Healthcare analytics, AI solutions for biological big data, providing an AI platform for the biotech, life sciences, medical and pharmaceutical industries, as well as for related technological approaches, i.e., curation and text analysis with machine learning and other activities related to AI applications to these industries.
Metabolic analysis has been widely used in laboratory research applications. One of the main uses in this field was the metabolic phenotyping of mouse models of cardiovascular diseases; this approach was pioneered by the group of Julian Griffin mainly using models of Duchenne muscular distrophy where they were able to show different metabolic profiles associated with the expression of dystrophin and utrophin in heart muscle. In a later work the same group applied the FANCY approach (Functional Analysis by Co-responses in Yeast) to mouse models of cardiac diseases and showed that although the background strain of mice was an important source of metabolic variation, multivariate statistics were able to separate each disease model from the control strain.
Since the beginning of the 21st century the term ‘personalized medicine’ has continuously gained popularity and is now considered an essential trait of present and future medicine. For personalized medicine to be successful, it is necessary to properly identify subjects at increased risk of developing a disease, which patients will respond to a given therapy or how a disease will evolve in each case. In other words it is important to genotype and or phenotype the individual patient so that its individual response to disease and treatment can be predicted.
Sabatine et al. in 2005 showed that it was possible to apply metabolomic analysis in a carefully characterized cohort of patients undergoing exercise stress testing and to differentiate between patients that developed inducible ischemia from the ones that did not. This work was done by analyzing serum samples obtained before, during and after stress testing by high performance liquid chromatography coupled to mass spectroscopy; ischaemic patients had higher circulating levels of metabolites belonging to the citric acid pathway. Ischemic patients had relatively higher lactate levels than non ischemic suggesting an underlying ischemic process although it could not be directly related to myocardial ischemia.
It has been known for a time that patients with heart failure (HF) have an altered heart metabolism and that metabolic modulation (shifting the main substrate from free fatty acids to glucose) improved VO2max, left ventricular ejection fraction, symptoms, resting and peak stress myocardial function, and skeletal muscle energetics. Metabolic modulation as a tool to treat patients with heart failure has attracted interest but the metabolomic analysis has not followed suit until recently when Kang et al. 2011 showed by profiling urine by NMR spectroscopy that it was possible to detect changes between HF patients and controls. It could be interesting to evaluate possible changes in the urine metabolic profile of patients treated with drugs targeting heart metabolism for example, perhexiline or trimetazidine. In conclusion, the future of metabolomics is now. It is clear that metabolomics can be applied to various cardiovascular related diseases, although its clinical value in different settings remains to be determined; this is the next big challenge in the field.
Vascular Surgery: International, Multispecialty Position Statement on Carotid Stenting, 2013 and Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD
Author and Curator: Aviva Lev-Ari, PhD, RN
Article ID #66: Vascular Surgery: International, Multispecialty Position Statement on Carotid Stenting, 2013 and Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD. Published on 7/14/2013
WordCloud Image Produced by Adam Tubman
Part One:
Vascular Surgery International, Multispecialty Position Statement on Carotid Stenting, 2013
Part Two:
Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD, Chief, Division of Vascular and Endovascular Surgery Co-Director, Thoracic Aortic Center @ MGH
I. Recollection of a visit at Dr. Cambria’s Office, 2004
II. Shadowing Dr. Cambria in OR @MGH
III. Dr. Cambria: Selection of Contributions to Scientific Research on Vascular Surgery
IV. Cardiovascular Clinical Observational Experience – Aviva Lev-Ari, PhD, RN
V. Cases with Complications: CEA and CAS
Part Three:
On 8/1/2013, Cleveland Clinic Reports Equivalence between carotid endarterectomy (CEA) and open-heart surgery (OHS) and carotid artery stenting (CAS) followed by coronary artery bypass graft (CABG) surgery or non-CABG cardiac surgery
Part One:
Vascular Surgery International, Multispecialty Position Statement on Carotid Stenting, 2013 Part
No other invasive intervention procedure in the history of Vascular Surgery has stormed the profession more than the two treatment options for carotid artery partial to complete blockage than Carotid endarterectomy (CEA) and Carotid angioplasty and stenting (CAS).
The debate required evidence based resolution for the two treatment options in terms of patient outcomes and adverse events. As the title of the Position statement explained below, the verdict is non equivocal: Routine Carotid Stenting is inferior to Carotid endarterectomy (CEA) from a patient safety and outcomes.
In conclusion, current global evidence shows that, even in the best academic centers, CAS is less effective (causing more strokes) and more expensive than CEA. It is premature that some guidelines have recently added support for routine practice CAS as an alternative to CEA for
asymptomatic43,44 and
low/ average surgical risk symptomatic patients43–45
because CAS may easily be misinterpreted by readers as being equivalent for
stroke prevention46 and
historical procedural standards were cited.
CAS, for these patients, should still only be performed and paid for within well‐designed, adequately powered trials. The US Center for Medicare and Medicaid Services is doing its job and setting an excellent global example. It is protecting Medicare beneficiaries from routine practice procedures, which are currently more likely to harm them and waste finite resources47 that could be used for their advantage. Meanwhile, we need to reassess the current routine practice role of CEA and deliver optimal current medical treatment to all who need it.
Clinical Trials Results
To avoid misguidance from calls for more routine practice (nontrial) carotid angioplasty/stenting (CAS), we need to distinguish relevant facts and patients’ best interests from all else (distractions). A recent editorial by White and Jaff1 is one publication which illustrates this need particularly well. First, these authors are correct in reminding us that the responsibility of physicians is to provide best patient care, putting aside personal interest. This is inherent in any profession.2 However, misconception, bias, and conflict of interest exist. Therefore, healthcare payment organizations, such as the US Center for Medicare and Medicaid Services are important gatekeepers to facilitate patient access to interventions that are likely to help them, as opposed to all others.
It is also true that CAS and carotid endarterectomy (CEA) result in better outcomes when patients are carefully selected and skilled operators perform the procedures in experienced centers.1 We would add that key indicators (such as 30‐day periprocedural stroke/death rates) must be accurately measured in routine (real‐world) practice, particularly as stroke and death rates here may be unacceptably higher than in trials. 3–5 Therefore, it is most appropriate, as suggested by White and Jaff,1 that coverage for carotid procedures be dependent on facility accreditation and audited measurement of key standards indicators in all practices performing these procedures.
This is a priority issue. White and Jaff1 also correctly state “a major change in evidence based stroke prevention strategies will require clinical trial data.,7,8 meta‐analyses, and routine practice.9–14 Most of these data relate to low/average risk symptomatic patients and demonstrate that, for these patients, even in the best academic centers, CAS is consistently associated with significantly higher rates of stroke or death (during or after the periprocedural period) compared with CEA.
It is incorrect that CREST “failed to show a difference in overall stroke rate between CAS and CEA” as stated by White and Jaff.1 In CREST, for average surgical risk symptomatic patients, the periprocedural stroke and death rates were 6.0% for CAS versus 3.2% for CEA (hazard ratio, 1.89; 95% confidence interval, 1.11–3.21; P=0.02).8
The higher periprocedural risk of stroke or death with CAS is particularly evident in the most senior patients (>68–70 years),13,15,16 those undergoing the procedure <7 days of incident cerebral or retinal ischemic symptoms17 (when CEA has the highest stroke prevention potential),18 those undergoing CAS outside clinical trials,19 and those with certain anatomic features.20 No study has shown that CAS is more effective than CEA in preventing stroke. Further, most analyses show that CAS costs considerably more,21–24 despite calculations derived from CREST results.25 No randomized trial has been adequately powered to compare the procedural and longer term risk of CAS on stroke or death in low/average risk asymptomatic patients. However, in CREST, the direction of effect was toward nearly twice the risk (periprocedural stroke/death rate was 2.5% for CAS versus 1.4% for CEA; hazard ratio, 1.88; 95% confidence interval, 0.79–4.42; P=0.15).8 This was consistent with the significantly higher periprocedural stroke rates seen in CREST CAS‐treated symptomatic patients8 and nontrial CAS‐treated asymptomatic patients.9,26
Meanwhile, medical treatment for asymptomatic carotid disease has improved significantly since past randomized trials of medical treatment alone versus additional CEA.27–32 Medical treatment consists of identification of risk factors for heart and vascular disease and risk reduction using healthy lifestyles and appropriate drugs. Improvement in medical treatment is clear from robust analyses of all published comparable, quality stroke rate calculations (including from, and within, randomized surgical trials) of patients with 50% to 99% asymptomatic carotid stenosis. This knowledge is not, as claimed by White and Jaff,1 derived from short‐cut extrapolation from coronary artery trials. Using the same standardized rate calculations, we are now seeing an average annual rate of ipsilateral stroke of ≈0.5% with medical treatment alone.30,33,34 This is about 3X— lower than that of asymptomatic CREST CAS‐treated patients and about half the rate of asymptomatic CREST CEA‐treated patients.7,9 This low rate with medical treatment is likely to fall further with improvements in efficacy, definition, and implementation.
However, recently published rate calculations indicate that, at most, only ≈2.5% of low/average CEA risk patients with 50% to 99% asymptomatic carotid stenosis will receive a stroke prevention benefit from CEA or CAS during their remaining average 10‐year lifetime if they receive good, current medical treatment (assuming the procedural risk of stroke/death is always zero).35 This indicates that a one‐size‐fits‐all procedural approach for these asymptomatic patients is now unlikely to be beneficial overall. We need to be much more selective. Research is required to determine which asymptomatic subgroups now benefit from carotid procedures in addition to current optimal medical treatment.
