of treatment.

The goals of CABG may include:

  • Improving your quality of life and reducing angina and other CHD symptoms
  • Allowing you to resume a more active lifestyle
  • Improving the pumping action of your heart if it has been damaged by a heart attack
  • Lowering the risk of a heart attack (in some patients, such as those who have diabetes)
  • Improving your chance of survival


The results of CABG usually are excellent. The surgery improves or completely relieves angina symptoms in most patients. Although symptoms can recur, many people remain symptom-free for as long as 10 to 15 years. CABG also may lower your risk of having a heart attack and help you live longer.

You may need repeat surgery if blockages form in the grafted arteries or veins or in arteries that weren’t blocked before. Taking medicines and making lifestyle changes as your doctor recommends can lower the risk of a graft becoming blocked.

(narrative resumed).

The Operating Theater:

(iii)     The nurses depilated the chest, checked the IV and injected a blood thinner. A local anesthetic was administered and the catheter with sensors inserted through the neck into my heart to monitor its vital signs in real time. The steps to be taken by the Cardiac Surgeon, some, while I was under anesthesia:

(a) Anesthesia CABG with Pump

(b) Insertion catheter, Artery

(c) Insert/Place Heart Catheter

(d) Echo Transeosophageal

(e) Doppler Echo Exam, Heart

(f) Doppler Color Flow Add-On

(iv)     The Operating Theater looked like a more (or better?) equipped version of the catheter/angiography lab. However, compared either to the version in the Movies or the ones I remember in India when I was the patient and operated on by an Uncle, Dr. Meherji P. Mehta, this one was sparse. Possibly to preserve sterility. Dr. Mehta was a pioneering Cardiac Surgeon who performed the 4th Ventricular Septum Reconstruction as well as some of the first Heart Transplants in the History of Cardiac Surgery at the K.E.M. Hospital in Mumbai (65, 66). He was also a contemporary of the renowned Pioneer of Cardiac Surgery Dr. Michael DeBakey with whom he exchanged Surgical visits. Although Dr. Mehta secured his F.R.C.S. degree in the UK his specialized training in Cardiothoracic Surgery was received at the Christian Medical Center in Vellore (C.M.C.V.) directed by Dr. Reeve Betts. This was one of the 3 Major Cardiac Centers established in India by British Surgeons who had mastered their craft in the Theater of the North African Desert in the Second World War (65, 66). Ironically Dr. Mehta, like my father (his step brother) Dr. Soli P. Nallaseth succumbed to Heart Attacks or Ventricular Fibrillations in their mid to late fifties. All of us in our immediate and several others in our more distant family either succumbed to or had Heart Attacks or Fibrillations when relatively young. However, in each case overwhelming additional factors complicated any simple interpretation of family history or a genetic cause (65, 66).

(v)     My brother was designated as the responsible relative to whom reports would be delivered and along with Mo waited outside the Operating Theater over the 4-5 hours of surgery.

(vi)     Dr. Batsides reassured me that his assistants ‘really knew their work’! But I had no doubt especially since everything the Surgical Team had done up till then was convincingly efficient, diligent and professional. I was as relaxed and accepting, as one can be under those circumstances, for the simple reason that I would have liked to live a little longer!

(vii)     I remember feeling some blood trickling down my neck from the ‘In Heart ‘ catheter and their fixing it in short order with a few stiches.

(viii)     Shortly after this the anesthetic was administered, I blacked out and assume that the CABG procedure described in (SIB-4) from the NHLBI (NIH) website began.

(ix)     I awoke on a low slung gurney in a line of gurneys in what presumably was the Intensive Care Unit (ICU). It was painted bright white with Nurses, Assistant Nurses. Technologists in white and urgent, purposeful but unhurried movements. There is a good description in NHLB – NIH outline of CABG in (SIB-4).

(x)     My throat was parched and when I tried speaking, no sound emerged, due to the effect of the anesthetics! So I could not get the drink of water that I desperately needed.

(xi)     My brother Cyrus was allowed into the ICU – I had that water soon. I don’t think I’ve ever been so glad to see him! And soon enough realized it was going to be a tough few days to normalcy.

(xii)     I was re-attached to a mobile Cardiac Monitor and intravenous IV feed and moved to the core-2 facility (Cardiac Wards) the next day.

(xiii)     The impression of the whole CABG process and its aftermath that lingers in my mind is not one of excruciating pain, but certainly one of labored attempts to move, resulting in acute discomfort, even sitting was difficult and conversations led to being easily winded within minutes! This low consequence was probably due to the excellent surgery and the thorough immobilization of the incision along the sternum, the pain killers and nursing all of which were excellent! Food did not seem at all appetizing – partly because of the fear of unleashing a ‘retching’ episode. One attempt, in that first 10 day period, at a Walker Assisted walk around the core-2 ward sent my blood pressure soaring! So walks were suspended!

(xiv)     Here too the Nurses, Nursing Assistants and Technical Staff taught me little tricks like building up my strength by sitting, rather than the more easily done, lying in the bed. One of the pieces of equipment used to ease the congestion in the lungs and keep them functional was the Spirometer – breathing into it to elevate the indicator, maximally without overshooting an easily overshot mark – 10x/day. The Nurses were insistent but in the only resistance I gave them, I found the Spirometer to be a waste of time – needless to say I was wrong!

(xv)     Dr. Amy Tilara, among others from Dr. Batsides group, checked my condition every day before and after surgery, e.g. making notes on the records of the vital signs. Dr. Tilara was also the ‘Enforcer of Spirometer Use’ and fairly dogged in extracting an accounting! She was also the one to deliver the message related to the 2nd discharge after I had been brought back from the Foothill Acres Rehab Center when the vital signs fluctuated again.

(xvi)     I was looked after and monitored closely in core-2, from the recording of vital signs to any of the ablutions and to the slightest need all of which were responded to when the buzzer brought them to my bedside. This besides their doing such things as recording ECGs with portable machines, administering medications at regular intervals at all times of the day and night.

(xvii)     I have never felt so dependent! Something that is anathema to me! Probably because of my professional experience!

(xviii)     The vital signs, particularly my temperature and blood pressure fluctuated sufficiently to cause some concern for the next 2 weeks. But considering the magnitude of the impact that the CABG procedure had to have on the body perhaps this was not entirely surprising.

(narrative interrupted).

Supplementary Information Box (SIB) – 5

What to expect in the ICU, the day after surgery, the second day after surgery, Recovery at home (60 – 62)


bcc5-985e7c77587e#.VVDybvDe-VN    (copy and paste into your browser)

(narrative resumed).


(i) Discharge from RWJUH core-2 on the 10th of January 2015 was administered by Dr. Leonard Lee, who was the Chief of Cardiac Surgery, and stopped by to check the scar and by Nurse Kelly Mayer-Delgado. Nurse Mayer-Delgado had spent time with and shown me several ways of managing the everyday problems that follow Bypass Surgery throughout my stay in the core-2 facility. She got me to stand for Dr. Lee without wobbling too much!

(ii) Dr. Lee caught sight of my Squash Bag (now serving as a garment bag) and that led to an exchange of some pleasantries about our mutual interests in the game, a friend and fellow Coach Geoff Mitchell from a Club (the Chatham Club) at which we had spent many years playing Squash (and I sometimes still do).

(iii) I was then prepared for the ambulance and transported to the Foothill Acres Rehab Clinic (FARC) for cardiac rehabilitation.

(iv) Little did I know that I would be returning to RWJUH the next day. The vital signs (blood pressure, heart rate, pulse and temperature) were high or fluctuated and a vigilant Nurse and Physician wanted the immediate results of a possible infection with microbial assays that were available at RWJUH but not at FARC.

(v) I was returned to the Emergency Room at RWJUH, with the vital signs elevated. Then tested for infections, other sources of problems, and while the vital signs stayed elevated.

(vi)I was kept under observation overnight. After Dr. Batsides’ and his Staff concluded this was normal given the magnitude of the impact that the surgical procedure would have had Dr. Tilara communicated the message and I was returned to the FARC Rehab Center the next day.

(vii)The Foothill Acres Rehab Center as its name implies imposed a regimen of a good diet, monitoring of the vital signs, good regimens for medications, therapies and physiotherapy. Which may explain the rapid recovery of patients.

(viii) One of my Room Mates at Foothills was an Engineer – Vincent Barone. Our conversations were entertaining.

(ix) On the 4th of February 2015 I had a long overdue follow-up visit with Dr. Batside’s Colleague and the Cardiothoracic Surgery Clinical Coordinator Rhonda Sabel RN.C.BSN. and was given permission for Discharge from the Rehab Clinic.

(x)By now I had started using my laptop and learned the sad news that my good friend Princeton Squash Coach Bob Callahan had finally fallen to the glioblastoma that he had resisted for 3 years on the 27th of January 2015! More than twice the mean time that other patients with this dread disease survive!

(xi) Players from the Rutgers Squash Club organized a memorial posting for Bob on the online journal Daily Squash Report and the social medium LinkedIn.

(xii) In thinking of the events of that past month I realized that my colleagues, mentors and friends in Squash at all the courts, in Science, at the New York Academy of Sciences, the Society for Developmental Biology, other Universities, Institutions, on Social Media like LinkedIn and ResearchGate among other places would want to know of the recent events and its strange biomedical contradictions! And so I sent out emails or posted the news on Social Sites and received nearly 300 deeply concerned, warm, supportive and encouraging replies!

(xiii) By the 30th of January 2015 I had been walking without a walker!!

(xiv) By the middle of that week of 4th of February 2015 I was climbing 78 steps on the FARC staircase which was equal to twice the numbers of stairs present at home, in addition to Physiotherapy administered by the expert Therapists of Foothills Acre Rehab Clinic.

(xv )By the end of that week, 6th of February 2015 I thanked the entire staff and personnel who had got me back up on my feet again and left. Iris brought me home.

(xvi) It was clean – Cyrus, Iris and Libby had done all the work!!

(xvii) I was still too unsteady to do much.

(xviii) On the 28th of February I could finally drive and make the overdue follow-up visit with Cardiologist Dr. Shanahan.

(xix) He put me through the necessary Stress Test on the 13th of March 2015.

(xx) I was cleared for cardiac physiotherapy at the University Medical Center of Princeton and made arrangements – but Squash and the Apartment Gym were  excluded for 6 months.

(xxi) I have now been writing regularly since 3.3.2015.

(narrative interrupted).

Supplementary Information Box (SIB) – 6 (62)

Cardiac Rehabilitation

During the recovery period, you may begin participation in a cardiac rehabilitation program, if prescribed by your physician. You may begin cardiac “rehab” while you are still in the hospital and continue it in the months moving forward. Cardiac rehab is, in part, a structured exercise program that can help you increase your physical activity level while under the direct supervision of medical professionals. The program also includes work with dieticians, occupational therapists, psychologists, and other healthcare providers who can help you recover from your surgery and feel confident that you have the skills to adopt a heart-healthy lifestyle. Regaining physical strength and eating a diet of nutrient-rich foods are critical to a successful recovery from coronary bypass surgery and to returning to the lifestyle you want to live. Studies have shown that cardiac rehab is more than just a good idea. It can be a lifesaver. Recent research has found that patients who complete cardiac rehab are more likely to be alive five years after a heart event than those who do not.

(narrative resumed).

(F)  A series of questions and issues related to my heart attack or MI arise that are addressed below.

  • As discussed the two types of traumatic cardiac pathologies resulting from either the deprivation or the complete cutoff of the supplies of blood flow and so O2 by plaques or fibrillation (fluttering heart muscles), respectively cause Myocardial Infarctions (Heart Attacks) and Sudden Cardiac Arrest (SCA) or Sudden Death (SD) (20, 23 – 27, 30). The Risk Factors for these 2 types of pathologies have also been discussed briefly but are dealt with in greater detail in the supplementary information box (SIB-7) and in even greater detail by multiple health agencies (8 – 27). As is clear from the above references cardiac diseases are considered to be multifactorial (genetic, environmental, behavioral, among other factors). It is useful to now specifically focus on the 5 principle elements of the cardiac event of 12.25.2914      (1) Risk Factors and the role of exercise in modifying or ameliorating them,(2) Squash ameliorates the Risk Factors as shown by results from recent studies that are in depth and so subsume contradicting results of older studies,(3) New research results support the interpretation that the intense competitive and exercise routine that I maintained in India, (high level overtraining) delivered conditioning that was at least partially retained in the US until 2006 and 2007,(4) This conditioning likely delayed the ongoing coronary artery disease (CAD) and the ongoing coronary heart disease (CHD), (5) Ameliorated the impact of a Heart Attack by preconditioning (IPC) cardiomyocytes.

The relevant literature, albeit selected, that will be drawn on, is listed in the (SIB-7). However a significantly more detailed version of the discussion of these events and the relevant literature on Sports Physiology and Clinical implications will be submitted to the appropriate Journal (1).

  • Salient and relevant features in the reconstruction of events from diagnosis and intervention to recovery, from: questions, medical reports and extrapolations of the literature:

 To summarize the details, the salient features of the cardiac events in my thorax culminating in the Coronary Artery Bypass Graft (CABG) Surgery and into ongoing recovery, as determined by (i) Cardiologist Dr. Andrew Shanahan, (ii) Cardiac Surgeon Dr. George Batsides, (iii) their teams, (iv) extrapolated from the literature, (v) those factors that remain unknown are enumerated as 1-14 below. The questions raised and possible reasons for survival are also considered.

(1)     Need for Oxygen: As it is indispensable as a terminal terminal e-1 acceptor required for generating molecules of ATP, the high energy vehicle which is required for most cellular functions, Oxygen is of fundamental importance to the survival of the vast majority of living organisms. The importance of Oxygen to the function and survival of cardiomyocytes and the heart has already been established in this article (SIB – 1).

(2)     Sequence of events leading to, and reasons for, the CAD and MI: As mentioned, in the 10 years from around 2005 to 2014, I had multiple chest spasms, underwent multiple tests of increasing rigor, for detecting cardiac malfunction, and in more than one institution. All of which had failed to implicate cardiac malfunction as the cause of my chest pains. Although there are several possible reasons for this interpretation: (a) the accumulated plaque in arteries (due to CAD), known to occur over decades, was likely already present during those Stress Tests but went undetected, (b) detection of cardiac mal-function or blood flow and so O2 supply in these Stress (and other) Tests are revealed by cardiac electrical (Electrocardiographs , ECG) perturbations of the discharge by cardiomyocytes which is caused by exercise dependent hypoxia (O2 deficits) and detected by (ECGs). These cardiomyocytes were not perturbed and so failed to reveal cardiac mal-function, (c) they were probably not perturbed because the cardiomyocytes were hypoxia tolerant, due to their overtraining based ischemic preconditioning (IPC) resulting from training for Squash, (d) this inference was supported by the necessity for having to elevate the Treadmill Settings (stress) 3x above normal settings for Stress Tests before hypoxia driven stress on the ECG, even registered, (e) this despite the likely hypoxia caused by the plaque ridden vessels (CAD) in addition to that caused by the Stress Tests, (f) Stress Tests are among those widely applied as a first line of investigation, but often may fail to detect cardiac malfunctions, as may have been so in my case, (g) however this explanation is the unlikely choice between known effects (IPC, 3x elevation of Treadmill settings) and a hypothetical premise (rate of failure of stress tests), (h) or alternatively significant blockage of coronary arteries (by CAD) and the resultant hypoxia may have set in relatively recently and rapidly (after the 30th of April 2010, which was the date of the most recent comprehensive cardiac tests) and (i) this explanation is also unlikely as an asintotic elevation of CAD is not commonly known.

(3)     Time course for plaque formation: The period of time that the plaque dramatically reduced or blocked, blood flow in 5 major coronary arteries, and so the Oxygen that they delivered to the cardiac tissues to induce hypoxia in cardiomyocytes, cannot be determined. The rate of deposition of plaques to attain a final blockage of 95% – 99% in 5 major coronary arteries is unknown. This level ranged from near complete 95% (hypoxia) and approached complete deprivation 99% (anoxia) of blood flow and oxygen delivery to cardiomyocytes, (personal communication from Dr. Shanahan and his Medical Report) is a condition which is likely to be lethal within 5 minutes.

(4)     How many cardiomyocytes succumbed? Yet only ~2% of cardiomyocytes were irreversibly dead as determined by Acoustic measurements during catheterization and angiography (personal communication by the performing Cardiologist Dr. Andrew J. Shanahan and Nurse Rhonda Sabel). They were presumably lost to apoptosis caused by anoxic conditions.

(5)     Why was there such a large disparity (~ 50x) between blockage of coronary arteries by plaques and cardiomyocyte cell death? Why were only ~2% of cardiomyocytes lost to cell death when the blockage of 5 major coronary (blood) vessels amounted to 95% – 99% with its corresponding reduction of blood, and so Oxygen, supplies? Although based on Retrospective Birth Dating (RBD) of cardiomyocytes, ~95.6% of cardiomyocytes could be expected to be resistant to hypoxia due to overtraining and IPC they would not be resistant to anoxia which is lethal within 5 minutes. This is shown experimentally as well as by the results of Atrial or Ventricular Fibrillations (fluttering heart muscles leading to a cutoff of blood and O2). It is possible that the ~2% of cardiomyocytes that succumbed were located in a cardiac segment that was anoxic.

(6)     What is the window of time between plaque deposition to complete arterial blockage and new blood vessel formation to relieve the pressures of hypoxia but not anoxia? It is known that new coronary blood vessel formation is induced as a compensatory response to hypoxia resulting from the blockage of coronary arteries by plaques through processes called angiogenesis or vasculogenesis (37). Their growth is stimulated by vasculogenesis endothelial growth factor (VEGF) and GATA nucleotide sequence binding protein, binds nucleotides (GATA 1-6), among other factors (37). However, fragments of plaques are broken off walls of blood vessels, either form dangerous and circulating clots or travel to new sites, where they are deposited and form nucleation foci for new deposits at rapid rates (SIB-4, NHLB(NIH). We neither know how quickly the plaque was deposited to block the blood vessels nor how quickly induction and new blood vessel formation occurred. But there must have been a window of time between, plaque deposition upto near complete blockage and the formation of new blood vessels vessel induced by VEGF, in which hypoxia had not yet progressed to anoxia. The length of this window of time that was sufficient to allow cardiomyocytes to survive is unknowable. However ~2% of cardiomyocytes did succumb to cell death and so there is evidence for this window having closed. This cell death (~2% cardiomyocytes) was either due to their location in a cardiac segment that was anoxic or due to an incomplete transfer of hypoxia (apoptosis) resistance from hypoxia resistant nuclei to newly born cardiomyocytes as is shown to occur in myonuclei (67). These new cardiomyocytes were likely born in the ~7 years after 2006/2007 the last 2 years of my low level overtraining for Squash in the US.

(7) (a)  How much hypoxia can cardiomyocytes tolerate and for how long do they do so in order to be able to resist cell death (apoptosis)? (b) How much anoxia can cardiomyocytes tolerate and for how long to be able to resist cell death (apoptosis)? The answer to both is unknowable without experiments. But the answer to (a) is complicated while the answer to (b) is the 5 minute period (maximally) and 10 minutes (survival with irreparable cardiac and neuronal damage) that emerges from Sudden Cardiac Arrest (SCA) or Sudden Cardiac Death (SCD) reports in the literature (SIB- 4, NHLB(NIH).