We have found no direct information about the influence of current medical treatment in patients with low/average CEA risk symptomatic carotid stenosis. However, improving results for medically treated asymptomatic patients27–32 and procedural trial asymptomatic and symptomatic patients8 indicate that a 6% periprocedural risk of
stroke or
death (the current standard) is now too high.
New randomized and risk stratification studies are required using current optimal medical treatment and procedural methods.36 For example,
improved plaque37 and
thrombus identification38 or
embolic signal detection39 above and below the stenosis
may help better identify carotid plaques responsible for carotid territory ischemic symptoms. Further, the best approach for patients with high surgical risk carotid stenosis remains uncertain because risk of stroke or death has not been measured with any standard of medical treatment or adequate procedural trials. However, some registries show significantly higher risks of stroke/death with CAS compared with CEA in asymptomatic and symptomatic high surgical risk patients.40
Incidence of MI
Calls from other authors for more routine CAS on the grounds of lower periprocedural myocardial infarction (MI) rates compared with CEA are distracting.41 MI is not a measure of stroke prevention efficacy, even though it is an important procedural complication. The inclusion of periprocedural MI with stroke and death in the primary outcome measure in CREST resulted in primary outcome equivalence between CAS and CEA. However, it did not result in efficacy equivalence. In CREST, 1.1% (14/1262) of CAS patients had periprocedural clinical MI (biomarkers plus chest pain/ECG evidence) compared with 2.3% (28/1240) of CEA patients7 (P=0.03). However, periprocedural stroke was nearly twice as common (81/2502; 3.2%)7 as periprocedural clinical MI (42/2502; 1.7%) and, as mentioned above, CAS caused almost twice as many of these strokes as CEA.Further, in CREST, the mortality rate up to 4 years was equally poor for CREST patients with periprocedural stroke (20%),42 periprocedural clinical MI (19%),41 or periprocedural biomarker‐positive only MI (25%).41 Finally, nonfatal stroke was associated with a poorer quality of life at 1 year than nonfatal MI.7 Therefore, MI is a measure of carotid procedural risk (not benefit) and must be considered separately from stroke risk. Moreover, in CREST, CAS‐associated stroke was more troublesome for patients than CEA‐associated MI.
Conclusion
Calls for More Routine Carotid Stenting Are Currently Inappropriate, 3/2013
Carotid artery disease, also called carotid artery stenosis, occurs when the carotid arteries, the main blood vessels that carry oxygenated blood to the brain, become narrowed. The narrowing of the carotid arteries is most commonly related to atherosclerosis (a buildup of plaque, which is a deposit of fatty substances, cholesterol, cellular waste products, calcium, and fibrin in the inner lining of an artery). Atherosclerosis, or “hardening of the arteries,” is a vascular disease (disease of the arteries and veins). Carotid artery disease is similar to coronary artery disease, in which blockages occur in the arteries of the heart, and may cause a heart attack.
Click Image to Enlarge
To better understand how carotid artery disease affects the brain, a basic review of the anatomy of the circulation system of the brain follows.
What are the carotid arteries?
The main supply of blood to the brain is carried by the carotid arteries. The carotid arteries branch off from the aorta (the largest artery in the body) a short distance from the heart, and extend upward through the neck carrying oxygen-rich blood to the brain.
There are four carotid arteries: the right and left internal carotid arteries and the right and left external carotid arteries. One pair (external and internal) is located on each side of the neck. Just as a pulse can be felt in the wrists, a pulse can also be felt on either side of the neck over the carotid arteries.
Click to Enlarge
Why are the carotid arteries important?
Because the carotid arteries deliver blood to the brain, carotid artery disease can have serious implications by reducing the flow of oxygen to the brain. The brain needs a constant supply of oxygen in order to function. Even a brief interruption in blood supply can cause problems. Brain cells begin to die after just a few minutes without blood or oxygen. If the narrowing of the carotid arteries becomes severe enough to block blood flow, or a piece of atherosclerotic plaque breaks off and obstructs blood flow to the brain, a stroke may occur.
What causes carotid artery disease?
Atherosclerosis is the most common cause of carotid artery disease. It is unknown exactly how atherosclerosis begins or what causes it. Atherosclerosis is a slow, progressive, vascular disease that starts as early as childhood. However, the disease has the potential to progress rapidly. It is generally characterized by the accumulation of fatty deposits along the innermost layer of the arteries. If the disease process progresses, plaque formation may take place. Plaque is made up of deposits of smooth muscle cells, fatty substances, cholesterol, calcium, and cellular waste products. This thickening narrows the arteries and can decrease blood flow or completely block the flow of blood to the brain.
Risk factors associated with atherosclerosis include:
Older age
Male
Family history
Race or ethnicity
Genetic factors
Hyperlipidemia (elevated fats in the blood)
Hypertension (high blood pressure)
Smoking
Diabetes
Obesity
Diet high in saturated fat
Lack of exercise
A risk factor is anything that may directly increase or be associated with a person’s chance of developing a disease. It may be an activity, such as smoking, diet, family history, or many other things. Different diseases have different risk factors.
Although these risk factors increase a person’s risk, they do not necessarily cause the disease. Some people with one or more risk factors never develop the disease, while others develop disease and have no known risk factors. Knowing your risk factors to any disease can help to guide you into the appropriate actions, including changing behaviors and being clinically monitored for the disease.
What are the symptoms of carotid artery disease?
Carotid artery disease may be asymptomatic (without symptoms) or symptomatic (with symptoms). Asymptomatic carotid disease is the presence of a significant amount of atherosclerotic buildup without obstructing enough blood flow to cause symptoms. However, a sufficiently tight stenosis will not always cause symptoms. Symptomatic carotid artery disease may result in either a transient ischemic attack (TIA) and/or a stroke (brain attack).
A transient ischemic attack (TIA) is a sudden or temporary loss of blood flow to an area of the brain, usually lasting a few minutes to one hour. Symptoms go away entirely within 24 hours, with complete recovery. Symptoms of a TIA may include, but are not limited to, the following:
Sudden weakness or clumsiness of an arm and/or leg on one side of the body
Sudden paralysis (inability to move) of an arm and/or leg on one side of the body
Loss of coordination or movement
Confusion, decreased ability to concentrate, dizziness, fainting, and/or headache
Numbness or loss of sensation (feeling) in the face
Numbness or loss of sensation in an arm and/or leg
Temporary loss of vision or blurred vision
Inability to speak clearly or slurred speech
TIA may be related to severe narrowing or blockage or from small pieces of an atherosclerotic plaque breaking off, traveling through the bloodstream, and lodging in small blood vessels in the brain. With TIA, there is rarely permanent brain damage.
Call for medical help immediately if you suspect a person is having a TIA, as it may be a warning sign that a stroke is about to occur. Not all strokes, however, are preceded by TIAs.
Stroke is another indicator of carotid artery disease. The symptoms of a stroke are the same as for a TIA. A stroke is loss of blood flow (ischemia) to the brain that continues long enough to cause permanent brain damage. Brain cells begin to die after just a few minutes without oxygen. The area of dead cells in tissues is called an infarct.
The area of the brain that suffered the loss of blood flow will determine what the physical or mental disability may be. This may include impaired ability with movement, speech, thinking and memory, bowel and bladder function, eating, emotional control, and other vital body functions. Recovery from the specific ability affected depends on the size and location of the stroke. A stroke may result in problems, such as weakness in an arm or leg or may cause paralysis, loss of speech, or even death.
The symptoms of carotid artery disease may resemble other medical conditions or problems. Always consult your doctor for a diagnosis.
How is carotid artery disease diagnosed?
In addition to a complete medical history and physical examination, diagnostic procedures for carotid artery disease may include any, or a combination, of the following:
Auscultation (listening to) of carotid arteries. Placement of a stethoscope over the carotid artery to listen for a particular sound called a bruit (pronounced brew-ee). A bruit is an abnormal sound that is produced by blood passing through a narrowed artery. A bruit is generally considered a sign of an atherosclerotic artery; however, an artery may be diseased without producing this sound.
Carotid artery duplex scan. A type of vascular ultrasound study performed to assess the blood flow of the carotid arteries. A carotid artery duplex scan is a noninvasive (the skin is not pierced) procedure. A probe called a transducer sends out ultrasonic sound waves at a frequency too high to be heard. When the transducer (like a microphone) is placed on the carotid arteries at certain locations and angles, the ultrasonic sound waves move through the skin and other body tissues to the blood vessels, where the waves echo off of the blood cells. The transducer picks up the reflected waves and sends them to an amplifier, which makes the ultrasonic sound waves audible. Absence or faintness of these sounds may indicate an obstruction to the blood flow.
Magnetic resonance imaging (MRI). A diagnostic procedure that uses a combination of large magnets, radiofrequencies, and a computer to produce detailed images of organs and structures within the body. To have this test done, you lie inside a big tube while magnets pass around your body. It is very loud. Sometimes it is done with IV contrast injected into your veins and sometimes not.
Magnetic resonance angiography (MRA). A noninvasive diagnostic procedure that uses a combination of magnetic resonance technology (MRI) and intravenous (IV) contrast dye to visualize blood vessels. Contrast dye causes blood vessels to appear opaque on the MRI image, allowing the doctor to visualize the blood vessels being evaluated.
Computed tomography scan (also called a CT or CAT scan). A diagnostic imaging procedure that uses a combination of X-rays and computer technology to produce horizontal, or axial, images (often called slices) of the body. A CT scan shows detailed images of any part of the body, including the bones, muscles, fat, and organs. CT scans are more detailed than general X-rays. Like an MRI, it is sometimes done with IV contrast injected into your veins and sometimes not.
Angiography. An invasive procedure used to assess the degree of blockage or narrowing of the carotid arteries by taking X-ray images while a contrast dye in injected. The contrast dye helps to visualize the shape and flow of blood through the arteries as X-ray images are made.
Treatment for carotid artery disease
Specific treatment for carotid artery disease will be determined by your doctor based on:
Your age, overall health, and medical history
Extent of the disease
Your signs and symptoms
Your tolerance of specific medications, procedures, or therapies
Expectations for the course of the disease
Your opinion or preference
Carotid artery disease (asymptomatic or symptomatic) in which the narrowing of the carotid artery is less than 50 percent is most often treated medically. Asymptomatic disease with less than 70 percent narrowing may also be treated medically, depending on the individual situation.
Medical treatment for carotid artery disease may include:
Modification of risk factors. Risk factors that may be modified include smoking, elevated cholesterol levels, elevated blood glucose levels, lack of exercise, poor dietary habits, and elevated blood pressure.
Medications. Medications that may be used to treat carotid artery disease include:
Antiplatelet medications. Medications used to decrease the ability of platelets in the blood to stick together and cause clots. Aspirin, clopidogrel, and dipyridamole are examples of antiplatelet medications.
Antihyperlipidemics. Medications used to lower lipids (fats) in the blood, particularly cholesterol. Statins are a group of antihyperlipidemic medications, and include simvastatin, atorvastatin, and pravastatin, among others. Studies have shown that certain statins can decrease the thickness of the carotid artery wall and increase the size of the lumen (opening) of the artery.
Antihypertensives. Medications used to lower blood pressure. There are several different groups of medications which act in different ways to lower blood pressure.
In people with narrowing of the carotid artery greater than 50 to 69 percent, a more aggressive treatment may be recommended, particularly in people with symptoms. Surgical treatment decreases the risk for stroke after symptoms such as TIA or minor stroke, especially in people with an occlusion (blockage) of more than 70 percent who are good candidates for surgery.
Surgical treatment of carotid artery disease includes:
Carotid endarterectomy (CEA). Carotid endarterectomy is a procedure used to remove plaque and clots from the carotid arteries, located in the neck. Endarterectomy may help prevent a stroke from occurring in people with symptoms with a carotid artery narrowing of 70 percent of more.
Illustration of Carotid Endarterectomy (Click to Enlarge)
Carotid artery angioplasty with stenting (CAS). Carotid angioplasty with stenting is an option for patients who are high risk for carotid endarterectomy. This is a minimally invasive procedure in which a very small hollow tube, or catheter, is advanced from a blood vessel in the groin to the carotid arteries. Once the catheter is in place, a balloon may be inflated to open the artery and a stent is placed. A stent is a cylinder-like tube made of thin metal-mesh framework used to hold the artery open. Because there is a risk of stroke from bits of plaque breaking off during the procedure, an apparatus, called an embolic protection device, may be used. An embolic protection device is a filter (like a small basket) that is attached on a guidewire to catch any debris that may break off during the procedure.
Carotid Artery Angioplasty with Stenting (CAS) Click to Enlarge
Carotid Artery Disease and Stroke: Prevention and Treatment – John Hopkins
VIEW VIDEO –
Carotid Endarterectomy with Temporary Bypass – A Fifty year old procedure
Docteur Jean VALLA
Chirurgien Cardiovasculaire et Thoracique
AIHR/ACCA – Ancien Chirurgien des Hôpitaux Universitaires.
Membre de la Société de Chirurgie Thoracique et Cardiovasculaire de Langue Française Conventionné
Carotid artery stenosis is the narrowing of the carotid arteries. These are the main arteries in the neck that supply blood to the brain. Carotid artery stenosis, also called carotid artery disease, is a major risk factor for ischemic stroke.The narrowing is usually caused by plaque in a blood vessel. Plaque forms when cholesterol, fat and other substances build up in the inner lining of an artery.Depending on the degree of stenosis and the patient’s overall condition, carotid artery stenosis can usually be treated with surgery. The procedure is called carotid endarterectomy. It removes the plaque that caused the carotid artery to narrow. Carotid endarterectomy has proven to benefit patients with arteries stenosed (narrowed) by 70 percent or more. For people with arteries narrowed less than 50 percent, anti-clotting medicine is usually prescribed to reduce the risk of ischemic stroke.
VIEW VIDEO –
Carotid angioplasty and stenting (CAS) – Mayo Clinic
In carotid angioplasty and stenting, a long hollow tube called a catheter is inserted in the femoral artery in the groin area. The catheter is then maneuvered through the arteries until it reaches the narrowing in the carotid artery in the neck. An umbrella-shaped filter is inserted beyond the narrowing to catch any plaque or debris that may break off during the procedure. Then, a tiny balloon at the end of the catheter is inflated to push the plaque to the side and widen the vessel. A small metal coil called a stent is inserted into the vessel. The stent serves as a scaffold to help prevent the artery from narrowing again.
Contributions of a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD, Chief, Division of Vascular and Endovascular Surgery Co-Director, Thoracic Aortic Center @ MGH
I. Recollection of a visit at Dr. Cambria’s Office @MGH, 2004
The author arrived for a 4PM appointment @ MGH with a referral from NWH for a Carotid artery duplex scan that in 2004 was not performed at NWH. The consultation appointment with Dr. Kwolek CJ, a vascular surgeon trained under Dr. RP Cambria, took place in Dr. Cambria’s Office. Few minutes into the patient Medical History interview, Dr. Kwolek was called for an emergency in the OR and asked me to wait for him till he comes back. I looked around and found myself in a 14’x22′ Room, the Office of Dr. Richard Cambria @ MGH, Chief Vascular Surgery and among the Top ten in the World. Except for the glass entrance door and the wide window to the right of the entrance – 3 1/2 walls from the ceiling to one yard above the floor where completely covered with framed Awards, licenses, renewed licenses, Pictures with graduating Medical Students, Pictures with Faculty, with Patients and in the OR. I waited for Dr. Kwolek’s return for the completion of my Medical History Interview about 30 minutes. I used that time to walk along the walls in Dr. Cambria’s Office and read the framed Exhibits. It was clear to me that this Office will need, one day, in the future, to become a Museum @MGH, for most significant milestones in Vascular Surgery, a branch of Cardiothoracic Surgery. Dr. Kwolek returned and completed the interview, scheduled my Lab appointment and the next appointment to discuss the duplex scan results.
II. Shadowing Dr. Cambria in OR @MGH
Per section IV, below which described the author’s Cardiovascular Clinical Observational Experience, I recorded my Shadowing experience at the OR @MGH, including Dr. Cambria performing a CEA on a 84 year old women under going aorta valve replacement (performed by Dr. Walker) priot to a CEA performed by Dr. Cambria. It was all captivating to watch his double gloved hands performing sutures on a >95% blocked carotid artery prior to incision.
The dexterity and the speed of Dr. Cambria’s fingers’ movement, could only have reminded me of World #1 Harp Player: Nicanor Zabaleta, which I met in person, in the presence of my prominent Harp teacher, on his US Tour in 11/1989. He was awarded the Premio Nacional de Música of Spain in 1982 and six years later, in 1988, he was elected to the Real Academia de Bellas Artes de San Fernando. Dr. Cambria’s and Mr. Zabaleta’s fingers dexterity and eye hand coordination, both are of the rarest endowments in fine motor precision and perfection with Worldly finest outcomes in art, Surgery is Art, the mastering of the Harp is Art, too.
The Author in the OR — Mass General Hospital, Boston
Cardiac Surgery – Operating Room
Supervisor: Dr. J. Walker, Cardiac Surgeon
Experience: Shadowing Open Heart Surgery at MGH
1/24/2005: Carotid Artery endarterectomy operation by Dr. Richard Cambria
1/24/2005: Mitral Valve Replacement by Dr. Jennifer Walker
1/26/2005: Aorta Valve Replacement and Coronary Artery Bypass Grafting by Dr. Jennifer Walker
[Saphenous vein harvested from the leg and Radial vein harvested from the right arm]
III. Dr. Cambria: Selection of Contributions to Scientific Research on Vascular Surgery
The Author covered In Part One, Dr. Cambria’s participation in and contribution to the International, Multispecialty Position Statement on Carotid Stenting, 2013.
In Part Two Section II, I share with the e-Reader watching Dr. Cambria in the Surgical Theater performing CEA
In Part Two Section III, I am carrying with me the heavy weight of my Recollections from a Visit to his Office in 2004, my experience shadowing Dr. Cambria in the OR @MGH on 1/24/2005. Now I am giving back.
I became aware that both events have impacted favorably my 7/2013, Editorial decision, for a forthcoming book on Cardiovascular Disease in 2013. The Editorial decision is two fold:
the selection and representation of a prominent Vascular Surgery Center in the US, @MGH, and
my personal decision to select a Vascular Surgeon at Peak Career – Richard Paul Cambria, MD @MGH.
The decision to focus on Peripheral Vascular Surgery @MGH as described in Dr. Richard P Cambria’s research had yielded one Sub-Chapter (5.5) in Chapter 5
Chapter 5
Invasive Procedures by Surgery versus Catheterization
in Volume Three in a forthcoming three volume Series of e-Books on Cardiovascular Diseases
This very Sub-Chapter, 5.5, represents milestones in Dr. Cambria as a Vascular Surgeon. His eminent profile as a Vascular Surgery Researcher, is now in:
IV. Cardiovascular Clinical Observational Experience – Aviva Lev-Ari, PhD, RN
Brigham and Women’s Hospital, Boston. MA
Cardiac ICU, Coronary Care Unit, Medical Rounds [100 hours] June 2006-November 2006
Brigham and Women’s Hospital, Boston. MA
CDIC – Cardiovascular Diagnostic and Interventional Center
Angiography & Interventional Radiology [100 hours] March 2006-August 2006
Experience shadowing the daily activities of three Physician Assistants
1. attended consultation appointments with patient candidate for procedures: fibroid embolization
2. patient candidate for intra-vertebral cement injection in fractured vertebrae in spinal column, L-9 – Kyphoplasty vertebral augmentation
3. drainage of bile leakage – biliary duct obstruction
4. attended invasive procedures in the Angiography Lab
5. attended 7:30AM department meeting on all cases scheduled for procedures in the Lab for the day
6. discussed procedure outcomes and patient follow ups with PAs
7. Shadowing PAs and Interventional Radiologists performing angiography.
– VENOUS ACCESS PROCEDURES – TUNNELED CATHETER AND PORT PLACEMENT
– DIALYSIS ACCESS MANAGEMENT – ARTERIOVENOUS FISTULA/GRAFT.