(8)     How long and how much did ischemic preconditioning (IPC) contributed to the observed disparity between coronary artery blockage (95-99%) and cardiomyocyte cell death (~2%)? A further complication arises from applying interpretations of results from experimental mammalian systems (mouse and rat) to humans. In rodents it has been shown that an initial and transient application of hypoxia (e.g. for 20 minutes) induces a state of tolerance (resistance) to subsequent prolonged challenges of hypoxia even 72 hours after transient exposure. This is known as ischemic pre-conditioning (IPC) and molecules either encoded by genes such as Akt, JAK-STAT, Bcl2, VEGF, GATA 1-6 BF, p38 kinase, HIF1, EPAS1, or hormones Estrogen or the signaling molecule NOX2, and the anti-inflammatory drug Sulindac all contribute to this effect through known pathways and mechanisms (36 – 51). Although overtraining dependent ischemic preconditioning (IPC) pre-conditioning in Squash probably facilitated survival of cardiomyocytes during the Heart Attack (MI) ~ 2% cardiomyocytes succumbed probably to anoxia. Some questions that follow. What was the distribution of blocked and new coronary (blood) vessels over the heart and did it supply the segment of the cardiac tissue spanning those ~2% cardiomyocytes that succumbed? What was the contribution of IPC in the blocked and supplied cardiac segments of cardiomyocytes? How long after this window of time between complete blockage and supply of new vascular vessels to populations of cardiomyocytes closed did they survive? These questions are unanswerable!

(9)     How many Cardiomyocytes were born after low level overtraining had ceased in 2006/2007? And were they resistant to hypoxia and apoptosis? Jonas Frisén, and his colleagues have innovated a method called retrospective birth dating (RBD) which measures the replicative loss of atmospheric residual 14C radioisotope with long half-life of 5,730±40 years, released from surface atomic tests and incorporated into our genomic DNA, by alterrations in 14C:12C ratios of tissues (58, 59). They used RBD to show that approximately 50% of cardiomyocytes were replaced in a human lifetime (58, 59). Based on this estimate and an average Life Span of 80 years the calculated number of newly formed cardiomyocytes in my heart since 2006/2007 (~7 years) is ~4.4% new cells. Can this number be used to calculate the numbers of cardiomyocytes that were ‘born’ after the cessation of low intensity overtraining (strenuous workouts) and hypoxic conditioning? These new cardiomyocytes (~4.4%) were not exposed to low intensity overtraining and despite predictions (67) may not have been equivalent to the ~95.6% of cardiomyocytes that were exposed to low intensity overtraining 7 years ago (in previous workouts) and so may not be preconditioned by IPC to resist hypoxia (67). Alternatively, either the transfer of resistance from the old hypoxia/apoptosis resistant templates was only partially complete in ~2% of cardiomyocytes, or they were resident in a segment of cardiac segment that was only partially vascularized nearly devoid of blood flow and so O2 thus becaming nearly completely anoxic. These questions are unanswerable.

(10)     Could high intensity overtraining for Squash which is a high intensity sport (METs index = 6 – 12 cals/kg/hr) in India 38 years ago (since 1976) have conferred IPC that was retained and so contributed to the survival of my cardiomyocytes in 2014? Could hypoxia resistance result from low intensity overtraining in the US (upto 2006/2007) and have lasted for ~7 years after nearly detraining (2006/2007 to 2014)? From experimental work done in rats it is known that skeletal muscle myocytes following strenuous training (overtraining) gain in numbers and sizes of myonuclei which results in hypoxia (and apoptosis) resistance (67). This increase in numbers and sizes of myonuclei correlates with hypoxia resistance and is retained after at least 3 months of detraining (67). After detraining these trained myonuclei remain resistant to hypoxia and apoptosis, and may serve as templates for the synthesis of new hypoxia and apoptosis resistant nuclei and are likely to extend conditioning into old age (67). This last observation is common knowledge among athletes! Based on several physical and physiological parameters of estimation (4), I had overtrained for Squash at a significantly higher intensity (or high intensity overtraining) more than 38 years ago in India until having arrived in the US in 1976. Based on the calculations in question 9, this would yield 23.8% of newly born cardiomyocytes since 1976 in the US, that were not exposed to the same high intensity overtraining. The intensity of overtraining in the US varied from low level overtraining to detraining (none) for Squash tournaments which would leave at least 23.8% of newly born cardiomyocytes either resistant or sensitive to hypoxia and apoptosis. This depends on whether this level of overtraining in the US was sufficient to induce hypoxia/apoptosis resistance. If sufficient does it explain the retention of hypoxia resistant conditioning over the 7-8 years since 2006/2007 when even the lower (US based) level of overtraining ceased? And are the ~2% cardiomyocytes that were not resistant among the calculated cardiomyocytes (~4.4%) that were ‘born’ in this period? Were these ~2% cardiomyocytes either (i) not exposed to sufficient overtraining and so endowed with low levels of hypoxia resistance or (ii) actually detrained or (iii) had they failed to acquire any resistance from hypoxia and apoptosis resistant nuclear templates or (iv) were they resident in a segment of cardiac tissue that was devoid of blood flow and O2 and so completely anoxic thus so succumbing to cell death? These are unanswerable questions.

(11)     Can cardiomyocytes survive anoxia? How many cardiomyocytes must be lost to apoptotic death to result in Sudden Cardiac Arrest (SCA) or Sudden Death (SD) fatality rather than Myocardial Infarction (MI) or Heart Attack ?

Cardiomyocytes may survive anoxia for more than 5 minutes but the damage is irreparable and after 10 minutes anoxia is invariably lethal. Finally there is a threshold of cardiomyocyte cell death that must be attained for the Myocardial Infarction to become irreversible. Why and What is that number? In Sudden Death (SD) or Sudden Cardiac Arrest (SCA) syndromes it is known that the entire Atrium or Ventricle fibrillates (flutters due to uncoordinated electrical discharges required for contraction) and so blood supply and Oxygen are cut-off. And lethality results in as little as 5 minutes This shows that inactivity of either of these 2 chambers is sufficient to prove fatal.

(narrative interrupted).

Supplementary Information box (sib) # 7:


(SIB-7A) Well established Risk Factors and reporting organizations.

(SIB-7B) Establishing Risk Factors by controlled Genome Wide Association Studies (GWAS).

(SIB-7C) Significant numbers of cardiomyocytes are replaced (~50%) in a lifetime.

(SIB-7D) Known cellular and molecular mechanisms for coping with cardiac stress and protecting hypoxic cardiomyoctes.

(SIB-7E) Preliminary results – Ongoing Discoveries, Identification of Potential New Risk Factors & Modifiers of Risk In Cardiac Disease States.

(SIB-7F) Exercise and Squash – optimal health to injury ratios, modification of Risk Factors for and induction of, Coronary Heart Disease (CHD), Coronary Artery Disease (CAD), Coronary Vein Disease (CVD) and Sudden Cardiac Arrest (SCA).


Review of the salient points of the relevant literature in each of the 6 categories listed in the Supplementary Information Box (SIB) -7:

To enable a meaningful discussion of the events of the MI I had, requires a minimal discussion of the last 15 years of methods and analyses that have turned multifactorial traits or pathologies, that were previously intractable to analytical resolution into those that can be resolved. These include Cardiology, Sports Medicine and Physiology, Molecular and Cellular Biology of Cardiac functions, and their interrelated dimensions such as Risk Factors and Intensity/Vigor of Sports Activities. Most have been exhaustively treated in each of the references. These references are restricted to those listed and their links in (SIB – 7A to 7F).

(SIB-7A) Risk Factors: The definition of Risk Factors, their types and numbers for the various Coronary diseases and Sudden Cardiac Arrest have been briefly outlined and are discussed in the links distributed in each of the categories (some with overlapping functions and definitions) in (SIB-7A to 7F). There are those Risk Factors that can be ameliorated by altering life styles, diet, weight, exercise, etc… and those that cannot be ameliorated such as incidences of Arterial Fibrillation, Gender, Age, Family Backgrounds (Genetics?), etc… Those Risk Factors provided by the National Heart Lung and Blood Institute (NHLBI) of the National Institutes of Health (NIH) section (11). However several other Risk Factors have been identified by a number of other methods and organizations e.g. (NHS (UK) and WebMD) have been listed (18, 19). Organizations such as those listed on Wikipedia not only include the standard definitions but also their pathophysiology (8 – 27). The Centers for Disease Control (8) classifies Risk Factors into 3 major categories (Conditions, Behavior and Heredity), the National Library of Medicine (9) categorizes 17 distinct Risk Factors into 2 major groups of those that (a) cannot be changed and (b) can be changed. The former group (a) also depends on excluding negative behaviors (smoking, foods raising levels of cholesterol, not exercising, alcohol consumption above moderate levels, etc..) and cultivating positive proactive (controlling diet, eating nuts, vegetables and fruits, lean meats, non-hydrogenated foods) behaviors (9). These are dealt with in detail via the links to these and other websites of other Public Service Organizations (8 – 23).

However, application of genetics (e.g. Genome Wide Association Studies (GWAS) has not only reduced the frequency of errors but also marginalized the uncertainties of the highly multifactorial field of cardiology so as to reinforce its parameters e.g. Risk Factors but has also gone far beyond. It has revealed new and surprising information on sources of Risk Factors and how they may either be exacerbated or ameliorated in ongoing research and unfolding discoveries. GWAS in the analyses of cardiac conditions (e.g. Risk Factors) and the influence of Sports Physiology on these conditions will be discussed in greater detail in a Journal concentrating on Sports Physiology or Sports and Clinical Medicine (1).

(SIB-7B, -7F) Well defined and improved contemporary approaches including combinations, such as Genome Wide Association Studies (GWAS), high numbers of reporter alleles (SNPs), Large Cohort Sizes, ranges of Metabolic Equivalent Task indices (METs), known and controlled quotients of stress and Personal Record Maintenance (PRM) have significantly elevated the reliability of measuring Risk Factors for Cardiac Heart Disease (CHD), Cardiac Arterial Disease (CAD), Cardiac Vein Disease (CVD), Sudden Cardiac Death (SCD) or Sudden Cardiac Arrest (SCA).

The large numbers of environmental, genetic, developmental, behavioral, dietary, emotional and other factors that contribute to Cardiac Heart Disease (CHD), Cardiac Arterial Disease (CAD), Cardiac Vein Disease (CVD), Sudden (Cardiac) Death (SD) or Sudden Cardiac Arrest (SCA), represent the multiple contributing Risk Factors. Making the evaluation of their contributions to these pathological conditions multifactorial and highly error prone, subjective and complicated (SIB-7A to SIB-7F) see references 8 – 96). To firmly establish these Risk Factors or for that matter any other dimensions of these diseases requires the robust analytical methods which have emerged in the last ~15 years. Most significant of these analytical developments are the combinatorial application of: (i) Genome Wide Association Studies (GWAS), (ii) with higher distributions and numbers of small nucleotide polymorphic SNPs/genome equivalent (upto 1.6 x106 SNPs) as reporter sequences, (iii) newer complementary robust statistical and analytical methods such as large Cohort Sizes (6000 to 215,413) elevating resolution of quantified dimensions,(iv) measurements of physiological parameters such as well-established Metabolic Equivalence Task Indices (METs) (a wide range of METs from a low of 2 to a high of 16 cals/kg/hr), (v) a range of known and controlled quotients of stress delivered by sports such as Walking, Racket Sports, Boxing and Marathon and (vi) Personal Record Maintenance (PRM) with high correlation factors to e.g. METs (0.6) which together significantly elevate the resolution and reliability or confidence intervals in measuring Risk Factors for the above pathologies.

What is GWAS? Also known as Whole Genome Analyses (GWA) or Common-Variant Association Study (CVAS) it is an epidemiological method examining large numbers of Variables including genes or short strings of reporter genetic code letter words called Small Nucleotide Polymorphisms (SNPs) and Clinical conditions to establish a clear associative relation between the two parameters (68).

The significance of this GWAS based studies (76 – 79, 81) and 2 studies predating GWAS (80, 82) will become clear in the interpretation of the role of Squash, high intensity overtraining exercise resulting in IPC and the hypoxia tolerance of cardiomyocytes as they relate to 2 variables in my case. They relate to the inability to detect CHD/CAD by stress tests, despite chest spasms for 10 years, as well as the minimal numbers (~2%) of cardiomyocytes that were lost in the Heart Attack despite the magnitude of the blockage of coronary arteries (95% – 99%/CAx5CA).

A point of note, there were 4 Sudden Cardiac Arrest (SCA) or Sudden Deaths (SD) among 215,413 Marathon runners in the US or 0.002% per race over 30 years (81). Although this 0.002% rate is 5x higher than the rate of Sudden Deaths 4 SDs/1000000 athletes or 1:250,000 or 0.0004% among all athletes in the US, it is significantly lower than the death rate recorded for many activities (80, 81, 82). Still other GWAS examine risk factors for CHD that are unique to distinct populations such as African Americans (78) and are strongly linked to their economic circumstances. In other reports such as longitudinal GWAS studies (following the development of a trait over time) of children in Finland whose risks for adult disease of Coronary Vascular Disease (CVD) are predicted during their development into adults and are also examined in detail by another group (79).

Additionally single nucleotide polymorphisms (SNP) based studies have established the role of adaptation of an evolutionarily modified form of Hypoxia Inducible Factor (HIF1) namely, Endothelial PAS (Per Arnt Sim) domain transcriptional factor (42, 43, 44). The gene encoding prolyl hydroxylase 2 which degrades HIF1 has acquired a protective SNP mutation in Tibetan populations that lowers the Km for O2 (42). Thus degrading HIF1 in hypoxic conditions and preempting its induction of polycythemia under hypoxic conditions at high altitude (42). EPAS1 as sensor and regulator of physiologically protective responses to O2 deficits at altitude (42) and in athletes has been previously referenced (43, 44). GWAS with 12 SNPs across EPAS1 and normal controls revealed that specific SNPs were enriched in each of 2 power:time groups and was further reinforced by a 3rd haplotype (43). The authors proposed that the SNPs associated with EPAS1 functions influenced adaptation and the relative contribution of aerobic and anaerobic metabolism and hence the maximum sustainable metabolic power for a given event duration (43). In a final study 5 SNPs associated with EPAS1 which regulates delivery of oxygen to the tissues were surveyed as plausible candidates to influence athletic performance (44). Using innovative statistical methods, the authors found SNPs that were highly predictive of sprint/power athletic performance, while interactions between other SNPs were less likely to contribute to elevated sprint/power athletic performance (44).

(SIB-7C) Significant numbers of cardiomyocytes are replaced (~50%) in a lifetime:

In a seminal body of work done in the laboratory of Dr. Jonas Frisén a method for dating the birth and replacement of cells in a tissue was designed (58, 59). During surface atomic tests of the mid 1960s the release of the radioisotope 14C into the atmosphere led to its incorporation into human genomic DNA at a level that reflected its level in the atmosphere (58). The half-life of 14C is 5,730±40 years but the predominant form of Carbon in nature is 12C. By measuring the ratio of 14C to 12C in a tissue which changes with the DNA replication associated with cell division the loss/replacement the numbers of new cells can be determined (58). This method was termed as Retrospective Birth Dating (RBD) and its application allowed Dr. Frisén and his colleagues to establish that all tissues except the cerebellum underwent cell replacement. This included the Heart with approximately 50% of its cardiomyocytes being replaced in a lifetime (58, 59). The significance of the number for the turnover of cardiomyocytes in the interpretation of numbers of my cardiomyocytes that were lost in the Heart Attack will become clear.

(SIB-7D) Known cellular and molecular mechanisms for coping with cardiac stress and protecting hypoxic cardiomyoctes.

Although it was always known that stress puts a strain on the cardio-pulmonary system the insidious role of chronic stress on all dimensions of health including cardiac disease is now much better appreciated as even being dangerous (53). New genetics and molecular biological approaches are identifying new risk factors beyond traditional targets for Coronary Artery Disease (CAD) (54, 55) such as the cardioprotective effects of IL1 against heart disease which is subverted by anti-inflammatory agents that are inhibitory for this factor (55). Furthermore, additional factors beyond weight gain act together with it to elevate the magnitude of Risk Factors for health problems (54).

As has been pointed out the principal source of cardiac stress is the deprivation of O2 (hypoxia) due to various factors affecting coronary blood flow. Hypoxia is responsible for pathologies such as heart disease, cancer, stroke, and chronic lung disease, which are responsible for 60% of deaths in the United States (38 – 44). Hypoxia Inducible Factor 1 (comprising of HIF1α and its partner HIF1β) is the molecule playing a principal role in ameliorating the consequences of low O2 in all mammalian cell types including cardiomyocytes. HIF1α has evolutionarily diverged into the related to Endothelial PAS (Per Arnt Sim) domain 1 (EPAS1) also interacting with the same partner HIF1β to initiate transcription. In poorly vascularized embryos EPAS1 responds to hypoxia as a developmental signal during embryogenesis and is responsible for vasculogenesis and angiogenesis (38 – 44). HIF1 and EPAS1 belong to the class of molecules known as transcription factors as they regulate the expression of genes necessary for physiological processes that elevate blood and O2 supply (angiogenesis, vasculogenesis, erythropoiesis and hematopoiesis) and are all essential for coping with O2 deficits. [In molecular biology and genetics, a transcription factor (sometimes called a sequence-specific DNA-binding factor) is a protein that binds to specific DNA sequences, thereby controlling the rate of transcription of genetic information from DNA to messenger RNA (46)]. Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator regulated by O2 and plays essential roles in mammalian development, physiology and disease pathogenesis. HIF1 was discovered by its ability to bind the enhancer and upregulate the transcription of the gene encoding Erythropoietin (EPO) a hormone required to elevate erythropoiesis (Red Blood Cell production (38 – 44). In the presence of O2 the HIF-1α subunit undergoes ubiquitination and proteasomal degradation – processes that are arrested in the absence O2. Interaction of HIF-1α transactivation domains with coactivators is induced by hypoxia. The signal transduction pathway is unresolved, but does involve generation of reactive oxygen species (ROS), (38 – 44).

HIF1 also plays a direct role in ischemic preconditioning (IPC) which is of critical importance in moderating the effects of CAD, CHD and SCA. Remote ischemic preconditioning (IPC) is induced by 5 minute cycles of limb ischemia and reperfusion, which are induced in mice by cyclical clamping and unclamping of the femoral artery and in human subjects by inflating and deflating a blood pressure cuff. Even after a period of 72 hours IPC results in protection of the heart against a subsequent prolonged induction of ischemia and reperfusion. The mechanisms possibly involve signals generated by the nervous system and by secreted factors, such as the cytokine interleukin-10 (IL-10) The transcriptional activator hypoxia-inducible factor 1 (HIF-1) has been shown to be necessary and sufficient for remote IPC in vivo, reduction of infarct size as well as for the up-regulation of Il10 mRNA in cultured mouse myocytes. Induction of HIF-1 activity may confer cardioprotection on patients undergoing cardiac bypass surgery (40).

Similarly the anti-inflammatory molecule Sulindac an inhibitor of cyclo oxygenase (COX1/COX2) also induces IPC in myocardial tissues via a pathway that includes protein kinase c (PKC), Nitric Oxide Synthase, Hsp27 protect cardiac tissues against ROS and oxidative damage (36 – 51). Similar protective effects against ROS are conferred on Retinal Pegmented Epithelial (RPE) cells (41, 45). Several of the genes listed above also deliver IPC to cardiomyocytes and include Akt, Bcl2, IL1, PPAR-a, CDC29, p38 kinase, and JAK-STAT (36 – 51).

Others have proposed therapeutic options based on in vitro cardiomyocytes and work done on IPC either demonstrating resistance due to IPC under conditions of hypotonic shock documented with cell biological methods or with molecular, cellular and immunological approaches (68, 69).

Other labs have studied additional mechanisms documented for cardiomyocyte cell death (68). These include the overload of Ca ++, perforative permeabilization of mitochondrial membranes and tendency for breakage of cytoskeletal and membrane components induced by protease activation which are also transferred to adjacent cardiomyocytes through gap junctions. Similarly these cell death signals are also received from blood cells and other cardiomyocytes via gap junctions. Most forms of protective treatment against reperfusion injury are in early stages of development, with atrial natriuretic peptide, inhibition of mitochondrial permeabilization and ischemic postconditioning holding some promise. Rescue from Myocardial Infarction by the therapeutic effect of an adjuvant during coronary recanalization presents a new therapeutic option (68).

The adaptive evolutionary response of the genes encoding HIF1 and EPAS1 to low O2 conditions mimicking CAD and CHD are clearly illustrated by Tibetans resident at high altitudes (>15000 meters) and Athletes (42 – 44). Tibetans do not exhibit increased hemoglobin concentration and polycythemia which is hypoxia-induced and HIF1 mediated at the rarefied atmosphere of high altitudes (42). A high-frequency missense mutation c.[12C>G; 380G>C] in the EGLN1 gene, which encodes prolyl hydroxylase 2 (PHD2), contributes to this adaptive response. PHD2 causes degradation of HIFs which regulate responses to hypoxia, e.g. erythropoiesis (42). The PHD2 p.[Asp4Glu; Cys127Ser] variant has a lower Km value for oxygen, which correlates with continued binding low density of O2 at high altitude and so increased HIF degradation under hypoxic conditions. Although hypoxia stimulates the proliferation of wild-type erythroid progenitors, the proliferation of progenitors with the c.[12C>G; 380G>C] mutation in EGLN1 is retarded under hypoxic culture conditions thus decreasing HIF-mediated polycythemia. The c.[12C>G; 380G>C] mutation originated ~8,000 years ago on the same haplotype previously associated with adaptation to high altitude (42).

The adaptive evolutionary relationship between SNPs in EPAS1 and athletic performance was documented in 2 studies (43, 44). In one study of athletes, SNPs and 2 power:time ratios the authors proposed that specific SNPs associated with each power:time ratio (43). EPAS1 functioning as a sensor with its additional ability of integrating cardiovascular function, energetic demand, muscle activity and oxygen therefore influenced adaptation and the relative contribution of aerobic and anaerobic metabolism and hence conferred the maximum sustainable metabolic power for a given event duration (43). In a second study, 2 of 5 SNPs across EPAS1 were found to be highly predictive of sprint/power athletic performance, while interactions between 3 SNPs were less likely to contribute to elevated sprint/power athletic performance (44).

Additionally, beyond established genes and mechanisms (36 – 51) results in several new, divergent and ongoing areas of research in cardiac, molecular, cellular and developmental biology illustrate the unfolding appreciation of the complexity of the Heart in Development. They identify the many new points of subversion leading to potential Risk Factors!

These mechanisms are discussed in detail in the references and in section SIB-7C to 7E. Furthermore, a select and representative sampling of the literature, molecules and mechanisms either inducing or offsetting the lethality of hypoxia-reperfusion or ischemia – reperfusion in neurons and cardiomyocytes by various mechanisms including apoptosis, has been addressed in previous sections. Molecules such as Akt, Bcl2, HIF1, EPAS1, VEGF, GATA binding factor, JAK-STAT, NOX2, Estrogen, p38 Kinase Isoforms, and Sulindac contribute to IPC through well-defined pathways (36 – 45, 47 – 51). HIF1 up-regulates VEGF and GATA nucleotide sequence (GATA 1-6) binding protein to induce angiogenesis and vasculogenesis in response to hypoxia and so retard ischemic cell death by apoptosis (36 – 45, 47 – 51). While other mechanisms also contribute to IPC and the survival of cardiomyocytes (36 – 45, 47 – 51).

However a cautionary qualification is essential at this point! It may be the striking qualification of the above results assembled in lab mice (52). These results which afford the analytical power of mammalian molecular genetics, in lab mice may be qualified by evolutionary genetics of wild populations of another species – teleost fish (52). Thus, although HIF1 and EPAS1 in their cardioprotective responses to hypoxia and ischemia have been covered in detail in model organisms e.g. mice they may not be completely applicable to humans (36 – 44).

Although only 1x-2x differences in levels of expression of genes in Inbred Strains of mice can result in pathologies like cardiac diseases and cancer, in an organism with identical or similar tissue specific expression patterns and levels of the same genes, teleost fish, different results were obtained (52). A wide variation in gene expression among tissues was observed, with only a small fraction (31%) of known tissue-specific differences being conserved between all feral or wild populations of these fish (52). Thus the application of these interpretations from mice to patients may involve a large step, which is complicated by these alternative results. This parallels the disparity in application of therapeutic results obtained from mice to humans that is often noted in cancers. However, each of these approaches brings its own analytical power, and it is likely that eventually they will all be integrated to contribute to enhancing the understanding and therapeutic offsetting of CAD, CHD, CVD and SCA or SD in humans.

(SIB-7E) Preliminary Results – Ongoing Discoveries, Identification of Potential New Risk Factors & Modifiers of Risk In Cardiac Disease States

In contrast, results emerging from research in the molecular, cellular and developmental biology of coronary vessel – myocardial systems is providing an entirely new perspective for determining Risk Factors and therapeutic applications. A select and representative sampling of the literature, molecules and mechanisms either inducing or offsetting the lethality of hypoxia-reperfusion or ischemia – reperfusion in neurons and cardiomyocytes by various mechanisms including apoptosis, has been addressed in previous sections (SIB-1, 7A, 7B, 7C & 7D) and references (36 – 45, 47 – 59, 67 – 69).

The results of these relatively new studies and results, some of which have been touched on before are sketched over here (36 – 45, 47 – 52, 53 – 59, 67 – 74). Studies on detraining of muscle myocytes following strenuous training (overtraining) which show that neither the numbers and sizes of myonuclei nor hypoxia and apoptosis resistance are lost and are retained for at least 3 months if not longer (67). Other mechanisms including the development of the heart and its cardiomyocytes, surprising new findings, molecules and mechanisms that play similar roles or contribute to the development and function of cardiomyocytes in heretofore unknown ways that have also been discussed in previous sections (67 – 74).

Still more sources of environmental and developmental variation potentially contributing cardiac Risk Factors and identifying therapeutic interventions have been reported (67 – 74). These include, results showing the dependence of maximal amplitude of contraction and pumping action of the cardiomyocytes, (and so the heart) on the optimal alignment of subunits of its filaments (of actin, myosin and troponin) as well as the flexibility of filament bundles in cardiomyocytes (70). Another group demonstrated the elevation of the viscosity of cardiomyocytes in response to decreasing flexibility of the collagen framework in the surroundings of the thorax is important for its efficiency and amplitude of contraction (71). Additionally, a range of results from molecular genetics of cardiology provide new therapeutic recourse and have already been discussed (72). In the introduction to the pumping amplitude of the heart, the role of Nup10 molecules regulating ER/NPC as well as the differentiation of muscles has been outlined (SIB-1) and references (67 – 74).

Finally the contributions of various inhibitors and genes of hypoxia induced apoptotic death of cardiomyocytes have also been discussed (ref: ref: 17 – 31, 38, 39, 66 – 74 ).

Three new areas of results illustrate the unfolding appreciation of the complexity of Cardiac Development and the many points at which its subversion could lead to the accumulation of Risk Factors!

To expand on the first set of new and ongoing fields of study and their results show that the synchronized beating of cardiomyoctes caused by their multi filament content organization is dependent on specific events which must have occurred during the early development of the embryonic heart (70). For this coordinated beating to attain maximal amplitude of contraction of the muscle cells the filament subunits and their boundaries must be properly aligned in bundles which are thus dependent on numbers of coordinately contracting bundles. Additionally the appropriate physical environment such as the elasticity of the Extracellular Matrix (ECM) is also a determinant of the amplitude of contraction (70). Other groups have shown that the flexibility of the Heart is optimized for amplitude of contraction by adjusting its myosin concentration in response to stiffening collagen in its surroundings, during development (71)!

Additionally the differentiation of the heart is regulated by a unique mechanism involving gp210/Nup210 a lynchpin nucleoporin regulating muscle and neuronal differentiation. The conserved N terminus of gp210/Nup210 inserts into the perinuclear space and induces muscle cell differentiation (75). This gp210/Nup210 molecule also plays a critical role in the maintenance of homeostasis in its interactions between the Nuclear Envelope and the Endoplasmic Reticulum through its large luminal domain. It does so independently of its binding to the Nuclear Pore Complex (NPC). Molecules of gp210/Nup210 block the stress specific caspase cascade response and retain their muscle cell differentiation capacity despite the absence of the C terminus and the NPC binding domain in the N-terminus (75).

In other work a newly discovered molecule RBFox2 in mice (73) plays a role in the compensatory phase (supports increased work and blood flow) as well as the decompensatory phase (which induces decreased work and blood flow progressing to failure) post Cardiac Heart Disease (CHD). The expression of RBFox2 in the decompensatory phase was the mirror image of developmental ‘remodeling’ (genetic reinforcement) of the heart. This pivotal role of RBFox2 in heart failure has been experimentally verified and could be a Risk Factor (73).

Furthermore, as shown, surprising new perceptions of other Risk Factors for CAD, CHD and SD such as interleukin-1 (IL-1) mediated inflammation are emerging (54). It is now shown that anti-inflammatory mediated suppression of inflammation, via inhibition of IL-1, may actually elevate the risk for Coronary Heart Disease (54).

Finally there are neuroprotective globins such as neuroglobin and cytoglobin that sequester ROS and may bind O2 within hypoxic mammalian brains (74). Their levels range significantly between terrestrial aquatic species (74). Running, swimming and diving elevates levels and modifies these neuroprotecting globins in the mammalian brain (74). They are expressed in all tissues including cardiac tissues, are upregulated by hypoxia and likely to play a cardioprotective role (74).

(SIB-7F) Exercise and Squash – Optimal Health/Injury Ratios, Modification of Risk Factors for, Coronary Heart Disease (CHD), Coronary Artery Disease (CAD), Coronary Vein Disease (CVD) and Sudden Cardiac Arrest (SCA)

The prominent role of exercise in reducing the risk of all Coronary Aretery Diseases (CAD), Coronary Heart Diseases (CHD) including Sudden Cardiac Arrest (SCA) has been well established (76, 77, 80 – 96). The known and hypothetical mechanisms for this protection have been characterized and some of the prominent ones include: (1) raising levels of fitness and physical activity (80 – 90), (2) ischemic pre-conditioning (IPC) of cardiomyocytes, that is protective even from late (up to 72 hour) ischemic challenges (36 – 51, 67 – 69), (3) involvement of a range of mediating molecules and mechanisms (36 – 51, 67 – 69, 80 – 96), (4) retention of overtraining generated hypoxia (and apoptosis) resistant myonuclei for at least 3 months if not longer into old age after detraining (67), (5) retention despite RBD confirming replacement of 50% of cardiomyocytes/lifetime (58, 59) . Having reviewed this literature it is useful to find that it proposes a role for high intensity (METs index of 6 – 12 cals/lg/hr) sports like Squash Rackets in reducing the Risk Factors (4 -22%) of these various cardiac diseases. Squash also represents an activity promoting high Health Benefit to Injury Ratios (5-7, 67 – 69, 80 – 96).

The Risk of Sudden Death or Sudden Cardiac Arrest among all athletes in the USA is 4/106 or 1:250,000 or 0.0004% and in the Republic of Ireland it is 1:600000 or 0.000167% (80, 81). In the last 5 decades of my life Competitive Squash and training for it, at various levels of intensity was the major physical activity. To understand any role that Squash may have played in my surviving the MI, it is worth reviewing studies and analyzing whether and how much it contributes to either elevating or decreasing the risk of all forms of cardiac pathologies (5 – 7, 67 – 69, 80 – 96). Analyses that were drawn on, included 4 groups of studies applying:

(1) older less representative methods which serve a useful purpose as indices (80, 82 – 84, 86),

(2) more contemporary, highly quantitative, statistically robust, defined and representative studies from 2000 – 2013, some based on GWAS/METs, with a Scientific emphasis (81, 85, 90),

(3) studies that are still scientifically systematic, quantitative or statistically robust and yet somewhat more representative of Racket Sports, especially Squash, that embodies arhythmicity, explosivity of basal to peak velocities, upper to lower body coordination, highly developed skills, (hand-eye coordination, racketwork, spatial dimensions, postures, on court moves and footwork). They are based on criteria selected by Players and Coaches in conjunction with Sports Physiologists (who may also be Physicians (MDs) and Research Scientists (PhDs). They are still restricted to a small range of skills, explosivity and relatively rhythmic movements (87 – 90),

(4) studies that are low on scientific and quantitative dimensions and statistical robustness but are significantly more representative of Racket Sports, especially Squash that embodies, arhythmicity, explosivity of basal to peak velocities, upper to lower body coordination, highly developed skills, (hand-eye coordination, racketwork, spatial dimensions, postures, on court moves and footwork). They are based on criteria selected by Players and Coaches in conjunction with Sports Physiologists (who may also be Physicians (MDs) and Research Scientists (PhDs) (5 – 7, 80, 91 – 94).

(1)  Does Squash have a high Metabolic Equivalent Task Index (MET), Work (wattage) or Cardiorespiratory Fitness (CRF) value? And is it higher than that measured in other sports?

Yes! Whether Squash has a higher Metabolic Equivalent Task Index (MET), work wattage or Cardiorespiratory Fitness (CRF) value than other sports depends on how it is measured but in all cases, the complexities of the game make the maximal values far lower than the actual values! This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar METs 6 – 12, work of 120 – 210 watts, are considered to represent high intensity exercise but due to the manner tested (without inclusion of all the variables identified in the above questions) it can only remain a minimal estimate of the true value for Squash (SIB-7B,-7F) and references (5 – 7, 67 – 69, 80 – 96).

An example of this discrepancy in evaluation is provided by the results of 7 studies (82, 85 – 90).This whole section will be covered in a more detailed Sports Physiology and Cardiac Risk Factor to be for oriented and submitted to a Journal dealing with Sports physiology or Clinical Medicine and Sports (1).

Study 1 (82): The study by Jette et al, 1990, (82) is both quantitative and thorough with an older definition of METs Index at (mls of O2/kg/min x 3.5 at rest (sitting).This work does not include e.g. ways of measuring all the variables defining Squash that were identified in questions 3 and 4. Thus, as the authors noted, this study lacks quantification of many of the determinants of rigor/intensity in Squash that distinguish its higher intensity over other sports including Racket Sports. Accepting this limitation, they showed that of 100 physical activities or sports tested, some at multiple intensities/rigors, 7 (Squash, Racquetball, Orienteering, Jogging, Judo, Karate and Boxing) had an intensity of 12 METs/210 watts. Another 13 sports had equal or ~3 had greater maximal intensity with Cross Country Skiing and Rowing at 13 METs/228 watts and running at up to 16 METs/280 watts (92). The relative energetic output, physiological output and thus the intensity of workouts in Squash relative to other sports obtained with contemporary methods have superseded this original ranking and distribution and been based on a Squash Specific quantifications (5 – 7, 85 – 90).

Studies 2 & 3 (5 – 7, 85 – 90): Squash is well known as a highly arrhythmic, explosive and spatially dynamic sport with a high density and wide range of movements, racketwork and skills that introduce variations which are extremely difficult to detect let alone quantify even for the experienced experimental observer! This is confirmed by the clusterings of tournament performance results of similarly ranked professionals in the Professional Squash Association (PSA). It is impossible to adequately cover let alone quantify the density, range and depth of these strokes and movements in the lexicon of current Sports Physiology. Given these limitations some attempts at quantification coupled with more qualitative estimates remain the best and only recourse. The strokes and movements include the whole range of Motor-Sensory-Spatial processes and their various permutations and combinations that are translated into the ‘Read (Stroke)->Get (Ball)->Stroke (Make)’ triad on the Squash Court either determined by, or in response to, a wide range of Sensory Perceptions or cues read in fractions of seconds as time periods (5 -7, 93, 94). These are best communicated in colloquial terms known to Players, Coaches and Exercise or Sports Physiologists rather than in formal scientific terminology (5 – 7, 93, 94, 87 – 90).

The range of Moves and Strokes in Squash although dependent on improvisation are mostly precise, technically demanding and occur in a varied and sequential intermix. Yet in the absence of time and space on the court all of this must be compressed into an improvised response! Adaptability is a core requirement in Squash. This is why Squash Players operate at high skill levels that involve a high density, arhythmicity and range of sudden (explosive) moves and strokes, upper and lower body coordination all producing high torque, intensity, caloric and metabolic expenditure (5 – 7, 93, 94, 87 – 90). The relative energetic (METs) Index, physiological (glycolytic and aerobic) output and the intensity of workouts in Squash relative to other sports have been obtained with contemporary methods based on a method known as Squash Specific Tests (ST) or Field Tests that have superseded its original ranking and distribution based on standard Treadmill Tests (TT) or Laboratory Tests (5 – 7, 93, 94, 87 – 90).

The first Squash Specific Test (ST) or Field Test was a computerized variation on the ‘Ghosting’ (or Star Drills in the USA) invented by Jonah Barrington, the former 6 time British Open (Wimbledon of Squash) Winner and the Coach of the Player currently ranked number 1 in the World – Mohammed El Shorbagy (7). Star Drills involve moves made on the Squash Court without a ball for efficiency, high and sustained pressure (7). Barrington is known to Players and Coaches, for maximizing Physical Conditioning for Squash (7). The computerized commands (introducing arhythimicity and explosivity) in Star Drills consists of 6 points (2 lateral points in addition to the 4 corners) on the court, identified by audio-visual commands leading the players from the strategic T junction (center of the court), to the designated points (displacements) with the swinging of the Racket at an imaginary ball on arrival (87). This sequence has high numbers of repetitions and with occasional breaks at standard intervals. In the Field Test or the Squash Specific Test (ST) players were monitored for physiological, biochemical and physical parameters such as Heart Rate, levels of Blood Lactate (mmol/L), time taken for the last step, VO2 max (mls/min/kg or METs) and Performance at the Anaerobic Threshold (Te) light flashes/hour). The same parameters for the same Players were also monitored in the Treadmill or Laboratory Test (TT) with the exception that final Threshold performance was recorded in km/Hr (87). Players, who were Juniors in German Squash, were assigned rank performances for both methods. It was established that there was a significantly greater correlation (>1.7x with p range >50x) between the Squash Specific or Field Test (ST = 0.90, p<0.001) and the rank established by the various physical, physiological and biochemical parameters than between the Treadmill and Laboratory Test (TT= 0.52, p>0.05) and these 3 performances (87). Of most importance the ST predicted the performance of the players in routine competitive play (tournaments) far better than the TT (87).