ANGIOGRAMS/ANGIOPLASTIES
Mass General Hospital, Boston
Cardiac Catheterization Lab
Supervisor: Dr. Igor Palacios, Director, Cath Lab
Experience Shadowing in the Cath Lab at MGH
1/19/2005: stenting – MI case, mitral valve opening with balloon
The cerebral hyperperfusion syndrome is a very rare complication after revascularization of the carotid artery and accompanied by postoperative or postinterventional hypertension in almost all patients. We report a case of a 77-year-old man who developed a complete aphasia and increased right-sided weakness following endovascular treatment of severe occlusive disease of the left internal carotid artery. We discuss the risk and management of cerebral hyperperfusion syndrome after carotid artery stenting.
Introduction
Neurological complications following carotid artery stenting (CAS) are usually ischemic in nature, due to embolization or occlusion of the carotid artery. However, in a small subset of patients, cerebral hyperperfusion causes postinterventional neurological dysfunction, characterized by ipsilateral headache, focal seizure activity, focal neurological deficit, and ipsilateral intracerebral edema or hemorrhage. A high clinical suspicion and early diagnosis will allow early initiation of therapy and preventing fatal brain swelling or bleeding in patients with peri- and postinterventional cerebral hyperperfusion syndrome (CHS).
Discussion
In 1981, Sundt et al. [1] described a triad of complications that included atypical migrainous phenomena, transient focal seizure activity, and intracerebral hemorrhage after CEA and used the term cerebral hyperperfusion syndrome (CHS). The first report on CHS after CAS was published by Schoser et al. [2]. They described a 59-year-old woman with ipsilateral putaminal hemorrhage that was diagnosed on the 3rd day after CAS of a high-grade stenosis of the left ICA. Outcome in this case was not fatal. The patient recovered with a mild upper limb paresis. McCabe et al. [3] were the first to report the occurrence of fatal ICH soon after CAS. Only a few hours after the procedure, neurological symptoms occurred without any prodromata (severe headache, nausea, and seizures) postulated by Sundt et al. [1] to be an obligate component of CHS. CT of the brain revealed extensive ICH and the patient died 18 days later. Abou-Chebl et al. [4] reported a retrospective single-center study on 450 patients who had been treated with CAS. Three patients (0.67%) developed ICH after the intervention. Further reports on results and complications after CAS have been published [5]. Nearly all reports on CHS after carotid revascularizations in general and CAS in particular have in common patients who had high-grade stenoses in the treated vessel.
CHS following surgical or endovascular treatment of severe carotid occlusive disease is thought to be the result of impaired cerebral autoregulation, hypertension, ischemia-reperfusion injury, oxygen-derived free radicals, baroreceptor-dysfunction, and intraprocedural ischemia [6]. Chronic cerebral hypoperfusion due to critical stenosis leads to production of vasodilatory substances. Autoregulatory failure results in the cerebral arterioles being maximally dilated over a long period of time, with subsequent loss of their ability to constrict when normal perfusion pressure is restored. The degree of microvascular dysautoregulation is proportional to the duration and severity of ischemia determined by the severity of ipsilateral stenosis and poor collateral flow.
Hypertension plays an important role in the development of CHS. In the absence of cerebral autoregulation, cerebral blood flow is directly dependent on the systemic blood pressure. The restoration of normal blood flow to chronically underperfused brain can result in edema, capillary breakthrough, and perivascular and macroscopic hemorrhages aggravated by peri- and postinterventional hypertension [6, 7]. The risk factors for CHS after CAS are summarized in Table 1.
The classic clinical presentation includes ipsilateral headache, seizures or focal neurological deficit, and ipsilateral intracerebral edema or hemorrhage. The diagnosis can be made readily with color Doppler ultrasound of the carotid artery and especially with transcranial Doppler (TCD) of the middle cerebral artery [9]. An increase in peak blood flow velocity of >100% is predictive of postinterventional hyperperfusion. Diffusion weighted MRI or single photon emission computed tomography (SPECT) could also be performed for diagnosis [10]. Angiography normally shows normal findings.
The prognosis of CHS depends on timely recognition of hyperperfusion and adequate treatment of hypertension before cerebral edema or hemorrhage develops. The prognosis following intracerebral bleeding is very poor, with mortality over 50% and significant morbidity of 80% in the survivors [4, 6]. The prognosis of CHS in patients without cerebral edema or hemorrhage is clearly better especially when they are identified and treated early. The most important aspects in preventing and treating this syndrome are early identification, careful monitoring, and control of blood pressure ideally in a high-dependency unit setting. In our special case, early diagnosis of CHS and immediate intensive medical treatment of blood pressure could prevent devastating cerebral edema or hemorrhage following CAS.
Conclusion
CHS, which is characterized by ipsilateral headache, hypertension, seizures, and focal neurological deficits, is a rare but devastating complication following carotid artery stenting. Hypertension is the most important risk factor. The diagnosis can be confirmed quickly by TCD, DWI, or SPECT. Especially peri- or postinterventional TCD monitoring should be available to identify patients with hyperperfusion who may benefit from intensive blood pressure management ideally in a specialized intensive care unit.
Abbreviations
CAS:
Carotid artery stenting
CCA:
Common carotid artery
CEA:
Carotid endarterectomy
CHS:
Cerebral hyperperfusion syndrome
CT:
Computed tomography
CVR:
Cerebrovascular reactivity
DWI:
Diffusion-weighted imaging
ICA:
Internal carotid artery
ICH:
Intracerebral haemorrhage
MRI:
Magnetic resonance imaging
SPECT:
Single photon emission computed tomography
TCD:
Transcranial Doppler.
REFERENCES
T. M. Sundt Jr., F. W. Sharbrough, and D. G. Piepgras, “Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy. With results of surgery and hemodynamics of cerebral ischemia,” Mayo Clinic Proceedings, vol. 56, no. 9, pp. 533–543, 1981.View at Scopus
B. G. H. Schoser, C. Heesen, B. Eckert, and A. Thie, “Cerebral hyperperfusion injury after percutaneous transluminal angioplasty of extracranial arteries,” Journal of Neurology, vol. 244, no. 2, pp. 101–104, 1997. View at Publisher · View at Google Scholar · View at Scopus
D. J. H. McCabe, M. M. Brown, and A. Clifton, “Fatal cerebral reperfusion hemorrhage after carotid stenting,” Stroke, vol. 30, no. 11, pp. 2483–2486, 1999. View at Scopus
A. Abou-Chebl, J. S. Yadav, J. P. Reginelli, C. Bajzer, D. Bhatt, and D. W. Krieger, “Intracranial hemorrhage and hyperperfusion syndrome following carotid artery stenting: risk factors, prevention, and treatment,” Journal of the American College of Cardiology, vol. 43, no. 9, pp. 1596–1601, 2004. View at Publisher · View at Google Scholar · View at Scopus
J.-H. Buhk, L. Cepek, and M. Knauth, “Hyperacute intracerebral hemorrhage complicating carotid stenting should be distinguished from hyperperfusion syndrome,” American Journal of Neuroradiology, vol. 27, no. 7, pp. 1508–1513, 2006. View at Scopus
W. F. Morrish, S. Grahovac, A. Douen et al., “Intracranial hemorrhage after stenting and angioplasty of extracranial carotid stenosis,” American Journal of Neuroradiology, vol. 21, no. 10, pp. 1911–1916, 2000. View at Scopus
R. Gupta, A. Abou-Chebl, C. T. Bajzer, H. C. Schumacher, and J. S. Yadav, “Rate, predictors, and consequences of hemodynamic depression after carotid artery stenting,” Journal of the American College of Cardiology, vol. 47, no. 8, pp. 1538–1543, 2006. View at Publisher · View at Google Scholar · View at Scopus
M. B. Sánchez-Arjona, G. Sanz-Fernández, E. Franco-Macias, and A. Gil-Peralta, “Cerebral hemodynamic changes after carotid angioplasty and stenting,” American Journal of Neuroradiology, vol. 28, pp. 640–644, 2007.
Y. Kaku, S. I. Yoshimura, and J. Kokuzawa, “Factors predictive of cerebral hyperperfusion after carotid angioplasty and stent placement,” American Journal of Neuroradiology, vol. 25, pp. 1403–1408, 2004.
Patient came to her appointment as part of a standard pre-operative evaluation for removal of a uterine myoma. She had a history of stroke with residual slurred speech, making it difficult to understand her. Accordingly, I assumed I would see some carotid stenosis, but her ultrasound showed a stunning 70-99% stenosis in her right internal carotid artery and full occlusion of her left internal carotid artery.
Flow in the common carotid arteries looked fine. The plaque itself in the internal carotid arteries was relatively hypoechoic and not easily visualized in brightness mode, so bidirectional color flow at the proximal internal carotid arteries was surprising. Adding power Doppler allowed me to conclude that there was presence of flow on the right, though minimal, and absolutely no flow in the left internal carotid artery.