In a third study (88, 89), essentially the same methods of Squash Specific or Field Tests (ST), Treadmill or Laboratory Tests (TT) were again compared with some changes introduced. Firstly, the conditioning and performance of the tested players was exponentially elevated by changing the subjects tested to Professional Squash Association (PSA) Players including the top ranked player in the world (World #1) in the years of the study (2004/2005). Secondly the Squash Specific Tests (ST) were graded with distance, directions and times calibrated with PSA tournament level performances by taped audio-visual cues. Thirdly, the computational programs were more sophisticated and could introduce greater arrhythmicity into the graded ST with specific audiovisual cues. Finally the numbers and resolution of physiological, physical and biochemical parameters was elevated and more sophisticated. They included heart rate (HR), VCO2/VO2, time to exhaustion (Te) and VO2 parameters under various conditions in ST and TT (88, 89). In both the graded ST and TT neither the heart rate (HR) nor the %VO2max, at VT and RCP were significantly different for the PSA Pros. However, other indicators such as VO2, VCO2 and breathing frequency values measured at maximal loads were significantly higher levels in ST than in TT. As with the Juniors, results of parameters determined in ST and TT correlated with known performances of the PSA Pros recorded in tournaments (88, 89).

Of most importance differences in the ST and TT results for the Junior Players and PSA Pro Players were revealing (87, 88, and 89). For the Juniors the values obtained in the TT and ST were significantly different (87) while for the PSA Pros they were mostly similar (88, 89) confirming the greater facility of the Pros with the higher rigor of the ST. This confirms a determining factor in the game that is well known to Squash Players. As expected the Pros are physically stronger and faster than the Juniors. But of more importance, the Pros have integrated the critical elements of Squash specific movements, racketwork, footwork and spatial dimensions to a significantly higher level than that of mastered by the Junior Players. This mastery by the Pros brings a significantly greater economy of energetic expenditures to the graded ST that is not required in the TT thus diminishing the rigor of the graded ST and the disparity between the 2 tests (87, 88, 89). Therefore the calculations of intensity for Squash e.g. METs by even graded ST methods is almost certainly an underestimate.

Another reason for this underestimate is drawn from the magnitude, density and range of movements and strokes from the ‘Read-Get-Stroke’ triad in an Amateur match let alone a high level PSA Squash match that would simply overwhelm even the graded ST or Field Test (87, 88, and 89). The energetic requirements of movements on the Squash Court are akin to overcoming the Inertia with all their Activation Energy Barriers (quantities from Formal Physics) that a Sprinter would overcome in (i) launching from the Starting Blocks, then (ii) coming to a hard stop and (iii) finally re-launching from mid track! And all this in Sprinting would be devoid of the many vectors that would present additional Activation Energy Barriers such as switched spatial orientations and directions that Squash Players have to routinely overcome in a match! The density and range of movements in the ‘Get’ segment of the ‘Read-Get-Stroke’ triad of Squash includes Sprint-Walk-Step, Dive, Twist, Turn, Stretch , Bend, Jump, Reach, Upper and Lower Body Coordination, Basal-Peak Velocities either in rapid succession or in overlapping or in a varied and sequential interchanges (87, 88, 89). The depth, range and spectrum of these movements as well as their energetic requirements are not adequately definable let alone measurable by scientific or Sports Physiological methods. This has led to the significant underestimate between the calculations of energetic demands and metabolic intensities for Squash e.g. METs indices by even graded ST methods relative to other sports (1, 4 – 6, 80 – 94).

To assay these factors more realistically requires inclusion of the less, controlled, quantitative, statistically robust and scientific methods designed by Athletes, Players, Coaches, Sports and Exercise Physiologists. It is an analyses more reflective of muscle strength, muscle endurance, cardiorespiratory endurance, flexibility and speed, semi-quantitatively measured and reported by Forbes and (TopTen) ESPN Sports (5 – 7, 87 – 89). These answers to this question requires experimental verification.

(2) Does Squash have a high workout intensity (calories per kilogram per hour (unit time)) as measured by studies done by Players, Coaches in conjunction with Sports Physiologists? Does Squash have a high Health Benefit/Injury ratio as measured by Forbes? And by ESPN(Top10)?

Yes to both questions. Controlled, systematic, physiologically and statistically robust methods for measuring METs indices was addressed in the answer to the above question as well as in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar METs indices (6 – 12) lower Risk Factors for MI, CHD, CAD, and SD or SCA by 22% – 40% (SIB-7B,-7F) and references (5 – 7, 80 – 94).

However, these scientifically robust methods were also shown not to be completely representative of the intensity and energetic requirements of the game. To appreciate the full magnitude of the physiological and physical intensity of the game, Competitors, Personal Trainers, Coaches and Exercise Physiologists quantified 6 parameters in 10 sports with the results being published in ForbesOnline (5, 6).

Parameters that were quantified on a scale of 1 – 5 (direct relationship) with the exception of injury risk on a scale of 3 -1 (inverse relationship) and were tallied for:

  • Cardio-respiratory endurance
  • Muscle strength
  • Muscle endurance
  • Flexibility
  • Calories/30 minutes
  • Injury risk

The highest scores for (1) energy consumption (517 calories/30 minutes), (2) ratio of Injury risk/calories per 30’(is 0.44 when corrected for differential of 1.1 in calories from rock climbing) and (3) total score of 22.5 were all assigned to Squash – making it the healthiest of the 10 sports tested (5, 6). They provide the alternative more realistic combinatorial approach and independent confirmation of Squash being one of the most energy and work intensive sports with the lowest risk of Injury and so the healthiest sport tested.

In contrast there are reports of serious injuries, such as concussion and even Parkinson’s Disease resulting from competition in other sports such as football, boxing and soccer (95, 96). These injuries have neither been included in evaluating, the Risk Factors nor in interrupted, unsustained and diminished training intensities associated with these sports (95, 96).

The above questions were addressed in a different way by ESPN(Top 10) with different results (91). They identified 10 attributes of athleticism, and then asked a group of experts made up of sports scientists, kinesiology academics and sporting journalists to assign a number from 1 to 10 to each of these skills. This analysis was applied to 60 sports from around the world, and the final results are shown in the table here. See also the sports lists for each of the components of athleticism.

The results from this ESPN(Top10) (91) are inconsistent with and even contradict the results from all other studies spanning the last 3 decades (1, 5 – 7, 80 – 94). Some of the reasons for the problems leading to this disparity are addressed elsewhere (1, 5, 6, 91 – 94) and suggest a lack of familiarity of the evaluators with the dynamics of Racket Sports, the relevant literature distinguishing their properties as well as with much of the literature in Sports Physiology in general (91: Table I; 1, 5 – 7, 80 – 94). These include e.g. the non-interchangeable nature of the differences in power generation between, Racket Sports and Boxing (its top rated sport) or Weight Lifting. In the Racket Sports e.g. Badminton power generation is predominantly based on technique and the timing of strokes while in Boxing (its top rated sport) or Weight Lifting it is based more on muscle mass and force than in technique. The qualities acquired in the latter would actually impede power generation in the former. This study contrasts sharply with the others and is cited as an example of the dangers of complexity, subjectivity and ad hoc attempts at quantifications of Sports in general (1, 5 – 7, 80 – 94).

(3) Does Squash cause Sudden Death or Sudden Cardiac Arrest (SCA)?

Only when pre-existing cardiac pathologies such as CHD, CAD, CVD have seriously compromised the cardiac health of the Players! There are 3 older references (83, 84, 86) that claim that Squash “causes Sudden Death” while a fourth paper and the contemporary literature suggest that these data reflect increases of the risk of Sudden Death among those with various pre-existing cardiac pathologies. Unlike either more comprehensive older or more systematized contemporary (GWAS, METs, PRM based) methods the above studies fail to show that Squash and similar activities actually register a decrease (22 – 40%) in the Risk Factors of CVD, CAD and MI ( (80, 82, 85, 87 – 90).

An exhaustive pre-GWAS study by Dr. Fionnuala Quigley (80) clarified some of these results and presciently revealed data that would be consistent with the contemporary studies of a decade later. In an unbiased survey of the population of 3,000,000 in the Republic of Ireland over a 10 year period, from 1987 – 1996, by including ALL people who died while exercising ostensibly of Sudden Death in ALL sports was obtained from postmortems done by 45 of 49 coroners contacted (80). It was found that of 15 sports surveyed it was Golf that was the game leading to the highest frequency of Sudden Deaths. Golf is the most popular participant sport in Ireland and the ages of the deceased Golfers ranged from 32 to 36 years. Thus age could not have been a predisposing factor (80). An uncritical reading of the data might have suggested that the frequency of Sudden Deaths caused by Golf was 16x higher than that caused by Rugby or Squash (1 each). Dr. Quigley points out that her paper clearly illustrates that despite an assiduous attempt at preventing this source of error – surveyed populations and methods can affect the interpretation with false positives or mis-interpretations which the author has carefully excluded (80).

At best these types of studies show that those with CHD, CVD and CAD should, as has been recommended, be medically counselled before taking to the Squash Court (ref 43, 44).

All the contemporary methods with large Cohort sizes, high resolution GWAS, high intensity sports METs, with strong correlations with Personal Record Maintenance, etc.. included in the analyses show that vigorous physical and fitness activities of intensity (METs = 6 – 12 cals/kg/hr) including Squash, actually decreased the Risk of Cardiac Heart Disease by 30% (SIB-7B,-7F), references: (82 – 90) & therein). And another independent study showed an inverse relationship between vigor of physical activity of sports such as Squash (with METs of 6 – 12 cals/kg/hr and work of 140 – 210 Watts) and Risk Factors actually leading to an even greater decrease of the risk of Coronary Heart Disease CHD by 22% – 40% (SIB-7B,-7F);references: (85 – 90)..

(4) Does Squash cause Coronary Heart Disease (CHD), Coronary Artery Disease (CAD) or Coronary Vein Disease (CVD)?

No! This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar METs actually lower these risk factors by 22% – 40%. Thus Squash would also be expected to slow down the rate of plaque deposits and the resultant CAD (SIB-7B,-7F); references: (82 – 90). These answers to this question requires experimental verification.

(5) Does Squash decrease the Risk Factors associated with Sudden Death or Sudden Cardiac Arrest (SCA)?

Yes! This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar METs 6 – 12 cals/kg/hr, work of 120 – 210 watts, lowers these risk factors by 22% – 40% (SIB-7B,-7F); references: (82 – 90).  This means that the rate of CHD leading to SCA would also be decreased by high intensity sports like Squash. (SIB-7B,-7F); references: (82 – 90). These answers to this question requires experimental verification.

(6) Does Squash decrease the Risk Factors associated with Heart Attacks (Myocardial Infarctions) or Sudden Death?

Yes! This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar METs 6 – 12 cals/kg/hr, work of 120 – 210 watts, lowers these risk factors by 22% – 40% (SIB-7B,-7F); references: (82 – 90). These answers to this question requires experimental verification.

(7)Coronary Artery Disease causes plaque buildup gradually leading to increased hypoxia and when the block is complete it results in (complete) anoxia and cell death. Could cardiomyocytes capable of resisting hypoxia due to increased numbers and sizes of cardiomyonuclei due to overtraining be expected to retain resistance after decades of detraining? Are there plausible molecular mechanisms for sensing and physiologically responding to hypoxia as in squash?

Yes to both questions. This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). The literature clearly demonstrated that Sports of maximal intensity like Squash (conservatively estimated: 6 – 12 cals/kg/hr METs, 12 watts and 517 calories/30 minutes) lowered the risk of all Coronary Diseases (CHD, CAD, CVD, SD) by 22% – 40% has also been reviewed (80 – 90). Additionally the role of molecules such as HIF1, EPAS1, Bcl2, JAK-STAT, Akt, NO2 , Estrogen, IL10, IL1 and Sulindac among others in IPC and cardioprotection that would provide a mechanistic basis for lowering these Risk Factors has also been well documented. Both lowered rates of plaque buildup from CAD and thus the delayed CHD as well as IPC induction by hypoxia reinforcing cardiomyocyte survival could be expected to be elevated by high intensity sports like Squash (SIB-7B,-7F); references: (82 – 90).

Furthermore, the adaptive evolutionary response of the genes encoding HIF1 and EPAS1 to low O2 conditions mimicking CAD and CHD are clearly illustrated by Tibetans resident at high altitudes (>15000 meters) and that of high performance athletes could be expected to set a parallel for selecting Squash Players with similar SNPs (42 – 44).

Of most importance it is now known that detraining of skeletal muscle myocytes following overtraining does not result in the loss of myonuclear resistance to hypoxia induced apoptosis and so the conditioning capacity is retained or restored for at least 3 months if not longer. These trained myonuclei resistant to hypoxia and apoptosis, can serve as templates for newly born myonuclei that are also hypoxia and apoptosis resistant – even extending conditioning well into old age as noted by athletes (67). So cardiomyocytes of Squash Players should be similarly capable of resisting hypoxia due to increased numbers and sizes of myonuclei conferring resistance to hypoxia even after decades of detraining. These answers to all these question requires experimental verification.

(8)Does Squash and training for it qualify for over-training levels which generate long lasting hypoxia induced and apoptosis resistant cardiomyocyte nuclei based on the studies with myocytes ?

Our ‘on- and off-court’ training in Squash met the standards of rigor and intensity by most criteria, including levels of my own game that have been reviewed in previous sections (SIB – 7D); narrative page 7 and references: (4, 94). The literature clearly established that Sports of maximal intensity (6 – 12 METs index, 12 watts and 517 calories/30 minutes) like Squash lowered the risk of all Coronary Diseases (CHD, CAD, CVD, SD) by 22% – 40% and this literature has also been reviewed (85 – 90). The work considered to meet the criteria of overtraining in experimental systems such as rodents was generated by partially ablating their major synergist leading to an overload of their Extensor digitorum longus (EDL) muscles situated at the lateral and front of the leg (SIB – 7D); reference: (67). Additionally SNPs in, prolyl hydroxylase 2 regulating HIF1 stability in high altitude adaptations of Tibetans and SNPs in EPAS1 correlated with Elite Athlete performances with hypoxia apparently serving as an (evolutionary) selective agent in both cases (42 – 44). Hypoxia in Squash could also be expected to correlate with similar SNPs and an elevated frequency of high performance in tournaments among Squash Players harboring them (42 – 44). Taken within the context of the above literature our training regimens in India qualified for high intensity overtraining (4, 94) while in the US it dropped to low intensity overtraining followed by detraining. These answers to this question require experimental verification.

(9) Based on Retrospective Birth Dating (RBD) in a 7- 8 year period of detraining, (2007 – 2014), how many new cardiomyocytes could be expected to be born and become susceptible to hypoxia and apoptosis? Is there a difference between the cardiomyocytes exposed to high intensity overtraining in India 38 years ago (ending in 1976), those exposed to low intensity overtraining in the US (ending in 2006/2007) and those exposed to detraining(ending in 2014)? How many cardiomyocytes would be susceptible to anoxia?

This question was partially addressed in 2 earlier sections in the narrative as well as in (SIB-7C; reference: (58, 59). For various Professional and non-Sports related reasons alluded to and based on various estimated physical and physiological parameters, my personal levels of overtraining for Squash in India were significantly higher than in the US. Based on Dr. Jonas Frisén’s Retrospective Birth Dating (RBD) data for replacement of cardiomyocytes an estimate of ~4.4% of cardiomyocytes would be replaced over the 7 years of detraining (low to non-existent training) in the US (post 2006/2007). This number would rise to ~23.8% of cardiomyocytes that would be replaced during low intensity overtraining in the US over 38 years post 1976. Overtraining at high intensity for Squash in India ceased since 1976 or 38 years ago (narrative pages 7, 39 – 40), (SIB-7C; reference: (4, 58, 59). Contradicting the study on myonuclei (67) and assuming that hypoxia resistance is NOT transferred to these ~4.4% new cardiomyonuclei, at least 95.6% (or 96% – 98% based on experimental error) of the cardiomyocytes would still retain resistance to hypoxia induced apoptosis (SIB-7D; reference: (58, 59). Alternatively, according to the published study the hypoxia resistant cardiomyocyte nuclei in turn should have acted as templates expected to confer hypoxia and apoptosis resistance even on these newly born ~4.4% cardiomyocyte nuclei. This agrees with the general observations of athletes on the long term retention of effects of overtraining! Which makes incomplete transfer of hypoxia resistance to new cardiomyonuclei an unlikely explanation (58, 59, 67)?

That still requires an explanation for the observed disparity between the magnitude of the blockage and the low levels of cardiomyocyte cell death. Despite the near complete blockage of (95-99%/CA x 5 CA) in blood flow and so O2 supply through 5 major coronary arteries only ~2% of cardiomyocytes succumbed to cell death as determined by Acoustic ECG during catheterization and angiography (personal communication: Dr. Andrew Shanahan, MD, Cardiologist and Nurse Rhonda Sabel, RN).

An alternative possibility is provided by the known lethality of 5 minutes of anoxia for cardiomyocytes which could reveal their cardiac location and so yield a more plausible explanation. Those ~2% (of a total of ~4.4% new cells) of either old or newly born cardiomyocytes that succumbed to cell death could have been localized in a segment of the Heart in which the ‘cutoff’ of blood and so O2 supply was complete, thus sending them into a lethal anoxic condition.

The anoxic condition is equivalent to that of a ‘cutoff’ of all O2 during Atrial Fibrillation (AF) or Ventricular Fibrillation (VF) both of which cause Sudden Cardiac Arrest (SCA) or Sudden Death (SD) within 5 minutes in the absence of intervention with an Automated External Defibrillator (AED). Anoxia for these ~2% cells would be lethal regardless of the presence of hypoxia and apoptosis resistant 98% cardiomyocyte nuclei as templates as even they would succumb to anoxia,and through various pathways of lethality (SIB- 7A, 7B, 7C, 7D, 7E, 7F). These answers to this question requires experimental verification.

(10)Would ~98% of these cardiomyocytes be sufficient to confer the resistance that explains the difference between the level of the block 95% – 99% in 5 major coronary arteries and ~2% cardiomyocyte cell death?

This question was addressed in the answer to the above question and in the section on GWAS and Risk Factors for MI, CHD, CAD, and SD or SCA (SIB-7B,-7F). Squash and activities of similar intensity (METs = 6-12 cals/kg/hr), lowers these risk factors for CAD 22% – 40%, so slows down CAD and induces IPC in 98% cardiomyoctes through hypoxic and apoptotic survival which translated to survival during an MI incident (SIB-7B,-7F; references: (36 – 45, 85 – 90). However, the ~2% cardiomyocytes that succumbed were likely resident in a cardiac segment that did not receive any supply of blood and so O2 and thus became anoxic and suffered lethality. Thus the ~98% hypoxia and apoptosis resistant cardiomyocytes were irrelevant to the survival of the ~2% in an anoxic cardiac segment and so succumbed to lethal anoxia. The answers to this question requires experimental verification.

narrative resumed:


  1. In other words, the literature supports the inference that, my competitive days in the game of Squash Rackets and high intensity overtraining for it, had delayed the deposition of plaques by CAD so it only gradually rose to 95-99%/CA/5xCA and conferred hypoxia and apoptosis resistance due to IPC that was retained on ~98% of my cardiomyocytes. When this near complete blockage and other Risk Factors (professional pressures, family background, etc..) finally precipitated the MI the extent of cell death and so cardiac damage was limited to ~2% cardiomyocytes. Thus enabling the Cardiologists, Cardiac Surgeons and their teams to save my life!
  2. Although we cannot prove it for the MI affecting my heart, the current literature establishes that overtraining in high intensity sports like Squash (with an underestimated METs index of 6 – 12 cals/kg/hr), elevates the level of general and cardiac conditioning, both slowing down and diminishing the risk of Coronary Artery Disease (CAD) or Coronary Heart Disease (CHD) by 22% – 40% while also allowing cardiomyocytes to resist oxygen deprivation (hypoxia) from constricted coronary arteries due to ischemic preconditioning or IPC (SIB-7).
  3. As far as the Open Heart Surgery goes, there were mixed reactions as is to be expected. Although there was post-surgical pain, some unpredictable vacillations of vital signs, an acute weakness that permeated my being, including a temporary 30 lb loss of weight (which was much needed), for a period from a week to a month, the overall impression I have is one in which all of these factors were of much lower intensity than expected for such a drastic procedure. I have changed my life style drastically at least partly in gratitude for all that was done by these professionals to save my life!
  4. We begin with the central players in all this! Despite the conceptual and technical complexities of the procedures involved, namely the catheterization and angiography done by Dr. Andrew Shanahan and the coronary artery bypass graft (CABG) done by Dr. George Batsides and their respective teams, they met the requirements of the daunting success rate of 98% because their work was carried out flawlessly. This, despite the various pathological obstacles that arose and the impending urgency of the circumstances in my thorax! The CABG procedure involved surgically opening a chamber, the thorax, which has remained hermetically sealed, for good reason, across Vertebrate Evolution. This was followed by their Bypass work on the heart, which as robust and active an organ as it is, is still susceptible to all manner of electrical and other failings. All this was done while I as the patient was on pump assisted breathing and circulation! And finally there was the required resealing of the thorax without allowing a leak to develop (the consequences of which are amply demonstrated by the associated pathologies). All this is done with the high success rate of 98% – which is unbelievable for those of us who are Experimental Biologists! All the Physicians, Surgeons, Nurses, Technological Staff were always completely professional, dedicated and technically skilled and yet remained kind, warm and deeply concerned about my wellbeing! There was never any panic on their part despite the unpredictable pathological problems that arose under highly urgent circumstances – in which the possibility of fatality always loomed! And this only led to further reassurance for me as the patient!
  5. The entire sequence of pre-events and events related to the Myocardial Infarction (heart Attack) that I had, from its beginnings on the 25th of December 2014 to the present day and the time of submission of the manuscript (9th May 2015) was played out flawlessly by the Biomedical Professionals, Physicians, Surgeons, Nurses, Technological Staff, Family and Friends with myself as the beneficiary. Which is probably why I am alive! They are all listed in the copied Portable Document Format (or pdf) file entitled ACKNOWLEDGEMENTS.
  6. My family and friends, some with whom I had lost touch, simply leapt to my rescue when the news got out! They were on the phone or appeared by my hospital bedside dropping urgent matters in their own lives, and in some cases risking their own healths with long and arduous journeys, to do so. None more so than my brother Cyrus Nallaseth who despite his own dangerous health circumstances, caught the first available flight out of Mumbai (Bombay) India to be by my bedside! This alone gives me the impetus to not waste their time and effort! I am still soaking up the enormous sense of having been sheltered and so remaining alive!
  7. My fellow patients and I at the Cardiac Pulmonary Rehab Facility at UMCPrinceton at Plainsboro cannot overemphasize the importance of systematically surveying the usefulness of catheterization and angiography as opposed to non-invasive Stress Tests and Radioisotopic or Acoustic tests to detect certain ‘silent’ cardiac pathologies so as to establish their true frequency. Perhaps in conjunction with the development of a new more reliable method. This is especially so with athletes or those who have overtrained at one time, so as to acquire IPC, which is likely retained even if they have subsequently detrained. This as we saw since the cardiac muscles are likely to have retained the capacity of hypoxia resistance and so are not stressed by standard Stress tests and would mask cardiac pathologies. In my case, despite chest spasms, and the likely presence of advanced CAD the other non-invasive tests had failed to detect effects of cardiac or coronary artery plaques over a period of a decade. So cardiac involvement was inaccurately if understandably excluded with a 95% confidence a short 4.5 years ahead of the MI incidence.
  8. So while the hypoxia resistance of the cardiomyocytes prevented the various cardiac Stress Tests from stressing the heart sufficiently to allow detection of CHD/CAD, for 10 years, when the Myocardial Infarction (Heart Attack) finally occurred, ~98% of the cardiomyocytes could resist prolonged hypoxia and I likely escaped a major and possibly lethal, attack! As was inferred those ~2% cardiomyocytes that succumbed to cell death during or prior to the MI were either anoxic for more than 5 minutes or less likely not resistant to hypoxia due to the incomplete transfer of hypoxia resistance from the resistant templates (page 38 – 39 of narrative, SIB-7). The former parallels events in Sudden Death or in Sudden Cardiac Arrest (induced by Atrial or Ventricular Fibrillation, (SIB-7). The latter could occur when cardiomyonuclei may not have acquired hypoxia (and apoptosis) resistance from the resistant template nuclei of overtrained cardiomyonuclei (SIB-7).
  9. Although invasive tests (catheterization and angiography) are more revealing and reliable than non-invasive tests (Stress, Acoustic, ECG, Tests etc..) in diagnosing Cardiac mal-function, they bring greater associated risks to the process. A need exists for the development of an alternative method of diagnosis which incorporates all the advantages without the risks associated with these 2 methods. Of necessity preceded by a re-evaluation of the methods for detection of all types of silent diseases affecting the Cardiac system. For example considering development of various Tomography approaches e.g. Multi Spectral Optoacoustic Tomography (MSOT) without catheterization (97, 98)
  10. An attempt has also been made to come to terms with perhaps an insidious process that is still underway – somewhere in the back of my mind. This includes, the many communities in any life – family, friends, medical, professional and social networks. Those who were either at one with me, or leapt to my rescue, and also included adversaries or onlookers who seemed to be genuinely concerned. Possibly as the Specter of Mortality is always intriguing?
  11. Of course work that is unfinished due to unavoidable circumstances that were alluded to earlier, and the transience of life were the compelling, if sub conscious, forces over the past ~40 years that also occupied my thoughts immediately after the Myocardial Infarction episode. I am now moving as quickly as possible to put this and other unfinished work into the literature!
  12. Last but not the least I simply cannot but marvel at the magnificent social processes that were at play in all the Biomedical facilities and which represented the most redeeming characteristics of Humankind! It left me as the beneficiary with a new lease on Life! I was, as someone unknown, to the Biomedical communities in those hospitals, carried in from the street, and yet in effect made as one of their own! They showed remarkable concern, kindness, warmth, empathy, generosity, graciousness, and yet retained all the skill, dedication and the professionalism that was so important to the recovery of the patient – myself (99)! And so they will remain among those to whom I owe my life!

Addendum added by FSN

 Something that might have contributed to my escape from certain death by MI and by the minimal odds of 48:1 requires emphasis! In the paper by Northcote et al (83), which is actually often misquoted on Google as Squash Causing Heart Attacks), of 60 deaths on the Squash Court, postmortems showed that at least 48 players had advanced CAD/CHD. They were ~20 or 30 years younger than I, could not possibly have had a greater extent of CAD than I did (95%-99%/CAx 5CA) and were certainly in  better condition than I was at age 62. So why did I live – at 48:1 if not greater odds? The answer may be that I had stopped playing at anywhere near the intensity (maximal METs index) as hard as I did, ~7 years earlier. Although I almost certainly had IPC preconditioned cadiomyocytes they may not be able to survive this combination of maximal intensity and CAD which is the reason for the reported fatalities on the court (83)! And since I did not get anywhere near that level on the court after 2007, I survived!​


I cannot express enough gratitude for the innumerable and different ways in which all of those listed below contributed to saving my life. As well as in making it possible for me to eventually emerge from Open Heart Surgery while remaining as comfortable as was possible given the circumstances! Should I have inadvertently left out a name please accept my sincerest apology. Ferez

See additional acknowledgemnents at the following link: Acknowledgements.5.9.2015.pdf

FSN would like to acknowledge the editorial assistance of Dr. Stephen J. Williams, Ph.D.


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(80) Quigley, F. A survey of the causes of sudden death in sport in the Republic of Ireland, Br J Sports Med, 34: 258-261 (2000), http://bjsm.bmj.com/content/34/4/258

(81) Maron, BJ, Poliac, LC, Roberts, WO. Risk for sudden cardiac death associated with marathon running, Journal of the American College of Cardiology, http://content.onlinejacc.org/article.aspx?articleID=1121267

(82) Jette, M., Sidney, K., Blumchen, G., Metabolic Equivalents (METS) in Exercise Prescription, an Evaluation of Functional Capacity, Clin. Cardiol. 13: 555-565 (1990)


(83) Northcote, R.J., Flannigan, C., and Ballantyne, D., Sudden death and vigorous exercise—a study of 60 deaths associated with squash, Br Heart J 55(2): 198 – 203 (1986), http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1232118/

(84) Brady, HR, Kinirons, M, Lynch, T, Ohman, EM, Tormey, TW, O’Malley, KM, Horgan, JH.  European Heart Journal, 10 (11): 1029-1035, Heart rate and metabolic response to competitive squash in veteran players: identification of risk factors for sudden cardiac death, (1989), http://www.ncbi.nlm.nih.gov/pubmed/2591394

(85) Chomistek, AK, Chiuve, SE, Jensen, MK, Cook, NR, Rimm, EB, Vigorous physical activity, mediating biomarkers, and risk of myocardial infarction; Med Sci Sports Exerc. 43(10): 1884 – 1890 (2011) , http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249756/

(86) Locke S., Colquhan D., Briner M., Ellis L., O’Brien, Wollstein J., Allen G., Squash racquets. A review of physiology and medicine, Sports Med. 23 (2): 130 – 138 (1997), http://www.ncbi.nlm.nih.gov/pubmed/9068096

(87) Steininger, K., Dr. med. And Wodick, R.E., Prof. Dr. Dr. rer . nat , Sports- Specific Fitness Testing In Squash, Brit J. Sports Med. 21(2): 23 -26, (198&) http://bjsm.bmj.com/content/21/2/23.full.pdf+html

(88) Girard, O., Sciberras, P., Habrard, M., Hot, P., Chevalier, R., Millet, G.P., Specific incremental test in elite squash players; Br J Sports Med; 39: 921 – 926 (2005).


(89) Girard, O.,Sciberras, P., habrard, M., Hot, Chevalier, R., Millet, G.P., Specific incremental test in elite squash players, Br J Sports Med 39: 921 – 926 (2005), http://bjsm.bmj.com/content/39/12/921.full.pdf+html

(90) Chomistek, AK, Chasman, DI, Cook, NR, Rimm, EB, and Lee, I-M. Physical Activity, Genes for Physical Fitness, and Risk of Coronary Heart Disease, Med Sci Sports Exerc. 2013 April ; 45(4): 691–697. doi:10.1249/MSS.0b013e3182784e9f., http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605203/

(91) 2-17-15 Daily Squash Report, ESPN ‘Most Demanding Sports’ List Re-Visited ‘ Most Demanding Sports’ List Re-Visited On ESPN’, (TopEnd Sports/ESPN, 2001)

(92) 2-17-15 Daily Squash Report , Rebutting ESPN’s Debunking of Forbes’ Analyses of Squash As The Healthiest Sport by Ferez S. Nallaseth

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(95) Hirshberg, L. Traumatic brain injury: Football and boxing, sure. But soccer? Neurodevelopment Center, Inc., NDC tips, qEEG, 11. 07.201

(96) Viano, D.C., Casson, I.R., Pellman, E.J., Bir, C.A.,Zhang, L., Sherman, D.C., Boitano, M.A., Concussion in professional football: comparison with boxing head impacts—part 10, Neurosurgery, 57(6): 1154 – 1172; discussion 1154-1172, (12.2005)http://journals.lww.com/neurosurgery/Abstract/2005/12000/Concussion_in_Professional_Football__Comparison.13.aspx

(97) Multispectral optoacoustic tomography, http://en.wikipedia.org/wiki/Multispectral_optoacoustic_tomography

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No evidence to change current transfusion practices for adults undergoing complex cardiac surgery: RECESS evaluated 1,098 cardiac surgery patients received red blood cell units stored for short or long periods

Reporter: Aviva Lev-Ari, PhD, RN

No evidence to change current transfusion practices for adults undergoing complex cardiac surgery

A National Institutes of Health-funded study found no statistical difference in the primary clinical measure — which assessed changes in function of six organs from before to seven days after surgery — between complex cardiac surgery patients receiving transfusions of red blood cell units stored for short (up to 10 days) versus long (21 or more days) periods. These findings indicate there is no need to alter how hospitals currently transfuse blood in adults going through complex cardiac surgical procedures.

Results of the Red Cell Storage Duration Study (RECESS), supported by the NIH’s National Heart, Lung, and Blood Institute (NHLBI), appear today in the New England Journal of Medicine.

In the United States, red blood cell units can be stored up to 42 days after collection. Basic research has documented changes in red blood cell units the longer that they are stored. Some studies, primarily observational, have found an association between the transfusion of blood stored for a longer duration and increased morbidity and mortality. However, the clinical significance of these findings is difficult to determine due to study-design limitations.

RECESS was a multicenter trial conducted at more than two dozen U.S. hospitals from January 2010 to January 2014 by the NHLBI-funded Transfusion Medicine and Hemostasis Clinical Trial Network (TMH CTN). The TMH CTN includes 17 core clinical centers and a data coordinating center. Patients were enrolled at most TMH CTN core clinical centers and some non-network centers.

RECESS evaluated 1,098 cardiac surgery patients who were randomized to receive red blood cell units stored for short or long periods. Patients in the longer storage period group received their transfusions using current care practices.

There was no statistical difference in the change in the primary clinical measure, the Multiple Organ Dysfunction Score (MODS), or mortality from before cardiac surgery to seven or 28 days after the operation for both transfusion groups.  The MODS was evaluated because it is an objective and validated way to assess small changes in six organ systems, which includes respiratory, renal, hepatic, cardiovascular, hematologic and neurologic. There were no statistical differences in the mean number of serious and non-serious adverse events between the two groups.

“RECESS contributes to a long-standing question about whether red blood cell storage duration impacts a patient’s clinical outcome after transfusion.” said Keith Hoots, M.D., director of the NHLBI Division of Blood Diseases and Resources. “These findings are reassuring because they do not support the need to modify transfusion practices in adult patients undergoing complex cardiac surgery. In particular, there does not appear to be something gained by only transfusing red blood products stored for ten days or less.”

Because very few RECESS patients were under 18 years of age, findings primarily apply to adult patients undergoing complex cardiac surgery.

Centers that Participated in RECESS

TMH CTN Core Clinical Centers

  • BloodCenter of Wisconsin, Milwaukee
  • Children’s Hospital, Boston
  • Weill Cornell Medical College, Cornell University, New York City
  • Duke University, Durham, North Carolina
  • Emory University, Atlanta
  • Johns Hopkins Hospital, Baltimore
  • Massachusetts General Hospital, Boston
  • Puget Sound Blood Center, Seattle
  • University of Iowa, Iowa City
  • University of Maryland, Baltimore
  • University of Minnesota, Minneapolis
  • University of North Carolina, Chapel Hill
  • University of Oklahoma Health Sciences Center, Oklahoma City/UT Southwestern Medical Center, Dallas
  • University of Pittsburgh

TMH CTN Data Coordinating Center

  • New England Research Institutes, Watertown, Massachusetts

Non-Network Centers

  • Mayo Clinic, Rochester, Minnesota
  • Vanderbilt University, Nashville, Tennessee
  • Rutgers Robert Wood Johnson Medical School, New Brunswick, New Jersey
  • St. Luke’s Episcopal — Texas Heart Institute, Houston
  • Baystate Medical Center, Springfield, Massachusetts
  • Indiana/Ohio Heart, Fort Wayne, Indiana
  • Indiana/Ohio Heart, St. Joseph Hospital, Fort Wayne, Indiana
  • University of Florida, Gainesville
  • St. Elizabeth’s Medical Center, Brighton, Massachusetts,
  • Newark Beth Israel Medical Center, New Jersey
  • Aspirus Heart and Vascular Institute, Wausau, Wisconsin
  • Sanford Heart Center, Fargo, North Dakota
  • Columbia University Medical Center, New York City

The National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases, and sleep disorders. More information about NHLBI is available at http://www.nhlbi.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

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Fractional Flow Reserve vs. Angiography in Non-ST-segment Elevation Myocardial Infarction

Reporter: Aviva Lev-Ari, PhD, RN


Jamie Layland, Keith G. Oldroyd, Nick Curzen, Arvind Sood, Kanarath Balachandran, Raj Das, Shahid Junejo, Nadeem Ahmed, Matthew M.Y. Lee, Aadil Shaukat, Anna O’Donnell, Julian Nam, Andrew Briggs, Robert Henderson, Alex McConnachie, Colin Berry


Eur Heart J. 2015;36(2):100-111. 


We assessed the management and outcomes of non-ST segment elevation myocardial infarction (NSTEMI) patients randomly assigned to fractional flow reserve (FFR)-guided management or angiography-guided standard care.

Methods and results

We conducted a prospective, multicentre, parallel group, 1 : 1 randomized, controlled trial in 350 NSTEMI patients with ≥1 coronary stenosis ≥30% of the lumen diameter assessed visually (threshold for FFR measurement) (NCT01764334).

Enrolment took place in six UK hospitals from October 2011 to May 2013. Fractional flow reserve was disclosed to the operator in the FFR-guided group (n 1/4 176). Fractional flowreserve was measured but not disclosed in the angiography guided group (n 1/4 174). Fractional flowreserve ≤0.80was an indication for revascularization by percutaneous coronary intervention (PCI) or coronary artery bypass surgery (CABG). The median (IQR) time from the index episode of myocardial ischaemia to angiographywas 3 (2, 5) days. For the primary outcome, the proportion of patients treated initially by medical therapy was higher in the FFR-guided group than in the angiography-guided group [40 (22.7%) vs. 23 (13.2%), difference 95% (95% CI: 1.4%, 17.7%), P 1/4 0.022]. Fractional flow reserve disclosure resulted in a change in treatment between medical therapy, PCI or CABG in 38 (21.6%) patients. At 12 months, revascularization remained lower in the FFR-guided group [79.0 vs. 86.8%, difference 7.8% (20.2%, 15.8%), P 1/4 0.054]. There were no statistically significant differences in health outcomes and quality of life between the groups.