Upon completion of the exam, I called the ER and spoke with the doctor, who asked me to bring Rose to the ER. Unfortunately, due to the location of the right internal carotid artery stenosis in the bony canal and total occlusion of the left internal carotid artery, surgery was not an option for clearing out the carotid plaque, but doctors believed she could continue functioning well with collateral vasculature carrying blood to her brain.
Thankfully, the patient passed her other pre-operative tests, consented to her surgery, and underwent general anesthesia with no complications. An 8-cm malignant mass was removed from her uterus and her prognosis is good.
opinion/26redberg.html. Last accessed Jan 8, 2013.
Part Three:
Cleveland Clinic Reports Equivalence between carotid endarterectomy (CEA) and open-heart surgery (OHS) and carotid artery stenting (CAS) followed by coronary artery bypass graft (CABG) surgery or non-CABG cardiac surgery
Stent first, then heart surgery, for patients with severe carotid/coronary disease
Cleveland, OH – With the absence of randomized, controlled clinical trials to address the optimal management of patients with severe carotid and coronary artery disease, a new retrospective study suggests the best tactic is a staged approach that sees the patient undergo carotid artery stenting (CAS) followed by coronary artery bypass graft (CABG) surgery or non-CABG cardiac surgery [1].
Investigators report that a combined approach that includes carotid endarterectomy (CEA) and open-heart surgery (OHS) is equivalent in terms of short-term outcomes with the staged CAS-OHS procedure. Beyond one year, however, the staged CAS-OHS approach resulted in the lowest risk of all-cause mortality, stroke, and MI when compared with a combined CEA-OHS procedure and staged CEA-OHS.
“The surgeons get very worried about doing operations on these patients because they don’t want to do a beautiful job on the bypass only to have the patient have a stroke,” lead investigator Dr Mehdi Shishehbor(Cleveland Clinic, OH) told heartwire.
Shishehbor said that when patients are undergoing open-heart surgery, whether it’s CABG or valve surgery, they are screened for carotid artery disease, given the heightened risk of stroke when undergoing heart surgery. As a result, various teams from neurology, vascular surgery, and interventional cardiology are called to address the safety of the surgery in the setting of severe carotid disease, said Shishehbor.
“These patients are the sickest of the sick in the sense that they have two conditions that are occurring concomitantly,” he said. “These are not patients who just have carotid disease. There are many patients who have moderate or mild carotid disease who undergo open-heart surgery with no problem. These are people with severe disease, those with more than 80% stenosis in one of their carotid arteries or maybe both. They also have severe coronary artery disease. These are people with left-main or three-vessel disease who are destined to undergo bypass.”
The whole point is to prevent stroke
In the study, published this week in the Journal of the American College Cardiology, the investigators reported data on 350 patients who underwent carotid revascularization and cardiac surgery. These included 45 patients who were treated with a staged CEA-OHS approach (OHS performed a median of 14 days after CEA), 110 who were treated with a staged CAS-OHS procedure (OHS performed a median of 47 days after CEA), and 195 patients treated with a combined CEA-OHS procedure. OHS is defined as CABG, CABG plus other cardiac procedures, or non-CABG cardiac surgery (isolated valve or aortic-repair surgery). In total, just 8% of procedures were non-CABG surgeries.
In a propensity-adjusted analysis analyzed by intention-to-treat, the 30-day risk of death, stroke, and MI was similar between the staged CAS-OHS and combined CEA-OHS procedures. The highest risk of the composite end point was observed in patients who underwent staged CEA-OHS.
At one year and beyond (median follow-up was 3.7 years), the staged CAS-OHS patients had the lowest risk of death, stroke, and MI. Compared with staged CEA-OHS, those treated with CAS-OHS had a 67% lower risk of death, stroke, and MI and a 65% lower risk compared with combined CEA-OHS.
Unadjusted comparison of primary/secondary end points
Event
Staged CEA-OHS,n=45 (%)
Combined CEA-OHS,n=195 (%)
Staged CAS-OHS,n=110 (%)
p
Overall 30-d risk post-OHS
31
10
10
0.003
Death
7
5
6
0.75
Stroke
2
7
2
0.11
MI
24
0.5
3
<0.001
Overall composite risk 1 y and beyond
27
39
12
<0.001
Death
38
39
11
<0.001
Stroke
2.2
1.5
0
0.37
MI
0
3.1
2.7
0.5
“In the long term, stenting [followed by OHS] definitely did better than the combined approach,” said Shishehbor. “What’s also important is that with the combined approach, the reason they didn’t do very well is because they had a higher rate of stroke in the perioperative period. . . . Remember the whole point of doing this is to prevent stroke. This is why we feel the combined approach is a little bit inferior to the staged CAS/open-heart-surgery approach. If you have a 7% risk of stroke in the 30-day perioperative period, that doesn’t appear to be the best option for the majority of patients.”
To heartwire, Shishehbor said that while the patients were well matched, the patients undergoing stenting tended to be sicker. For example, they were more likely to have symptomatic carotid stenosis and were more likely to have undergone a previous carotid revascularization. Shishehbor also said that clinical events occurring between the initial carotid artery revascularization procedure and OHS were included in the analysis. These deaths, strokes, and MIs were identified and accounted for in the data.
In an editorial accompanying the study [2], Drs Ehtisham Mahmud and Ryan Reeves (University of California, San Diego) say the work by the Cleveland Clinic group is strengthened by the propensity-adjusted analysis and long follow-up beyond the perioperative period. Most important, they say the study provides clarity for the management of patients with carotid and coronary disease.
“For patients presenting with an acute coronary syndrome requiring urgent coronary revascularization in whom waiting three to four weeks is not safe, combined CEA-OHS is the optimum revascularization strategy, though associated with higher neurological ischemic events,” write Mahmud and Reeves.
“However, for patients with a stable or an accelerating anginal syndrome who can wait three to four weeks to complete dual antiplatelet therapy [DAPT] after carotid stenting, staged CAS followed by OHS leads to superior early and long-term outcomes.”
Since completing the analysis, Shishehbor said there have been discussions with colleagues in vascular surgery, vascular medicine, cardiac surgery, and cardiology to establish the optimum way to treat patients with severe carotid and coronary disease. “The bottom line is that there will never be a randomized, clinical trial in this setting,” he told heartwire. “I hope there would be, but I doubt it. So I think papers like this are critical because we’re doing these procedures to prevent stroke. It’s important that we pick the right procedure for the right patient.”
Confounded by registry requirements
Shishehbor is also concerned about the scrutiny carotid stenting is under from the Centers for Medicare&Medicaid Services(CMS). Currently, the CMS reimburses procedures for asymptomatic patients only if they are included in one of the industry-funded and -maintained registries. He believes the scrutiny has led to a dwindling number of clinicians with the expertise capable of doing the procedure, and this is concerning, since the present analysis shows there are cohorts of asymptomatic patients who would benefit from the treatment.In addition, to be included in a registry, an asymptomatic patient must receive DAPT with aspirin andclopidogrel for four weeks. If the patient does not meet the DAPT requirements, they can’t be included in the registry. However, Shishehbor said, many of these patients have significant coronary disease and can’t wait four weeks. As a result, they are treated with a combined CEA-OHS approach, an approach that is associated with a higher risk of stroke.
Shishehbor reports serving as a speaker and consultant for Abbot Vascular, Medtronic, and Gore but waives all compensation for his work. Mahmud reports trial support from Boston Scientific and Abbott Vascular. In addition,he consults for Cordis andthe Medicines Companyand serves on the speaker‘s bureau for Medtronic. Disclosures for the coauthors are listed in the paper.
Sources
Shishehbor MH, Venkatachalam S, Sun Z, et al. A direct comparison of early and late outcomes with three approaches to carotid revascularization and open heart surgery. J Am Coll Cardiol 2013; available at: http://content.onlinejacc.org.
Mahmud E, Reeves R. Carotid revascularization prior to open heart surgery: The data driven treatment strategy. J Am Coll Cardiol 2013; available at: http://content.onlinejacc.org.
2013 ACCF/AHA Guideline for the Management of Heart FailureA Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
Clyde W. Yancy, MD, MSc, FACC, FAHA; Mariell Jessup, MD, FACC, FAHA; Biykem Bozkurt, MD, PhD, FACC, FAHA; Javed Butler, MBBS, FACC, FAHA; Donald E. Casey, MD, MPH, MBA, FACP, FAHA; Mark H. Drazner, MD, MSc, FACC, FAHA; Gregg C. Fonarow, MD, FACC, FAHA; Stephen A. Geraci, MD, FACC, FAHA, FCCP; Tamara Horwich, MD, FACC; James L. Januzzi, MD, FACC; Maryl R. Johnson, MD, FACC, FAHA; Edward K. Kasper, MD, FACC, FAHA; Wayne C. Levy, MD, FACC; Frederick A. Masoudi, MD, MSPH, FACC, FAHA; Patrick E. McBride, MD, MPH, FACC; John J.V. McMurray, MD, FACC; Judith E. Mitchell, MD, FACC, FAHA; Pamela N. Peterson, MD, MSPH, FACC, FAHA; Barbara Riegel, DNSc, RN, FAHA; Flora Sam, MD, FACC, FAHA; Lynne W. Stevenson, MD, FACC; W.H. Wilson Tang, MD, FACC; Emily J. Tsai, MD, FACC; Bruce L. Wilkoff, MD, FACC, FHRS
We present below four National institutions with pubic mandate to promote all Healthcare aspects of Cardiovascular Diseases.