In NSTEMI patients, angiography-guided management was associated with higher rates of coronary revascularization compared with FFR-guided management. A larger trial is necessary to assess health outcomes and cost-effectiveness.



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Please see Further Information on the Sachs Associates 14th Annual Biotech in Europe Forum for Global Investing & Partnering at:




why-is-twitter-s-logo-named-after-larry-bird--b8d70319daON TWITTER Follow at





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One year Post-Intervention Mortality Rate: TAVR and AVR – Aortic Valve Procedures 6.7% in AVR, 11.0% in AVR with CABG, 20.7 in Transvascular (TV-TAVT) and 28.0% in Transapical (TA-TAVR) Patients

Reporter: Aviva Lev-Ari, PhD, RN


UPDATED on 4/8/2017

Routine Imaging After TAVR Suggested to Catch Thrombosis – German data supports ‘significant’ prevalence warranting routine check by Nicole Lou 

Reporter, MedPage Today/CRTonline.org, April 03, 2017

Clinical transcatheter heart valve thrombosis may be common enough to merit routine imaging after transcatheter aortic valve replacement (TAVR), a German study suggested.

A retrospective analysis of a single-center registry found a 2.8% incidence of clinical valve thrombosis, according to Mohamed Abdel-Wahab, MD, of Germany’s Segeberger Kliniken, and colleagues. No one on oral anticoagulation got bioprosthetic valve thrombosis, however, and no patients died from it.

Thrombosis was more likely with balloon-expandable valves (OR 3.45, 95% CI 1.22-9.81) and with valve-in-valve procedures (OR 5.93, 95% CI 2.01-17.51), the authors reported in the April 10 issue of JACC: Cardiovascular Interventions.



One year Post-Intervention Mortality Rate: TAVR and AVR – Aortic Valve Procedures 6.7% in AVR, 11.0% in AVR with CABG, 20.7 in Transvascular (TV-TAVR) and 28.0% in Transapical (TA-TAVR) Patients


The 1-year mortality rate was

  • 6.7% for conventional AVR patients (n = 6523) and
  • 11.0% for patients who underwent AVR with coronary artery bypass grafting (n = 3464).
  • The 1-year mortality rate was 20.7 and 28.0% in TV- and TA-TAVR patients, respectively (n = 2695 and 1181).

However, if patients were stratified into four risk groups by means of the EuroSCORE and the German AV Score, the

  • highest risk cohorts showed the same mortality at 1 year with either therapy.
  • More than 80% of patients in all groups were in the same or better state of health at 1 year post-intervention and were satisfied with the procedural outcome.


European Journal of Cardio-Thoracic Surgery

Eur J Cardiothorac Surg (2014)doi: 10.1093/ejcts/ezu290



The German Aortic Valve Registry: 1-year results from 13 680 patients with aortic valve disease


  1. Friedrich W. Mohra,*,
  2. David Holzheya,
  3. Helge Möllmannb,
  4. Andreas Beckmannc,
  5. Christof Veitd,
  6. Hans Reiner Figullae,
  7. Jochen Cremerf,
  8. Karl-Heinz Kuckg,
  9. Rüdiger Langeh,
  10. Ralf Zahni,
  11. Stefan Sackj,
  12. Gerhard Schulera,
  13. Thomas Waltherk,
  14. Friedhelm Beyersdorfl,
  15. Michael Böhmm,
  16. Gerd Heuschn,
  17. Anne-Kathrin Funkata,
  18. Thomas Meinertzo,
  19. Till Neumannp,
  20. Konstantinos Papoutsisq,
  21. Steffen Schneiderr,
  22. Armin Welzs and
  23. Christian W. Hammb
  24. for the GARY Executive Board

+Author Affiliations

  1. aHeart Center Leipzig, Leipzig, Germany

  2. bDepartment of Cardiology, Kerckhoff Heart Center, Bad Nauheim, Germany

  3. cDeutsche Gesellschaft für Thorax-, Herz- und Gefäßchirurgie, Langenbeck-Virchow-Haus, Berlin, Germany

  4. dBQS Institute for Quality and Patient Safety, Düsseldorf, Germany

  5. eDivision of Cardiology, 1st Department of Medicine, University Hospital of Jena, Jena, Germany

  6. fDepartment of Cardiovascular Surgery, University of Schleswig-Holstein, Kiel, Germany

  7. gAsklepios Klinik St. Georg, Hamburg, Germany

  8. hGerman Heart Center Munich, Department of Cardiovascular Surgery, Technische Universität München, Munich, Germany

  9. iDepartment of Cardiology, Medizinische Klinik B, Herzzentrum am Klinikum Ludwigshafen, Ludwigshafen, Germany

  10. jKlinik für Kardiologie, Pneumologie und Internistische Intensivmedizin, Klinikum Schwabing, Munich, Germany

  11. kKerckhoff-Herzzentrum, Abteilung für Herzchirurgie, Bad Nauheim, Germany

  12. lUniversitätsklinikum Freiburg, Chirurgische Klinik Abteilung Herz- und Gefäßchirurgie, Freiburg, Germany

  13. mMedizinische Klinik und Poliklinik, Universitätsklinik des Saarlandes, Innere Medizin III, Homburg/Saar, Germany

  14. nInstitut für Pathophysiologie, Universitätsklinikum Essen, Essen, Germany

  15. oDeutsche Herzstiftung, Frankfurt am Main, Germany

  16. pDepartment of Cardiology, University of Duisburg-Essen Medical School, Essen, Germany

  17. qGerman Cardiac Society, Düsseldorf, Germany

  18. rInstitut für Herzinfarktforschung, Ludwigshafen, Germany

  19. sDepartment of Cardiac Surgery, University of Bonn, Bonn, Germany
  1. *Corresponding author. Heart Center Leipzig, Struempellstrasse 39, 04289 Leipzig, Germany. Tel: +49-341-8651421; fax: +49-341-8651452; e-mail:mohrf@medizin.uni-leipzig.defriedrich.mohr@herzzentrum-leipzig.de (F.W. Mohr).
  1.  An excerpt of the 1-year data was first presented at the ACC in San Francisco in March 2013.

  • Received April 16, 2014.
  • Revision received May 27, 2014.
  • Accepted June 17, 2014.



OBJECTIVES The German Aortic Valve Registry (GARY) seeks to provide information on a real-world, all-comers basis for patients undergoing aortic valve interventions. This registry comprises patients undergoing the complete spectrum of transcutaneous and conventional surgical aortic valve interventions. The aim of this study was to use the GARY registry to evaluate conventional and catheter-based aortic valve interventions in several risk groups.

METHODS A total of 13 860 consecutive patients undergoing intervention for aortic valve disease [conventional aortic valve replacement (AVR) or transvascular/transapical TAVR (TV-/TA-TAVR)] were enrolled in 78 German centres in 2011. Baseline, procedural and outcome data, including quality of life, were acquired up to 1 year post-intervention. Vital status at 1 year was known for 98.1% of patients.

RESULTS The 1-year mortality rate was 6.7% for conventional AVR patients (n = 6523) and 11.0% for patients who underwent AVR with coronary artery bypass grafting (n = 3464). The 1-year mortality rate was 20.7 and 28.0% in TV- and TA-TAVR patients, respectively (n = 2695 and 1181). However, if patients were stratified into four risk groups by means of the EuroSCORE and the German AV Score, the highest risk cohorts showed the same mortality at 1 year with either therapy. More than 80% of patients in all groups were in the same or better state of health at 1 year post-intervention and were satisfied with the procedural outcome.

CONCLUSIONS Conventional AVR surgery yields excellent results after 1 year in lower-risk patients. Catheter-based AVR is a good alternative in high-risk and elderly patients.


Key words





FIFTY ARTICLES on TAVR and AVR were published in this Open Access Online Scientific Journal. All articles are included at the following URL:


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MedTech (Cardiac Imaging) and Medical Devices for Cardiovascular Repair – Curations, Co-Curations and Reporting by Aviva Lev-Ari, PhD, RN

MedTech (Cardiac Imaging) and Medical Devices for Cardiovascular Repair – Curations, Co-Curations and Reporting by Aviva Lev-Ari, PhD, RN

Cardiac Imaging and Cardiovascular Medical Devices in use for

Cardiac Surgery, Cardiothoracic Surgical Procedures and Percutaneous Coronary Intervention (PCI) / Coronary Angioplasty

List of Publications updated on 8/13/2018


Single-Author Curation by Aviva Lev-Ari, PhD, RN


42c       Experimental Therapy (Left inter-atrial shunt implant device) for Heart Failure: Expert Opinion on a Preliminary Study on Heart Failure with preserved Ejection Fraction

Article Curator: Aviva Lev-Ari, PhD, RN



41c       Spectranetics, a Technology Leader in Medical Devices for Coronary Intervention, Peripheral Intervention, Lead Management to be acquired by Philips for 1.9 Billion Euros

Reporter and Curator: Aviva Lev-Ari, PhD, RN



40c       Moderate Ischemic Mitral Regurgitation: Outcomes of Surgical Treatment during CABG vs CABG without Mitral Valve Repair

Curator: Aviva Lev-Ari, PhD, RN



39c       Patients with Heart Failure & Left Ventricular Dysfunction: Life Expectancy Increased by coronary artery bypass graft (CABG) surgery: Medical Therapy alone and had Poor Outcomes

Curator: Aviva Lev-Ari, PhD, RN



38c       Mapping the Universe of Pharmaceutical Business Intelligence: The Model developed by LPBI and the Model of Best Practices LLC

Author and Curator of Model A: Aviva Lev-Ari, PhD, RN and Reporter on Model B: Aviva Lev-Ari, PhD, RN



37c     MedTech & Medical Devices for Cardiovascular Repair – Curations by

Curator: Aviva Lev-Ari, PhD, RN



36c     Stem Cells and Cardiac Repair: Scientific Reporting by: Aviva Lev-Ari, PhD, RN

Curator: Aviva Lev-Ari, PhD, RN



35c       CVD Prevention and Evaluation of Cardiovascular Imaging Modalities: Coronary Calcium Score by CT Scan Screening to justify or not the Use of Statin

Curator: Aviva Lev-Ari, PhD, RN



34c       “Sudden Cardiac Death,” SudD is in Ferrer inCode’s Suite of Cardiovascular Genetic Tests to be Commercialized in the US

Curator: Aviva Lev-Ari, PhD, RN



33c       Transcatheter Valve Competition in the United States: Medtronic CoreValve infringes on Edwards Lifesciences Corp. Transcatheter Device Patents

Curator: Aviva Lev-Ari, PhD, RN



32c       Developments on the Frontier of Transcatheter Aortic Valve Replacement (TAVR) Devices

Curator: Aviva Lev-Ari, PhD, RN



31c       Market Impact on Global Suppliers of Renal Denervation Systems by Pivotal US Trial: Metronics’ Symplicity Renal Denervation System FAILURE at Efficacy Endpoint

Curator and Reporter: Aviva Lev-Ari, PhD, RN



30c     Stenting for Proximal LAD Lesions

Curator: Aviva Lev-Ari, PhD, RN



29c       Stent Design and Thrombosis:  Bifurcation Intervention, Drug Eluting Stents (DES) and Biodegrable Stents

Curator: Aviva Lev-Ari, PhD, RN



28c       Calcium Cycling (ATPase Pump) in Cardiac Gene Therapy: Inhalable Gene Therapy for Pulmonary Arterial Hypertension and Percutaneous Intra-coronary Artery Infusion for Heart Failure: Contributions by Roger J. Hajjar, MD

Curator: Aviva Lev-Ari, PhD, RN



27c       Call for the abandonment of the Off-pump CABG surgery (OPCAB) in the On-pump / Off-pump Debate, +100 Research Studies

Curator: Aviva Lev-Ari, PhD, RN



26c       3D Cardiovascular Theater – Hybrid Cath Lab/OR Suite, Hybrid Surgery, Complications Post PCI and Repeat Sternotomy

Curator: Aviva Lev-Ari, PhD, RN



25c       Vascular Surgery: International, Multispecialty Position Statement on Carotid Stenting, 2013 and Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD

Curator: Aviva Lev-Ari, PhD, RN



24c       Heart Transplant (HT) Indication for Heart Failure (HF): Procedure Outcomes and Research on HF, HT @ Two Nation’s Leading HF & HT Centers

Curator: Aviva Lev-Ari, PhD, RN



23c       Becoming a Cardiothoracic Surgeon: An Emerging Profile in the Surgery Theater and through Scientific Publications 

Curator: Aviva Lev-Ari, PhD, RN



22c       Fractional Flow Reserve (FFR) & Instantaneous wave-free ratio (iFR): An Evaluation of Catheterization Lab Tools (Software Validation) for Endovascular Lower-extremity Revascularization Effectiveness: Vascular Surgeons (VSs), Interventional Cardiologists (ICs) and Interventional Radiologists (IRs)

Curator: Aviva Lev-Ari, PhD, RN



21c       No Early Symptoms – An Aortic Aneurysm Before It Ruptures – Is There A Way To Know If I Have it?

Curator: Aviva Lev-Ari, PhD, RN



20c       Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

Curator: Aviva Lev-Ari, PhD, RN



19c       Revascularization: PCI, Prior History of PCI vs CABG

Curator: Aviva Lev-Ari, PhD, RN



18c       Minimally Invasive Structural CVD Repairs: FDA grants 510(k) Clearance to Philips’ EchoNavigator – X-ray and 3-D Ultrasound Image Fused.

Curator: Aviva Lev-Ari, PhD, RN



17c       Acute Chest Pain/ER Admission: Three Emerging Alternatives to Angiography and PCI

Curator: Aviva Lev-Ari, PhD, RN



16c       Clinical Trials on Transcatheter Aortic Valve Replacement (TAVR) to be conducted by American College of Cardiology and the Society of Thoracic Surgeons

Curator: Aviva Lev-Ari, PhD, RN



15c       FDA Pending 510(k) for The Latest Cardiovascular Imaging Technology

Curator: Aviva Lev-Ari, PhD, RN



14c       The ACUITY-PCI score: Will it Replace Four Established Risk Scores — TIMI, GRACE, SYNTAX, and Clinical SYNTAX

Curator: Aviva Lev-Ari, PhD, RN   https://pharmaceuticalintelligence.com/2013/01/03/the-acuity-pci-score-will-it-replace-four-established-risk-scores-timi-grace-syntax-and-clinical-syntax/

13c       Renal Sympathetic Denervation: Updates on the State of Medicine

Curator: Aviva Lev-Ari, PhD, RN



12c       Coronary artery disease in symptomatic patients referred for coronary angiography: Predicted by Serum Protein Profiles

Curator: Aviva Lev-Ari, PhD, RN



11c       CABG or PCI: Patients with Diabetes – CABG Rein Supreme

Curator: Aviva Lev-Ari, PhD, RN


10c       Clinical Trials Results for Endothelin System: Pathophysiological role in Chronic Heart Failure, Acute Coronary Syndromes and MI – Marker of Disease Severity or Genetic Determination?

Curator: Aviva Lev-Ari, PhD, RN



9c         Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

Curator: Aviva Lev-Ari, PhD, RN



8c         New Drug-Eluting Stent Works Well in STEMI

Curator: Aviva Lev-Ari, PhD, RN


7c         Coronary Artery Disease – Medical Devices Solutions: From First-In-Man Stent Implantation, via Medical Ethical Dilemmas to Drug Eluting Stents

Curator: Aviva Lev-Ari, PhD, RN



6c         DELETED, identical to 7r


5c         Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

Curator: Aviva Lev-Ari, PhD, RN



4c         Global Supplier Strategy for Market Penetration &amp; Partnership Options (Niche Suppliers vs. National Leaders) in the Massachusetts Cardiology &amp; Vascular Surgery Tools and Devices Market for Cardiac Operating Rooms and Angioplasty Suites

Curator: Aviva Lev-Ari, PhD, RN



3c         Competition in the Ecosystem of Medical Devices in Cardiac and Vascular Repair: Heart Valves, Stents, Catheterization Tools and Kits for Open Heart and Minimally Invasive Surgery (MIS)

Curator: Aviva Lev-Ari, PhD, RN



2c         Executive Compensation and Comparator Group Definition in the Cardiac and Vascular Medical Devices Sector: A Bright Future for Edwards Lifesciences Corporation in the Transcatheter Heart Valve Replacement Market

Curator: Aviva Lev-Ari, PhD, RN



1c         Treatment of Refractory Hypertension via Percutaneous Renal Denervation

Curator: Aviva Lev-Ari, PhD, RN



Lev-Ari, A. (2006b). First-In-Man Stent Implantation Clinical Trials & Medical Ethical Dilemmas.

Bouve College of Health Sciences, Northeastern University, Boston, MA 02115


Co-Curation Articles on MedTech and Cardiac Medical Devices by LPBI Group’s Team Members and Aviva Lev-Ari, PhD, RN

67co     ATP – the universal energy carrier in the living cell: Reflections on the discoveries and applications in Medicine

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN


66co     Eric Topol, M.D.

Curators: Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN



65co     Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



64co     Introduction to e-Series A: Cardiovascular Diseases, Volume Four Part 2: Regenerative Medicine

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



63co     Epilogue: Volume 4 – Translational, Post-Translational and Regenerative Medicine in Cardiology

Larry H Bernstein, MD, FCAP, Author and Curator, Consultant for Series B,C,D,E

Justin Pearlman, MD, PhD, FACC, Content Consultant for Series A: Cardiovascular Diseases

Aviva Lev-Ari, PhD, RN, Co-Editor and Editor-in-Chief, BioMed e-Series



62co     Introduction to Translational Medicine (TM) – Part 1: Translational Medicine

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



61co     Acute Myocardial Infarction: Curations of Cardiovascular Original Research A Bibliography

Curators: Aviva Lev-Ari, PhD, RN and Larry H Bernstein, MD, FCAP


60co     Mitral Valve Repair: Who is a Patient Candidate for a Non-Ablative Fully Non-Invasive Procedure?

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN



59co     Coronary Circulation Combined Assessment: Optical Coherence Tomography (OCT), Near-Infrared Spectroscopy (NIRS) and Intravascular Ultrasound (IVUS) – Detection of Lipid-Rich Plaque and Prevention of Acute Coronary Syndrome (ACS)

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN



58co     Normal and Anomalous Coronary Arteries: Dual Source CT in Cardiothoracic Imaging

Reporters: Justin D Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



57co     Alternative Designs for the Human Artificial Heart: Patients in Heart Failure –  Outcomes of Transplant (donor)/Implantation (artificial) and Monitoring Technologies for the Transplant/Implant Patient in the Community

Authors and Curators: Larry H Bernstein, MD, FCAP and Justin D Pearlman, MD, PhD, FACC and Article Curator and Reporter: Aviva Lev-Ari, PhD, RN



56co     Cardiovascular Complications: Death from Reoperative Sternotomy after prior CABG, MVR, AVR, or Radiation; Complications of PCI; Sepsis from Cardiovascular Interventions

Author, Introduction and Summary: Justin D Pearlman, MD, PhD, FACC, and Article Curator: Aviva Lev-Ari, PhD, RN



55co     The Cardiorenal Syndrome in Heart Failure: Cardiac? Renal? syndrome?

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



54co     Mechanical Circulatory Assist Devices as a Bridge to Heart Transplantation or as “Destination Therapy“: Options for Patients in Advanced Heart Failure

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



53co     Heart Transplantation: NHLBI’s Ten year Strategic Research Plan to Achieving Evidence-based Outcomes

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



52co     After Cardiac Transplantation: Sirolimus acts as immunosuppressant Attenuates Allograft Vasculopathy

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN


51co     Orthotropic Heart Transplant (OHT): Effects of Autonomic Innervation / Denervation on Atrial Fibrillation (AF) Genesis and Maintenance

Author and Curator: Larry H. Bernstein, MD, FCAP and

Curator: Aviva Lev-Ari, PhD, RN



50co     CABG Survival in Multivessel Disease Patients: Comparison of Arterial Bypass Grafts vs Saphenous Venous Grafts

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN


49co     Coronary Reperfusion Therapies: CABG vs PCI – Mayo Clinic preprocedure Risk Score (MCRS) for Prediction of in-Hospital Mortality after CABG or PCI

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



48co     Pre-operative Risk Factors and Clinical Outcomes Associated with Vasoplegia in Recipients of Orthotopic Heart Transplantation in the Contemporary Era

Writer and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



47co     Carotid Endarterectomy (CEA) vs. Carotid Artery Stenting (CAS): Comparison of CMMS high-risk criteria on the Outcomes after Surgery:  Analysis of the Society for Vascular Surgery (SVS) Vascular Registry Data

Writer and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



46co     Improved Results for Treatment of Persistent type 2 Endoleak after Endovascular Aneurysm Repair: Onyx Glue Embolization

Author and Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



45co     DELETED, was identical to 47co


44co     Open Abdominal Aortic Aneurysm (AAA) repair (OAR) vs. Endovascular AAA Repair (EVAR) in Chronic Kidney Disease (CKD) Patients – Comparison of Surgery Outcomes

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



43co     Effect of Hospital Characteristics on Outcomes of Endovascular Repair of Descending Aortic Aneurysms in US Medicare Population

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



42co     First case in the US: Valve-in-Valve (Aortic and  Mitral) Replacements with Transapical Transcatheter Implants – The Use of Transfemoral Devices

Author: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



41co     Survivals Comparison of Coronary Artery Bypass Graft (CABG) and Percutaneous Coronary Intervention (PCI) / Coronary Angioplasty

Curators: Larry H Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN



40co     Ventricular Assist Device (VAD): A Recommended Approach to the Treatment of Intractable Cardiogenic Shock

Author: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN


39co     Trans-apical Transcatheter Aortic Valve Replacement in a Patient with Severe and Complex Left Main Coronary Artery Disease (LMCAD)

Author: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



38co     Transcatheter Aortic Valve Replacement (TAVR): Postdilatation to Reduce Paravalvular Regurgitation During TAVR with a Balloon-expandable Valve

Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



37co     Acute and Chronic Myocardial Infarction: Quantification of Myocardial Perfusion Viability – FDG-PET/MRI vs. MRI or PET alone

Justin Pearlman, MD, PhD and Aviva Lev-Ari, PhD, RN


36co     On Devices and On Algorithms: Arrhythmia after Cardiac SurgeryPrediction and ECG Prediction of Paroxysmal Atrial Fibrillation Onset

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN



35co     Vascular Repair: Stents and Biologically Active Implants

Author and Curator: Larry H Bernstein, MD, FACP and Curator: Aviva Lev-Ari, PhD, RN



34co     Drug Eluting Stents: On MIT‘s Edelman Lab’s Contributions to Vascular Biology and its Pioneering Research on DES

Author: Larry H Bernstein, MD, FACP and Curator: Aviva Lev-Ari, PhD, RN



33co     Mitral Valve Repair: Who is a Patient Candidate for a Non-Ablative Fully Non-Invasive Procedure?

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC and Article Curator: Aviva Lev-Ari, PhD, RN



32co     Source of Stem Cells to Ameliorate Damaged Myocardium (Part 2)

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



31co     State of Cardiology on Wall Stress, Ventricular Workload and Myocardial Contractile Reserve: Aspects of Translational Medicine (TM)

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



30co  DELETED identical to 58co


29co  DELETED identical to 58co


28co  DELETED identical to 57co


27co  DELETED identical to 47co


26co     Cardiac Resynchronization Therapy (CRT) to Arrhythmias: Pacemaker/Implantable Cardioverter Defibrillator (ICD) Insertion

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



25co     Emerging Clinical Applications for Cardiac CT: Plaque Characterization, SPECT Functionality, Angiogram’s and Non-Invasive FFR

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



24co     Fractional Flow Reserve (FFR) & Instantaneous wave-free ratio (iFR): An Evaluation of Catheterization Lab Tools (Software Validation) for Ischemic Assessment (Diagnostics) – Change in Paradigm: The RIGHT vessel not ALL vessels

Reporters: Justin D Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



23co  DELETED identical to 24co


22co  DELETED identical to 49co


21co  DELETED identical to 52co


20co  DELETED identical to 50co


19co  DELETED identical to 57co


18co     Open Abdominal Aortic Aneurysm (AAA) repair (OAR) vs. Endovascular AAA Repair (EVAR) in Chronic Kidney Disease (CKD) Patients – Comparison of Surgery Outcomes

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



17co     Improved Results for Treatment of Persistent type 2 Endoleak after Endovascular Aneurysm Repair: Onyx Glue Embolization

Author & Curator: Larry H Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN


16co     Effect of Hospital Characteristics on Outcomes of Endovascular Repair of Descending Aortic Aneurysms in US Medicare Population

Author and Curator: Larry H. Bernstein, MD, FCAP and Curator: Aviva Lev-Ari, PhD, RN



15co     Comparison of Coronary Artery Bypass Graft (CABG) and Percutaneous Coronary Intervention (PCI) / Coronary Angioplasty

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN



14co     First case in the US: Valve-in-Valve (Aortic and Mitral) Replacements with Transapical Transcatheter Implants – The Use of Transfemoral Devices.

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN



13co     Phrenic Nerve Stimulation in Patients with Cheyne-Stokes Respiration and Congestive Heart Failure

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN



12co  DELETED identical to 40co

11co  DELETED identical to 38co

10co  DELETED identical to 39co


9co       Imaging Biomarker for Arterial Stiffness: Pathways in Pharmacotherapy for Hypertension and Hypercholesterolemia Management

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



8co       DELETED identical to 37co


7co       Treatment, Prevention and Cost of Cardiovascular Disease: Current & Predicted Cost of Care and the Potential for Improved Individualized Care Using Clinical Decision Support Systems

Author, and Content Consultant to e-SERIES A: Cardiovascular Diseases: Justin Pearlman, MD, PhD, FACC, Author and Curator: Larry H Bernstein, MD, FACP and Curator: Aviva Lev-Ari, PhD, RN



6co       Hypertension and Vascular Compliance: 2013 Thought Frontier – An Arterial Elasticity Focus

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



5co       DELETED identical to 36co


4co       Biomaterials Technology: Models of Tissue Engineering for Reperfusion and Implantable Devices for Revascularization

Author and Curator: Larry H Bernstein, MD, FACP and Curator: Aviva Lev-Ari, PhD, RN



3co       Cardiovascular Diseases: Decision Support Systems for Disease Management Decision Making

Curators: Justin D. Pearlman, MD, PhD, FACC and Aviva Lev-Ari, PhD, RN



2co    DELETED identical to 35co


1co    DELETED identical to 34co


Single-Author Reporting on MedTech and Cardiac Medical Devices by

Aviva Lev-Ari, PhD, RN


162r Rhythm Management Device Hardware (Dual-chamber Pacemaker) coupled with BackBeat’s Cardiac Neuromodulation Therapy (CNT) bioelectronic therapy for Lowering Systolic Blood Pressure for patients with Pacemakers

Reporter: Aviva Lev-Ari, PhD, RN



161r Pulmonary Valve Replacement and Repair: Valvuloplasty Device – Tissue (bioprosthetic) or mechanical valve;  Surgery type – Transcatheter Pulmonary Valve Replacement (TPVR) vs Open Heart, Valve Repair – Commissurotomy, Valve-ring Annuloplasty

Reporter: Aviva Lev-Ari, PhD, RN



160r Are TAVR volume requirements limiting rural and minority access to this life-saving procedure, or are they still necessary for patient safety?

Reporter: Aviva Lev-Ari, PhD, RN


159r Top 100 of 415 articles published on PubMed in 2018 on TAVR

Reporter: Aviva Lev-Ari, PhD, RN


158r Aortic Stenosis (AS): Managed Surgically by Transcatheter Aortic Valve Replacement (TAVR) – Search Results for “TAVR” on NIH.GOV website, Top 16 pages

Reporter: Aviva Lev-Ari, PhD, RN



157r Comparison of four methods in diagnosing acute myocarditis: The diagnostic performance of native T1, T2, ECV to LLC

Reporter: Aviva Lev-Ari, PhD, RN



156r   Left ventricular outflow tract (LVOT) obstruction (LVOTO): The Role of CT in TAVR and in TMVR

Reporter: Aviva Lev-Ari, PhD, RN



155r   CABG: a Superior Revascularization Modality to PCI in Patients with poor LVF, Multivessel disease and Diabetes, Similar Risk of Stroke between 31 days and 5 years, post intervention

Reporter: Aviva Lev-Ari, PhD, RN



154r   Stanford University researchers have developed a scanner that unites optical, radioluminescence, and photoacoustic imaging to evaluate for Thin-Cap Fibro Atheroma (TCFA)

Reporter: Aviva Lev-Ari, RN



153r   An Overview of the Heart Surgery Specialty: heart transplant, lung transplant, heart-lung transplantation, aortic valve surgery, bypass surgery, minimally invasive cardiac surgery, heart valve surgery, removal of cardiac tumors, reoperation valve surgery

Reporter: Aviva Lev-Ari, PhD, RN



152r   PCI, CABG, CHF, AMI – Two Payment Methods: Bundled payments (hospitalization costs, up to 90 days of post-acute care, nursing home care, complications, and rehospitalizations) vs Diagnosis-related groupings cover only what happens in the hospital.

Reporter: Aviva Lev-Ari, PhD, RN



151r   Expanded Stroke Thrombectomy Guidelines: FDA expands treatment window for use (Up to 24 Hours Post-Stroke) of clot retrieval devices (Stryker’s Trevo Stent) in certain stroke patients

Reporter: Aviva Lev-Ari, PhD, RN



150r   What is the Role of Noninvasive Diagnostic Fractional Flow Reserve (FFR) CT vs Invasive FFR for PCI?

Reporter: Aviva Lev-Ari, PhD, RN



149r   Renowned Electrophysiologist Dr. Arthur Moss Died on February 14, 2018 at 86

Reporter: Aviva Lev-Ari, PhD, RN



148r   Mitral Valve Repair Global Leader: Edwards LifeSciences acquired Harpoon Medical for $250 in 12/2017 followed by $690 million buyout of Valtech Cardio 1/2017 and $400 million acquisition of CardiAQ Valve Technologies in 8/2017

Reporter: Aviva Lev-Ari, PhD



147r   2017 American Heart Association Annual Meeting: Sunday’s Science at #AHA17 – Presidential Address

Reporter: Aviva Lev-Ari, PhD, RN



146r   Medical Devices Early Feasibility FDA’s Pathway – Accelerated Recruitment for Randomized Clinical Trials: Replacement and Repair of Mitral Valves

Reporter: Aviva Lev-Ari, PhD, RN



145r   Arrhythmias Detection: Speeding Diagnosis and Treatment – New deep learning algorithm can diagnose 14 types of heart rhythm defects by sifting through hours of ECG data generated by some REMOTELY iRhythm’s wearable monitors

Reporter: Aviva Lev-Ari, PhD, RN



144r   Cleveland Clinic: Change at the Top, Tomislav “Tom” Mihaljevic, M.D., as its next CEO and President to succeed Toby Cosgrove, M.D., effective Jan. 1, 2018

Reporter: Aviva Lev-Ari, PhD, RN



143r   Off-Label TAVR Procedures: 1 in 10 associated with higher in-hospital 30-day mortality, 1-year mortality was similar in the Off-Label and the On-Label groups

Reporter: Aviva Lev-Ari, PhD, RN



142r   Right Internal Carotid Artery Clot Aspiration: 4.5 Minute Thrombectomy Using the ADAPT-FAST Technique and the ACE68 Catheter

Reporter: Aviva Lev-Ari, PhD, RN



141r   Less is More: Minimalist Mitral Valve Repair: Expert Opinion of Prem S. Shekar, MD, Chief, Division of Cardiac Surgery, BWH – #7, 2017 Disruptive Dozen at #WMIF17

Reporter: Aviva Lev-Ari, PhD, RN


140r   What is the history of STEMI? What is the current treatment for Cardiogenic Shock? The Case Study of Detroit Cardiogenic Shock Initiative

Reporter: Aviva Lev-Ari, PhD, RN



139r   ACC 2017, 3/30/2017 – Poor Outcomes for Bioresorbable Stents in Small Coronary Arteries

Reporter: Aviva Lev-Ari, PhD, RN



138r   Edwards Lifesciences closes $690m a buy of Valtech Cardio and most of the heart valve repair technologies it’s developing

Reporter: Aviva Lev-Ari, PhD, RN



137r   First U.S. TAVR Patients Treated With Temporary Pacing Lead (Tempo Lead)

Reporter: Aviva Lev-Ari, PhD, RN



136r   2017 World Medical Innovation Forum: Cardiovascular, May 1-3, 2017, Partners HealthCare, Boston, at the Westin Hotel, Boston

Reporter: Aviva Lev-Ari, PhD, RN



135r   Advanced Peripheral Artery Disease (PAD): Axillary Artery PCI for Insertion and Removal of Impella Device

Reporter: Aviva Lev-Ari, PhD, RN



134r   CorPath robotic system for bifurcation lesions with placement of the Absorb GT1 Bioresorbable Vascular Scaffold (BVS) (Abbott Vascular)

Reporter: Aviva Lev-Ari, PhD, RN



133r   Hadassah Opens Israel’s First Heart Valve Disease Clinic

Reporter: Aviva Lev-Ari, PhD, RN



132r   Left Main Coronary Artery Disease (LMCAD): Stents vs CABG – The less-invasive option is Equally Safe and Effective

Reporter: Aviva Lev-Ari, PhD, RN



131r   Advances and Future Directions for Transcatheter Valves – Mitral and tricuspid valve repair technologies now in development

Reporter: Aviva Lev-Ari, PhD, RN



130r   New method for performing Aortic Valve Replacement: Transmural catheter procedure developed at NIH, Minimally-invasive tissue-crossing – Transcaval access, abdominal aorta and the inferior vena cava

Reporter: Aviva Lev-Ari, PhD, RN



129r   Robot-assisted coronary intervention program @MGH – The first CorPath Vascular Robotic System, lets Interventional Cardiologists position the right stent in the right place at reduces radiation exposure by 95%

Reporter: Aviva Lev-Ari, PhD, RN



128r   Second in the United States to implant Edwards Newly FDA-Approved Aortic Valve “Intuity Elite” Sutureless Valve at Northwestern Medicine

Reporter: Aviva Lev-Ari, PhD, RN



127r   First-in-Man Mitral Valve Repairs Device used for Tricuspid Valve Repair: Cardioband used by University Hospital Zurich Heart Team

Reporter: Aviva Lev-Ari, PhD, RN



126r   Inferior Vena Cava Filters: Device for Prevention of Pulmonary Embolism and Thrombosis

Reporter: Aviva Lev-Ari, PhD, RN



125r   Chest Radiation Therapy causes Collateral Damage to the Human Heart

Reporter: Aviva Lev-Ari, PhD, RN



124r   Clinical Trials for Transcatheter Mitral Valves Annulus Repairs and TAVR: CT Structural Software for Procedural Planning and Anatomical Assessments

Reporter: Aviva Lev-Ari, PhD, RN



123r   Lysyl Oxidase (LOX) gene missense mutation causes Thoracic Aortic Aneurysm and Dissection (TAAD) in Humans because of inadequate cross-linking of collagen and elastin in the aortic wall

Mutation carriers may be predisposed to vascular diseases because of weakened vessel walls under stress conditions.