A. 2020 Vision of the Heart Failure Society of America (HFSA)
Special Communication: The Heart Failure Society of America in 2020: A Vision for the Future
Journal of Cardiac Failure Vol. 18 No. 2 2012 written by BARRY H. GREENBERG, MD,1,3 INDER S. ANAND, MD, PhD,2 JOHN C. BURNETT JR, MD,2,3 JOHN CHIN, MD,2,3 KATHLEEN A. DRACUP, RN, DNSc,3 ARTHUR M. FELDMAN, MD, PhD,3 THOMAS FORCE, MD,2,3 GARY S. FRANCIS, MD,3 STEVEN R. HOUSER, PhD,2 SHARON A. HUNT, MD,2 MARVIN A. KONSTAM, MD,3 JOANN LINDENFELD, MD,2,3 DOUGLAS L. MANN, MD,2,3 MANDEEP R. MEHRA, MD,2,3 SARA C. PAUL, RN, DNP, FNP,2,3 MARIANN R. PIANO, RN, PhD,2 HEATHER J. ROSS, MD,2 HANI N. SABBAH, PhD,2 RANDALL C. STARLING, MD, MPH,2 JAMES E. UDELSON, MD,2 CLYDE W. YANCY, MD, MSc,3 MICHAEL R. ZILE, MD,2 AND BARRY M. MASSIE, MD2,3
From the 1Chair, ad hoc Committee for Strategic Development, Heart Failure Society of America; 2Member of Executive Council, Heart Failure Society of America and 3Member, ad hoc Committee for Strategic Development, Heart Failure Society of America.
They write:
The preceding 2 decades had been marked by unprecedented insights into the underlying pathophysiology of cardiac dysfunction that were paralleled by therapeutic advances that, for the first time, were shown to clearly improve outcomes in heart failure patients. At the same time, heart failure prevalence was rapidly increasing throughout the world because of the aging of the population, improved survival of patients with myocardial infarction and other cardiac conditions, and inadequate treatment of common risk factors such as hypertension.
More recently the Heart Failure Society successfully promoted establishment of Advanced Heart Failure and Transplant Cardiology as an American Board of Internal Medicine recognized secondary subspecialty of cardiology developed a board review course to help physicians prepare for the certification examination for the new subspecialty and created a national heart failure review course.
The Society has Advocacy goals, membership goals – to increase by 10% per year for 3 years from all disciplines of Heart Failure.
Education Goals:
The Heart Failure Society of America will be recognized for its innovative approaches to educating and content dissemination on heart failure targeting
healthcare professionals and patients
Grow and enhance the annual meeting through innovative approaches
Continue board review course
Increase web-based programs for patients and health care providers
Enhance the website as a portal for information dissemination for health care professionals and patients
Grow and enhance the relevance and value of the Journal of Cardiac Failure
Conceptual analysis of projection done by the AHA regarding the increase in the Cost of Care for the the American Patient in Heart Failure were developed in the following two articles:
National Heart, Lung, And Blood Institute Working Group identified the most urgent knowledge gaps in Heart Transplantation Research. These gaps require to address the following 4 specific research directions:
enhanced phenotypic characterization of the pre-transplant population
donor-recipient optimization strategies
individualized immunosuppression therapy, and
investigations of immune and non-immune factors affecting late cardiac allograft outcomes.
D. Donor-Recipient Optimization Strategies – 33,640 Cases in the United Network for Organ Sharing database – Organ Donor’s Age is BEST predictor for survival after Heart Transplant
IF the donor age is in the 0- to 19-year-old group the median survival of 11.4 years follows the Heart Transplant.
The effect of ischemic time on survival after heart transplantation varies by donor age: An analysis of the United Network for Organ Sharing database
The Journal of Thoracic and Cardiovascular Surgery ● February 2007
Mark J. Russo, MD, MS,a,b Jonathan M. Chen, MD,a Robert A. Sorabella, BA,a Timothy P. Martens, MD,a
Mauricio Garrido, MD,a Ryan R. Davies, MD,a Isaac George, MD,a Faisal H. Cheema, MD,a Ralph S. Mosca, MD,a Seema Mital, MD,c Deborah D. Ascheim, MD,b,d Michael Argenziano, MD,a Allan S. Stewart, MD,a Mehmet C. Oz, MD,a and Yoshifumi Naka, MD, PhDa
Objectives:
(1) To examine the interaction of donor age with ischemic time and their effect on survival and
(2) to define ranges of ischemic time associated with differences in survival.
Methods: The United Network for Organ Sharing provided de-identified patientlevel data. The study population included 33,640 recipients undergoing heart transplantation between October 1, 1987, and December 31, 2004. Recipients were divided by donor age into terciles: 0 to 19 years (n 10,814; 32.1%), 20 to 33 years (11,410, 33.9%), and 34 years or more (11,416, 33.9%). Kaplan-Meier survival functions and Cox regression were used for time-to-event analysis. Receiver operating characteristic curves and stratum-specific likelihood ratios were generated to compare 5-year survival at various thresholds for ischemic time.
Results: In univariate Cox proportional hazards regression, the effect of ischemic time on survival varied by donor age tercile: 0 to 19 years (P .141), 20 to 33 years (P .001), and 34 years or more (P .001). These relationships persisted in multivariable regression. Threshold analysis generated a single stratum (0.37-12.00 hours) in the 0- to 19-year-old group with a median survival of 11.4 years. However, in the 20- to 33-year-old-group, 3 strata were generated: 0.00 to 3.49 hours (limited), 3.50 to 6.24 hours (prolonged), and 6.25 hours or more (extended), with median survivals of 10.6, 9.9, and 7.3 years, respectively. Likewise, 3 strata were generated in the group aged 34 years or more: 0.00 to 3.49 (limited), 3.50 to 5.49 (prolonged), and 5.50 or more (extended), with median survivals of 9.1, 8.5, and 6.3 years, respectively.
Conclusions: The effect of ischemic time on survival after heart transplantation is dependent on donor age, with greater tolerance for prolonged ischemic times among grafts from younger donors. Both donor age and anticipated ischemic time must be considered when assessing a potential donor.
Procedures Outcomes of Heart Transplant (HT) Indication for Heart Failure (HF)
Center for Heart Failure @Cleveland Clinic, and
Transplant Center @Mayo Clinic
Center for Heart Failure @Cleveland Clinic: Institution Profile
Heart failure (sometimes called congestive heart failure or ventricular dysfunction) means your heart muscle is not functioning as well as it should. Either the left ventricle (lower chamber of the heart) is not contracting with enough force (systolic heart failure), or the ventricles are stiff and do not relax and fill properly (diastolic heart failure). The treatment of heart failure requires a specialized multidisciplinary approach to manage the overall patient care plan.
The George M and Linda H Kaufman Center for Heart Failure is one of the premier facilities in the United States for the care of people with heart failure.
The Kaufman Center Heart Failure Intensive Care was the recipient of the Beacon Award of Excellence for continuing improvements in providing the highest quality of care for patients. With over 6,000 ICUs in the Unites States, the Center joins a distinguished group of just 300 to receive this honor that recognizes the highest level of standards in patient safety and quality in acute and critical care.
In 2011, Cleveland Clinic received the American Heart Association’s Get With The Guidelines Heart Failure GOLD Plus Certification for improving the quality of care for heart failure patients. Gold Plus distinction recognizes hospitals for their success in using Get With The Guidelines treatment interventions. This quality improvement program provides tools that follow proven, evidence-based guidelines and procedures in caring for heart failure patients to prevent future hospitalizations.
The Kaufman Center for Heart Failure Team brings together clinicians that specialize in cardiomyopathies and ischemic heart failure. The team includes physicians and nurses from Cardiovascular Medicine, Cardiothoracic Surgery, Radiology, Infectious Disease, Immunology, Pathology, Pharmacy, Biothetics and Social Work with expertise in diagnostic testing, medical and lifestyle management, surgical procedures, and psychosocial support for patients with:
Patients at Cleveland Clinic Kaufman Center for Heart Failure have available to them the full array of diagnostic testing, treatments and specialized programs.
Outcomes of Heart Failure and Heart Transplant @Cleveland Clinic
1,570 Number of heart transplants performed at Cleveland Clinic since inception of the Cardiac Transplant Program in 1984.
The survival rates among patients who have heart transplants at Cleveland Clinic exceeds the expected rates. Of the 150 transplant centers in the United States, Cleveland Clinic is one of only three that had better-than-expected one-year survival rates in 2011.
Ventricular Assist Device Volume 2007 – 2011
2007 – N = 23
2008 – N = 48
2009 – N = 76
2010 – N = 51
2011 – N = 56
Mechanical circulatory support (MCS) devices are used in patients with heart failure to preserve heart function until transplantation (bridge-to-transplant) or as a final treatment option (destination therapy). Cleveland Clinic has more than 20 years of experience with MCS devices for both types of therapy.
LVAD In-Hospital Mortality 2007 – 2011
Cleveland Clinic continues to make improvements to reduce mortality rates among patients who are placed on mechanical circulatory support. The mortality rate among patients who have a left ventricular assist device (LVAD) has been drastically reduced over the past five years.5% in 2011
VAD Mortality 2011
The mortality rate among Cleveland Clinic patients placed on ventricular assist devices (VADs) was much lower than expected in 2011. Observed 10%, Expected 17.5%
Heart Failure – National Hospital Quality Measures
This composite metric, based on four heart failure hospital quality process measures developed by the Centers for Medicare and Medicaid Services (CMS), shows the percentage of patients who received all the recommended care for which they were eligible. Cleveland Clinic has set a target of UHC’s 90th percentile.
Cleveland Clinic, 2010 (N = 1,194) 93.9%
Cleveland Clinic, 2011 (N = 1,163) 96.9%
UHC Top Decile, 2011 99.2%
SOURCE
University HealthSystem Consortium (UHC) Comparative Database, January through November 2011 discharges.
The Centers for Medicare and Medicaid Services (CMS) calculates two heart failure outcome measures: all-cause mortality and all-cause readmission rates, each based on Medicare claims and enrollment information. Cleveland Clinic’s performance appears below.
Heart Failure All-Cause 30-Day Mortality (N = 762) July 2008 – June 2011
Cleveland Clinic 9.2%
National Average 11.6%
Heart Failure All-Cause 30-Day Readmission (N = 1,029) July 2008 – June 2011
Cleveland Clinic 27.3%
National Average 24.7%
SOURCE:
hospitalcompare.hhs.gov
Cleveland Clinic’s heart failure risk-adjusted 30-day mortality rate is below the national average; the difference is statistically significant. Our heart failure risk-adjusted readmission rate is higher than the national average; that difference is also statistically significant. To further reduce this rate, a multidisciplinary team was tasked with improving transitions from hospital to home or post-acute care facility. Specific initiatives have been implemented in each of these focus areas: communication, education and follow-up.
In 2011, 51% of lung transplant patients were from outside the state of Ohio.
Cleveland Clinic surgeons transplanted 111 lungs in 2011. Our Lung and Heart-Lung Transplant
Program is the leader in Ohio and among the best programs in the country.
July 2010 – June 2011
160 Performed in 2009
Liver-Lung
Heart-Lung
Double Lung
Single Lung
53.5% Idiopathic
Primary Disease of Lung Transplant Recipients (N = 101)
Source: Scientific Registry of Transplant Recipients. March 2011. Ohio, Lung Centers, Cleveland Clinic. Table 7
Cleveland Clinic surgeons transplanted 111 lungs in 2011. Our Lung and Heart-Lung Transplant Program is the leader in Ohio and among the best programs in the country.
Transplant Center @Mayo Clinic: Heart Transplant Procedures Outcomes
Mayo Clinic History
Dr. W.W. Mayo
Drs. William (left) and Charles Mayo
Mayo Clinic developed gradually from the medical practice of a pioneer doctor, Dr. William Worrall Mayo, who settled in Rochester, Minn., in 1863. His dedication to medicine became a family tradition when his sons, Drs. William James Mayo and Charles Horace Mayo, joined his practice in 1883 and 1888, respectively.
From the beginning, innovation was their standard and they shared a pioneering zeal for medicine. As the demand for their services increased, they asked other doctors and basic science researchers to join them in the world’s first private integrated group practice.
Although the Mayo doctors were initially viewed as unconventional for practicing medicine through this teamwork approach, the benefits of a private group practice were undeniable.
As the success of their method of practice became evident, so did its acceptance. Patients discovered the advantages to a “pooled resource” of knowledge and skills among doctors. In fact, the group practice concept that the Mayo family originated has influenced the structure and function of medical practice throughout the world.
Along with its recognition as a model for integrated group practice, “the Mayos’ Clinic” developed a reputation for excellence in individual patient care. Doctors and students came from around the world to learn new techniques from the Mayo doctors, and patients came from around the world for diagnosis and treatment. What attracted them was not only technologically advanced medicine, but also the caring attitude of the doctors.
Through the years, Mayo Clinic has nurtured and developed its founders’ style of working together as a team. Shared responsibility and consensus still provide the framework for decision making at Mayo.
That teamwork in medicine is carried out today by more than 55,000 doctors, nurses, scientists, students and allied health staff at Mayo Clinic locations in the Midwest, Arizona and Florida.
Alternative Solutions to Treatment of Heart Failure
Mayo Clinic, with transplant services in Arizona, Florida and Minnesota, performs more transplants than any other medical center in the world. Mayo Clinic has pre-eminent adult and pediatric transplant programs, offering cardiac, liver, kidney, pancreas and bone marrow transplant services. Since performing the first clinical transplant in 1963, Mayo’s efforts to continually improve and expand organ transplantation have placed Mayo at the leading edge of clinical and basic transplant research worldwide. Research activities in the Transplant Center at Mayo Clinic have contributed significantly to the current successful outcomes of organ transplantation.
People who survive a heart attack face the greatest risk of dying from sudden cardiac death (SCD) during the first month after leaving the hospital, according to a long-term community study by Mayo Clinic researchers of nearly 3,000 heart attack survivors.
Sudden cardiac death can happen when the hearts electrical system malfunctions; if treatment — cardiopulmonary resuscitation and defibrillation — does not happen fast, a person dies.
After that first month, the risk of sudden cardiac death drops significantly — but rises again if a person experiences signs of heart failure. The research results appear in the Nov. 5 edition of Journal of the American Medical Association.
Veronique Roger, M.D., a Mayo Clinic cardiologist provides an overview of the study and it’s findings.
For more information on heart attacks, click on the following link:http://www.mayoclinic.org/heart-attack/
VIEW VIDEOon Mayo Clinic Regenerative Medicine Consult Service – Stem Cell Transplantation post MI
In a proof-of-concept study, Mayo Clinic investigators have demonstrated that induced pluripotent stem (iPS) cells can be used to treat heart disease. iPS cells are stem cells converted from adult cells. In this study, the researchers reprogrammed ordinary fibroblasts, cells that contribute to scars such as those resulting from a heart attack, converting them into stem cells that fix heart damage caused by infarction. The findings appear in the current online issue of the journal Circulation.
Timothy Nelson, M.D., Ph.D., first author on the Mayo Clinic study, talks about the study and it’s findings.
Heart Transplant: Volumes and success measures Transplant Center@ Mayo Clinic
Mayo Clinic doctors’ experience and integrated team approach results in transplant outcomes that compare favorably with national averages. Teams work with transplant recipients before, during and after surgery to ensure the greatest likelihood of superior results.
Volumes and statistics are maintained separately for the three Mayo Clinic locations. Taken together or separately, transplant recipients at Mayo Clinic enjoy excellent results.
Volumes
Arizona
More than 100 heart transplants have been completed since the program began in 2005.
Florida
Surgeons at Mayo Clinic in Florida have performed more than 167 heart transplants and eight heart-lung transplants since the program began in 2001. Mayo surgeons have performed combined transplants, such as heart-kidney and heart-lung-liver transplants.
Minnesota
Mayo Clinic’s outcomes for heart transplantation compare favorably with national norms. Doctors at Mayo Clinic in Minnesota have transplanted more than 450 adult and pediatric patients, including both isolated heart transplants and combined transplants such as heart-liver, heart-kidney and others.
The Center for Heart Failure @Cleveland Clinic’s, and the Transplant Center @Mayo Clinic’s Institutions Profiles, Procedures Outcomes and Selection of their Research are now in:
Article ID #65: Becoming a Cardiothoracic Surgeon: An Emerging Profile in the Surgery Theater and through Scientific Publications. Published on 7/8/2013
WordCloud Image Produced by Adam Tubman
Two components of an Emerging Profile of a Young Cardiothoracic Surgeon were researched by the Author for the case of Dr. Isaac George, Assistant Professor of Surgery, Division of Cardiothoracic Surgery, Department of Surgery, New York Presbyterian Hospital/Columbia University Medical Center , New York, NY.
The two components being:
1. the Cardiothoracic Surgery Theater
2. the Scientific Publications
I noted with interest Dr. George’s second publication, to be about a very well known surgeon in the US and Europe, John Benjamin Murphy. written by Dr. George and two other colleagues, George I, Hardy MA, Widmann WD. published in Curr Surg. 2004 Sep-Oct;61(5):439-41.
I assume that Dr. Murphy’s contributions to Thoracic surgery were of interest to Dr. George to inspire him to write on the subject and elect that Specialty in Surgery.
Murphy was first in the U.S. to induce (1898) artificial immobilization and collapse of the lung in treatment of pulmonary tuberculosis. He was a pioneer in the use of bone grafting and made contributions to the understanding and management of ankylosis as well as independently proposing artificial pneumothorax to manage unilateral lung disease in tuberculosis.
«It is the purpose of every man’s life to do something worthy of the recognition and appreciation of his fellow men. . . . By their superior intellectual qualifications, their fidelity to purpose and above all their indefatigable labour the few become leaders.»