Reporter: Aviva Lev-Ari, PhD, RN



122r   SAPIEN 3 Transcatheter Aortic Valve Replacement in High-Risk and Inoperable Patients with Severe Aortic Stenosis: One-Year Clinical Outcomes

Reporter: Aviva Lev-Ari, PhD, RN



121r   Entire Family of Impella Abiomed Impella® Therapy Left Side Heart Pumps: FDA Approved To Enable Heart Recovery

Reporter: Aviva Lev-Ari, PhD, RN



120r   DELETED identical to 121r


119r   FDA approved Absorb GT1 Bioresorbable Vascular Scaffold System (BVS), Everolimus releasing and Absorbed by the body in 3 years

Reporter: Aviva Lev-Ari, PhD, RN



118r   TAVR with Sapien 3: combined all-cause death & disabling stroke rate was 8.4% and 16.6% for the surgery arm

Reporter: Aviva Lev-Ari, PhD, RN



117r   Boston Scientific implant designed to occlude the heart’s left atrial appendage implicated with embolization – Device Sales in Europe halts

Reporter: Aviva Lev-Ari, PhD, RN



116r   Issue with Delivery System Deployment Process: MitraClip Clip Recalled by Abbott Vascular

Reporter: Aviva Lev-Ari, PhD, RN



115r   Prospects for First-in-man Implantation of Transcatheter Mitral Valve by Direct Flow Medical

Reporter: Aviva Lev-Ari, PhD, RN



114r   Steps to minimise replacement of cardiac implantable electronic devices

Reporter: Aviva Lev-Ari, PhD, RN



113r Atrial Fibrillation Surgery Market worth $1.73 Billion by 2020

Reporter: Aviva Lev-Ari, PhD, RN



112r   Abbott’s Bioabsorbable Stent met its Primary Endpoint in a U.S. Clinical Trial, applications for FDA Approval follows

Reporter: Aviva Lev-Ari, PhD, RN



111r   Low-dose and High-resolution Cardiac Imaging with Revolution™ CT

Reporter: Aviva Lev-Ari, PhD, RN



110r   Hybrid Imaging 3D Model of a Human Heart by Cardiac Imaging Techniques: CT and Echocardiography

Reporter: Aviva Lev-Ari, PhD, RN



109r   Premature Ventricular Contraction percentage predicts new Systolic Dysfunction and clinically diagnosed CHF and overall Mortality

Reporter: Aviva Lev-Ari, PhD, RN



108r   ‘Mammogram for the heart’ can predict heart attack by Dr. James Min, Director of the Dalio Institute of Cardiovascular Imaging at New York-Presbyterian Hospital and Weill Cornell Medical College

Reporter: Aviva Lev-Ari, PhD, RN



107r   Abbott’s percutaneous MitraClip mitral valve repair device SUPERIOR to Pacemaker or Implantable Cardioverter Defibrillator (ICD) for reduction of Ventricular Tachyarrhythmia (VT) episodes

Reporter: Aviva Lev-Ari, PhD, RN



106r   No evidence to change current transfusion practices for adults undergoing complex cardiac surgery: RECESS evaluated 1,098 cardiac surgery patients received red blood cell units stored for short or long periods

Reporter: Aviva Lev-Ari, PhD, RN



105r   3-D BioPrinting in use to create Cardiac Living Tissue: Print Your Heart Out

Reporter: Aviva Lev-Ari, PhD, RN



104r   Fractional Flow Reserve vs. Angiography in Non-ST-segment Elevation Myocardial Infarction

Reporter: Aviva Lev-Ari, PhD, RN



103r   Transradial PCI Bests Transfemoral PCI in UK Analysis, regardless of Patient’s Age

Reporter: Aviva Lev-Ari, PhD, RN



102r   DELETED, identical to 101r


101r   Protein Clue to Sudden Cardiac Death: Research @Oxford University

Reporter: Aviva Lev-Ari, PhD, RN



100r   Culprit-Lesion Over Multivessel PCI in STEMI Patients

Reporter: Aviva Lev-Ari, PhD, RN



99r     Convergent Procedure addresses the progressive nature of A-Fib

Reporter: Aviva Lev-Ari, PhD, RN



98r     Paul Zoll, MD: Originator of Modern Electrocardiac Therapy – A Biography by Stafford Cohen, MD, BIDMC

Reporter: Aviva Lev-Ari, PhD, RN




97r     Surgical Options for Left Atrial Appendage (LAA) Removal for A-Fib Patients without Indication for Anticoagulant Therapy

Reporter: Aviva Lev-Ari, PhD, RN



96r     Intracranial Vascular Stenosis: Comparison of Clinical Trials: Percutaneous Transluminal Angioplasty and Stenting (PTAS) vs. Clot-inhibiting Drugs: Aspirin and Clopidogrel (dual antiplatelet therapy) – more Strokes if Stenting

Reporter: Aviva Lev-Ari, PhD, RN


95r     New Era for PAD as FDA approval in the US of 1st Drug-coated Balloon (DCB) for PDA – CAD Indication for DCB will follow

Reporter: Aviva Lev-Ari, PhD, RN



94r     Tethered–Liquid Perfluorocarbon surface (TLP): Biocoating Prevents Blood from Clotting on Implantables

Reporter: Aviva Lev-Ari, PhD, RN



93r     Medtronic’s CoreValve System Sustains Positive Outcomes Through Two Years in Extreme Risk Patients

Reporter: Aviva Lev-Ari, PhD, RN



92r     Thrombus Aspiration for Myocardial Infarction: What are the Outcomes One Year After

Reporter: Aviva Lev-Ari, PhD, RN



91r     Fractional Flow Reserve–Guided PCI vs Drug Therapy for Stable Coronary Artery Disease

Reporter: Aviva Lev-Ari, PhD, RN


90r     Capillaries: A Mapping Geometrical Method using Organ 3D Printing

Reporter: Aviva Lev-Ari, PhD, RN



89r     One year Post-Intervention Mortality Rate: TAVR and AVR – Aortic Valve Procedures 6.7% in AVR, 11.0% in AVR with CABG, 20.7 in Transvascular (TV-TAVT) and 28.0% in Transapical (TA-TAVR) Patients

Reporter: Aviva Lev-Ari, PhD, RN



88r     CEO of PolyNova: The Paradigm Shift in Heart Valve

Reporter: Aviva Lev-Ari, PhD, RN



87r     An FDA advisory committee unanimously recommended approval of the Lutonix drug-coated balloon PTA catheter for the treatment of patients with femoropopliteal occlusive disease.

Reporter: Aviva Lev-Ari, PhD, RN



86r     Patent Dispute over Heart Defect Repair Technology: Appeals court Upholds Gore win over St. Jude Medical – Helex septal occluder competes with the Amplatzer device made by AGA/St. Jude

Reporter: Aviva Lev-Ari, PhD, RN


85r     Chest Pain: Cardiac MRI provides the Picture of MI

Reporter: Aviva Lev-Ari, PhD, RN



84r     CardioMEMS sold to St. Jude Medical: Boston Millennia Partners announced that St. Jude Medical (NYSE: STJ) is acquiring the remaining 81 percent of CardioMEMS, Inc. it does not own for $375 million

Reporter: Aviva Lev-Ari,  PhD, RN



83r     Cardiovascular Biology  – A Bibliography of Research @Technion

Reporter: Aviva Lev-Ari, PhD, RN



82r     Asymptomatic Patients After Percutaneous Coronary Intervention: Low Yield of Stress Imaging – Population-Based Study

Reporter: Aviva Lev-Ari, PhD, RN




81r     Transcatheter Mitral Valve (TMV) Procedures: Centers for Medicare & Medicaid Services (CMS) proposes to cover Transcatheter Mitral Valve Repair (TMVR)

Reporter: Aviva Lev-Ari, PhD, RN



80r     Minimally Invasive Valve Therapy Programs: Recommendations by SCAI, AATS, ACC, STS

Reporter: Aviva Lev-Ari, PhD, RN



79r     Among those 26 exams deemed low-value, 12 involve medical imaging, in tests that range from preoperative chest radiography to carotid artery screening for asymptomatic patients, imaging for back pain, and CT for headache and rhinosinusitis (JAMA Internal Medicine, May 12, 2014)

Reporter: Aviva Lev-Ari, PhD, RN



78r     FDA on Medical Devices: Part 1 – User Fee Act (MDUFA) III and Part 2 – Expedited Access Program for Medical Devices that Address Unmet Medical Needs

Reporter: Aviva Lev-Ari, PhD, RN



77r     Settled Heart Valve Lawsuit: Medtronic to Pay Edwards: Edwards Lifesciences’ Sapien XT beat out Medtronic’s CoreValve

Reporter: Aviva Lev-Ari, PhD, RN



76r     Replacement of the Mitral Valve: Using the Edwards’ Sapien Aortic Valve Device

Reporter: Aviva Lev-Ari, PhD, RN



75r     Stem-Cell Therapy for Ischemic Heart Failure: Clinical Trial MSC Demonstrates Efficacy

Reporter: Aviva Lev-Ari, PhD, RN




74r     ATVB (Arteriosclerosis, Thrombosis and Vascular Biology) 2014 Conference  5/1 – 5/3/2014, Sheraton Centre Toronto – Toronto, Ontario

Reporter: Aviva Lev-Ari, PhD, RN



73r     Endovascular Aortic Repair: A New Tool for Procedure Planning

Reporter: Aviva Lev-Ari, PhD, RN



72r     Females and Non-Atherosclerotic Plaque: Spontaneous Coronary Artery Dissection – New Insights from Research and DNA Ongoing Study

Reporter: Aviva Lev-Ari, PhD, RN


71r     Of the Cardiac-specific Deaths, Deaths from Heart Attack and Sudden Heart Rhythm Disturbances declined steeply, no decline in Deaths from Heart Failure in a 20,000 PCI patients Study @ Mayo Clinic

Reporter: Aviva Lev-Ari, PhD, RN



70r     Cardiac Perfusion Exam, Rapid Heart Scanner, CT, MRI and PET imaging – Innovations in Radiology @ Beth Israel Deaconess Medical Center

Reporter: Aviva Lev-Ari, PhD, RN



69r     Maladaptive Vascular Remodeling found by four-dimensional (4D) flow MRI: Outflow Patterns, Wall Shear Stress, and Expression of Aortopathy are caused by Congenital bicuspid aortic valve (BAV) Cusp Fusion

Reporter: Aviva Lev-Ari, PhD, RN



68r     “Medicine Meets Virtual Reality” – NextMed-MMVR21 Conference 2/19 – 2/22/2014, Manhattan Beach Marriott, Manhattan Beach, CA

Reporter: Aviva Lev-Ari, PhD, RN



67r     Preserved vs Reduced Ejection Fraction: Available and Needed Therapies

Reporter: Aviva Lev-Ari, PhD, RN



66r     Developments on the Frontier of Transcatheter Aortic Valve Replacement (TAVR) Devices

Reporter: Aviva Lev-Ari, PhD, RN



65r     On-Hours vs Off-Hours: Presentation to ER with Acute Myocardial Infarction – Lower Survival Rate if Off-Hours

Reporter: Aviva Lev-Ari, PhD, RN



64r     Elastin Arteriopathy: The Genetics of Supravalvular Aortic Stenosis

Reporter: Aviva Lev-Ari, PhD, RN



63r     Abdominal Aortic Aneurysm: Matrix Metalloproteinase-9 Genotype as a Potential Genetic Marker

Reporter: Aviva Lev-Ari, PhD, RN



62r     Genetics of Aortic and Carotid Calcification: The Role of Serum Lipids

Reporter: Aviva Lev-Ari, PhD, RN



61r     St. Jude’s CEO is still betting on EnligHTN IV Study Renal Denervation System, despite Medtronic’s setback related to SYMPLICITY Phase IV

Reporter: Aviva Lev-Ari, PhD, RN



60r     Ischemic Stable CAD: Medical Therapy and PCI no difference in End Point: Meta-Analysis of Contemporary Randomized Clinical Trials

Reporter: Aviva Lev-Ari, PhD, RN



59r     Resistance Hypertension: Renal Artery Intervention using Stenting

Reporter: Aviva Lev-Ari, PhD, RN



58r   For Accomplishments in Cardiology and Cardiovascular Diseases: 2015 The Arrigo Recordati International Prize for Scientific Research

Reporter: Aviva Lev-Ari, PhD, RN



57r   Dalio Institute of Cardiovascular Imaging @ NewYork-Presbyterian Hospital and Weill Cornell Medical College

Reporter: Aviva Lev-Ari, PhD, RN



56r   ACC/AHA Guidelines for Coronary Artery Bypass Graft Surgery

Reporter: Aviva Lev-Ari, PhD, RN



55r     Risks for Patients’ and Physician’s Health in the Cath Lab

Reporter and Curator: Aviva Lev-Ari, PhD, RN



54r     Myocardial Infarction: The New Definition After Revascularization

Reporter: Aviva Lev-Ari, PhD, RN


53r     Echocardiogram Quantification: Quest for Reproducibility and Dependability

Reporter: Aviva Lev-Ari, PhD, RN


52r     Myocardial Strain and Segmental Synchrony: Age and Gender in Speckle-tracking-based Echocardiographic Study

Reporter: Aviva Lev-Ari, PhD, RN


51r   Hybrid Cath Lab/OR Suite’s da Vinci Surgical Robot of Intuitive Surgical gets FDA Warning Letter on Robot Track Record

Reporter: Aviva Lev-Ari, PhD, RN



50r     Abdominal Aortic Aneurysms (AAA): Albert Einstein’s Operation by Dr. Nissen

Reporter: Aviva Lev-Ari, PhD, RN


49r     Transposon-mediated Gene Therapy improves Pulmonary Hemodynamics and attenuates Right Ventricular Hypertrophy: eNOS gene therapy reduces Pulmonary vascular remodeling and Arterial wall hyperplasia

Reporter: Aviva Lev-Ari, PhD, RN



48r   First-of-Its-Kind FDA Approval for ‘AUI’ Device with Endurant II AAA Stent Graft: Medtronic Expands in Endovascular Aortic Repair in the United States

Reporter: Aviva Lev-Ari, PhD, RN



47r     Bioabsorbable Drug Coating Scaffolds, Stents and Dual Antiplatelet Therapy

Reporter: Aviva Lev-Ari, PhD, RN


46r     Svelte Medical Systems’ Drug-Eluting Stent: 0% Clinically-Driven Events Through 12-Months in First-In-Man Study

Reporter: Aviva Lev-Ari, PhD, RN



45r   Echo vs Cardiac Magnetic Resonance Imaging (CMRI): CMRI may be a useful adjunct in Hypertrophic Cardiomyopathy (HCM) family screening in higher risk

Reporter: Aviva Lev-Ari, PhD, RN



44r   iElastance: Calculates Ventricular Elastance, Arterial Elastance and Ventricular-Arterial Coupling using Echocardiographic derived values in a single beat determination

Reporter: Aviva Lev-Ari, PhD, RN



43r   CT Angiography (CCTA) Reduced Medical Resource Utilization compared to Standard Care reported in JACC

Reporter: Aviva Lev-Ari, PhD, RN



42r   Texas Heart Institute: 50 Years of Accomplishments

Reporter: Aviva Lev-Ari, PhD, RN



41r   Economic Toll of Heart Failure in the US: Forecasting the Impact of Heart Failure in the United States – A Policy Statement From the American Heart Association

Reporter: Aviva Lev-Ari, PhD, RN



40r   Sudden Cardiac Death invisible at Autopsy: Forensic Power of Postmortem MRI

Reporter: Aviva Lev-Ari, PhD, RN



39r   Advanced CT Reconstruction: Plaque Estimation Algorithm for Fewer Errors and Semiautomation

Reporter: Aviva Lev-Ari, PhD, RN



38r     Dilated Cardiomyopathy: Decisions on implantable cardioverter-defibrillators (ICDs) using left ventricular ejection fraction (LVEF) and Midwall Fibrosis: Decisions on Replacement using late gadolinium enhancement cardiovascular MR (LGE-CMR)

Reporter: Aviva Lev-Ari, PhD, RN



37r     Clinical Trials on transcatheter aortic valve replacement (TAVR) to be conducted by American College of Cardiology and the Society of Thoracic Surgeons

Reporter: Aviva Lev-Ari, PhD, RN



36r     Direct Flow Medical Wins European Clearance for Catheter Delivered Aortic Valve

Reporter: Aviva Lev-Ari, PhD, RN



35r     DELETED, identical to 15c


34r     PCI Outcomes, Increased Ischemic Risk associated with Elevated Plasma Fibrinogen not Platelet Reactivity

Reporter: Aviva Lev-Ari, PhD, RN



33r     Cardiac Surgery Theatre in China vs. in the US: Cardiac Repair Procedures, Medical Devices in Use, Technology in Hospitals, Surgeons’ Training and Cardiac Disease Severity

Reporter: Aviva Lev-Ari, PhD, RN



32r     DELETED, identical to 14c

31r     DELETED, identical to 12c


30r     Heart Renewal by pre-existing Cardiomyocytes: Source of New Heart Cell Growth Discovered

Reporter: Aviva Lev-Ari, PhD, RN



29r     Ablation Devices Market to 2016 – Global Market Forecast and Trends Analysis by Technology, Devices & Applications

Reporter: Aviva Lev-Ari, PhD, RN



28r     Abdominal Aortic Aneurysm: Endovascular repair and open repair resulted in similar long-term survival

Reporter: Aviva Lev-Ari, PhD, RN



27r     Renal Denervation Technology of Vessix Vascular, Inc. been acquired by Boston Scientific Corporation (BSX) to pay up to $425 Million

Reporter: Aviva Lev-Ari, PhD, RN



26r     DELETED, identical to 11c


25r     To Stent or Not? A Critical Decision

Reporter: Aviva Lev-Ari, PhD, RN



24r     FDA Approval for Under-Skin Defibrillator goes to Boston Scientific Corporation

Reporter: Aviva Lev-Ari, PhD, RN



23r     Absorb™ Bioresorbable Vascular Scaffold: An International Launch by Abbott Laboratories

Reporter: Aviva Lev-Ari, PhD, RN



22r     Carotid Stenting: Vascular surgeons have pointed to more minor strokes in the stenting group and cardiologists to more myocardial infarctions in the CEA cohort.

Reporter: Aviva Lev-Ari, PhD, RN



21r     FDA: Strengthening Our National System for Medical Device Post-market Surveillance

Reporter: Aviva Lev-Ari, PhD, RN



20r     Transcatheter Aortic-Valve Replacement for Inoperable Severe Aortic Stenosis

Reporter: Aviva Lev-Ari, PhD, RN



19r     Evidence for Overturning the Guidelines in Cardiogenic Shock

Reporter: Aviva Lev-Ari, PhD, RN



18r     Imbalance of Autonomic Tone: The Promise of Intravascular Stimulation of Autonomics

Reporter: Aviva Lev-Ari, PhD, RN


17r     Intravascular Stimulation of Autonomics: A Letter from Dr. Michael Scherlag

Letter received by Aviva Lev-Ari, PhD, RN on September 1, 2012



16r     New Definition of MI Unveiled, Fractional Flow Reserve (FFR)CT for Tagging Ischemia

Reporter: Aviva Lev-Ari, PhD, RN



15r     DELETED, identical to 8c


14r     Expected New Trends in Cardiology and Cardiovascular Medical Devices

Reporter: Aviva Lev-Ari, PhD, RN



13r     Patient Access to Medical Devices — A Comparison of U.S. and European Review Processes

Reporter: Aviva Lev-Ari, PhD, RN



12r   Coronary CT Angiography versus Standard Evaluation in Acute Chest Pain

Reporter: Aviva Lev-Ari, PhD, RN



11r     Updated Transcatheter Aortic Valve Implantation (TAVI): risk for stroke and suitability for surgery

Reporter: Aviva Lev-Ari, PhD, RN



10r     Transcatheter Aortic Valve Implantation (TAVI): FDA approves expanded indication for two transcatheter heart valves for patients at intermediate risk for death or complications associated with open-heart surgery

Reporter: Aviva Lev-Ari, PhD, RN



9r      Early Surgery May Benefit Some With Heart Infection

Reporter: Aviva Lev-Ari, RN



8r      Gaps, Tensions, and Conflicts in the FDA Approval Process: Implications for Clinical Practice

Reporter: Aviva Lev-Ari, PhD, RN



7r      Heart Remodeling by Design – Implantable Synchronized Cardiac Assist Device: Abiomed’s Symphony

Reporter: Aviva Lev-Ari, PhD, RN



6r      Percutaneous Endocardial Ablation of Scar-Related Ventricular Tachycardia

Reporter: Aviva Lev-Ari, PhD, RN



5r      Implantable Synchronized Cardiac Assist Device Designed for Heart Remodeling: Abiomed’s Symphony

Reporter: Aviva Lev-Ari, PhD, RN



4r      Percutaneous Transluminal Angioplasty and Stenting (PTAS) – Stenting versus Aggressive Medical Therapy for Intracranial Arterial Stenosis

Reporter: Aviva Lev-Ari, PhD, RN



3r      The Centers for Medicare & Medicaid Services (CMS) covers transcatheter aortic valve replacement (TAVR) under Coverage with Evidence Development (CED)

Reporter: Aviva Lev-Ari, PhD, RN



2r     Investigational Devices: Edwards Sapien Transcatheter Aortic Heart Valve Replacement Transfemoral Deployment

Reporter: Aviva Lev-Ari, PhD, RN



1r     Investigational Devices: Edwards Sapien Transcatheter Aortic Valve Transapical Deployment

Reporter: Aviva Lev-Ari, PhD, RN





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