SOURCEWhonamedit? A dictionary of medical eponyms, John Benjamin Murphy
I came across Dr. Isaac George’s name while researching clinical indications for Inhaled Nitric Oxide in June 2013, upon the recent publication of Leaders in Pharmaceutical Business Intelligence FIRST e-Book on Amazon (Biomed e-Books) [Kindle Edition]
Being myself in Analytics and quantitative model design, 1976-2004, I found of particular interest the range of quantitative methodologies used in the following article by Isaac George, assuming that his days at MIT, came very handy in 2006:
George, Isaac, Xydas, Steve, Topkara, Veli K., Ferdinando, Corrina, Barnwell, Eileen C., Gableman, Larissa, Sladen, Robert N., Naka, Yoshifumi, Oz, Mehmet C. Clinical Indication for Use and Outcomes After Inhaled Nitric Oxide Therapy Ann Thorac Surg 2006 82: 2161-2169
As a result of studying this article, I became aware that it has impacted favorably my 6/2013, Editorial decision, for a forthcoming book on Cardiovascular Disease in 2013. The Editorial decision regarding the selection and representation of prominent Cardiothoracic Surgery Theater in the US, and my personal decision to select a Young Cardiothoracic Surgeon
Dr. Isaac George, Assistant Professor of Surgery, Division of Cardiothoracic Surgery, Department of Surgery, New York Presbyterian Hospital/Columbia University Medical Center, New York, NY
Education Profile and Medical Training of a Cardiac Surgeon
NewYork-Presbyterian Hospital/Columbia University Medical Center, New York, NY
2012-present
Assistant Professor of Surgery
Division of Cardiothoracic Surgery, Department of Surgery, New York Presbyterian Hospital/Columbia University Medical Center , New York, NY
Clinical Specialties
Adult aortic and mitral valve surgery
Transcatheter aortic and mitral valve implantation
Hybrid coronary artery bypass surgery
Complex aortic surgery
Complex valvular surgery
Heart failure and transplant surgery
Reoperative cardiac surgery
Thoracic aortic endograft implantation
1. Regulation of myostatin signaling in human cardiomyopathy
2. TGFB regulation in non-syndromic aortic aneurysm formation
3. Valve interstitial cell activation mechanisms after surgical and transcatheter valve replacement
4. Clinical outcomes after valve and hybrid surgery
Education and Training
2011-2012
Interventional Cardiology/Hybrid Cardiac Surgery Fellowship
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2011
Ventricular Assist Device/Cardiac Transplant Fellowship, Minimally Invasive, Cardiac Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2009-2011
Fellow, Cardiothoracic Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2008-2009
Post-Doctoral Clinical Fellow, Cardiothoracic Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2006-2008
Resident, General Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2004-2006
Research Fellow, Cardiothoracic Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2002-2004
Resident, General Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
2001-2002
Internship, General Surgery
New York Presbyterian Hospital – Columbia University Medical Center, New York, NY
1997-2001
MD, Medicine
Duke University School of Medicine, Durham, NC
1993-1997
BS, Mechanical Engineering
Massachusetts Institute of Technology, Cambridge, MA
Board Certifications
American Board of Thoracic Surgery, 2012-
American Board of Surgery, 2008-
Certification, Pediatric Advanced Life Support, 2008-
Certification, Advanced Trauma Life Support, 2006-
MD, State of New York, 2005-
Certification, Advanced Cardiac Life Support/Basic Life Support, 2001-
United States Medical Licensing Examination Step 3, 2004
United States Medical Licensing Examination Step 2, 2001
United States Medical Licensing Examination Step 1, 2000
Professional Honors
2008 Blakemore Prize – Best Resident Research Award, Columbia University College of Physicians and Surgeons
2007 Blakemore Award – Best Resident Research Award, Columbia University College of Physicians and Surgeons
2006 Blakemore Award – Best Resident Research Award, Columbia University College of Physicians and Surgeons
2004 New Era Cardiac Surgery Conference Scholarship
1995 Pi Tau Sigma, Mechanical Engineering Honor Society
1993 Duke University Comprehensive Cancer Center Fellowship
The decision to focus on Cardiothoracic Surgery @Presbeterian as described in Dr. Isaac George’s research had yielded one Sub-Chapter (4.1) in Chapter 4
Cardiac Surgery, Cardiothoracic Surgical Procedures and Percutaneous Coronary Intervention (PCI)/Coronary Angioplasty – Heart and Cardiovascular Medical Devices in Use in Operating Rooms and in Catheterization Labs in the US
in Volume Three in a forthcoming three volume Series of e-Books on Cardiovascular Diseases
This very Sub-Chapter represents milestones in Dr. Isaac George – Becoming a Cardiothoracic Surgeon: An Emerging Profile through Scientific Publications, This profile is now in:
VIEW VIDEOon Mitral Valve Repair and Replacement – Dr. Karl H. Krieger
Dr. Karl H. Krieger, the Vice Chairman of the Department of Cardiothoracic Surgery at NewYork-Presbyterian Hospital/Weill Cornell Medical Center in New York City, discusses treatment for Mitral Valve Disease. Specifically, Dr. Krieger compares the options of Mitral Valve Repair with Mitral Valve Replacement.
This video with Dr. Krieger is from a web cast at the Ronald O. Perelman Heart Institute at NewYork-Presbyterian.
VIEW VIDEOon Left Ventricular Assist Devices (LVADs) – Dr. Jonathan Chen
Dr. Jonathan Chen, the Site Chief for Pediatric Cardiac Surgery at NewYork-Presbyterian Hospital/Weill Cornell Medical Center in New York City, explains how Left Ventricular Assist Devices (LVADs) work and how they can benefit patients with heart failure.
LVADs are implantable devices that help the heart pump blood. They can be used as a temporary therapy, allowing patients’ hearts to rest while they recover from cardiac events such as heart attacks, or while they wait for hearts to become available for transplants. For some patients whose hearts are unlikely to recover and are not candidates for heart transplants, the devices may be used as a permanent therapy. Heart failure, especially in severe forms, can force patients to lead restricted lives because often even very limited physical activity, such as walking from one room to another, will leave them breathless.
Dr. Chen is a pediatric cardiothoracic surgeon, yet the information in the video is applicable to adult patients as well.
Organ transplantation that prolongs and dramatically improves quality of life is nearly a daily occurrence at Columbia University Medical Center.
The success of solid organ transplantation – with improved surgical techniques, replacement organ procurement, and medical management – is advancing each year. Many of these advances have resulted from scientific and clinical research conducted at Columbia University Medical Center.
A Brief History of Transplantation at Columbia
Transplantation: Where we’ve been, where we’re going
Eric A. Rose, MD, former chairman of the department of surgery, left center, performing the first successful pediatric heart transplant in 1984. Transplant pioneer Keith Reemtsma, MD, who is overseeing the operating field (top of photo).
When he transplanted a chimpanzee kidney into a human patient in the late 1960’s, the late Keith Reemtsma, MD, then Department of Surgery Chairman at Tulane University, revolutionized treatment of end-stage organ failure and initiated an era of unprecedented exploration into organ transplantation that would affect the lives of patients around the world.
Transferring to Columbia-Presbyterian Medical Center in 1971, Dr. Reemtsma recruited Mark A. Hardy, MD, who laid another cornerstone of organ transplant medicine by founding the program for dialysis and kidney transplantation. Dr. Hardy based the new program on the principle of collaborative clinical care between surgeons and nephrologists. During a time when renal transplant programs were managed by one or the other discipline but never by both simultaneously, the medical community regarded the concept as folly. Yet the program grew steadily, as did the program’s immune tolerance research initiatives to induce the transplant recipient’s body to accept a donor organ. This multidisciplinary cooperation also led to major contributions in immunogenetics, immunosuppression, and treatment of autoimmune diseases and lymphoma — and it ultimately became the overarching principle for all the NewYork-Presbyterian Hospital transplant services.
Colleagues universally give credit to Eric A. Rose, MD, who co-founded the heart transplantation program with Dr. Reemtsma, for his successful transformation of the program into the outstanding center it is today. A parade of achievements marks the history of the heart transplant program, including the first mechanical bridge-totransplantation using intra-aortic balloon pumps in the 1970’s, and the first successful pediatric heart transplant, performed by Dr. Rose in 1984. Under the guidance of Dr. Rose and his successors, the program has pioneered research in immunosuppressant medications, mechanical assist devices, and minimally invasive surgical procedures. It currently performs over 100 heart transplants yearly, with among the highest success rates in the nation.
Also in 2004, Lloyd E. Ratner, MD, succeeded Dr. Hardy as director of the renal and pancreas transplant program. One of the first to perform laparoscopic donor operations, Dr. Ratner has found creative solutions to overcome immune barriers to kidney transplantation. The program now routinely uses extended-criteria donor organs, performs transplants among incompatible donors, and is a leader in coordinating “donor swaps” to maximize availability of compatible donor organs. Since Dr. Ratner’s arrival, Columbia has been designated one of ten regional islet resource centers in the U.S. that isolate and transplant pancreatic cells to treat type 1 diabetes as part of a limited protocol controlled by the FDA. Recent progress in visualization of pancreatic islets using PET technology, under the guidance of Paul Harris, PhD, has been recognized by the scientific community as a milestone in this developing field.
NYPH/Columbia received UNOS approval for pancreatic transplantation in January 2008. Our premier kidney transplant program is facilitating rapid growth of the new pancreatic transplantation program, which overlaps both in its patient population and its surgical and medical expertise. The northeast region of the U.S. has been consistently underserved as far as access to pancreatic transplantation, with relatively few centers serving a disproportionately large metropolitan population. The expanding program at NewYork-Presbyterian now provides much-needed access to patients with end-stage pancreatic disease in New York state, particularly those with the most complex medical and surgical challenges.
Transplantation of cells, rather than organs, is emerging as a therapy with enormous potential. Transplantation of either a patient’s own or a foreign donor’s bone marrow cells, for example, offers hope of regenerating the heart so that patients with heart failure may be able to avoid heart transplantation.
In introducing the transplantation programs, it would be remiss to neglect mention of the yet another dimension in which they excel — education. Physician training is a top priority, and NYPH/Columbia has trained many of the greatest transplant surgeons over the last 20 years, including many of the leaders of transplant programs throughout the U.S.
At NewYork-Presbyterian Hospital/Columbia University Medical Center, the Transplant Initiative (TI) has been launched to drive the growth of both clinical and research aspects of transplantation. This multi-year undertaking will involve Departments of Medicine, Pathology, Pediatrics, and Surgery and all of the solid organ transplantation programs, both adult and pediatrics. It is led by its Executive Director, Jean C. Emond, MD.
Although NYP/Columbia is already a national leader in clinical transplantation with respect to volume and patient outcomes, this initiative will further leverage the diverse expertise of its transplant scientists and clinicians.
Approximately 2,200 heart transplants are now performed each year in more than 150 heart transplant centers in the United States. The surgeons and cardiologists of Columbia University Medical Center of NYPH have a long and distinguished history of advancing “standards of care” and the survival rates of our patients by using innovative surgical techniques, by applying our basic scientific research in immunosuppression to the clinical setting, and by inventing and perfecting life-sustaining cardiac assist devices that prolong life while waiting for organ availability.
Columbia University Medical Center’s lung and heart-lung transplantation program, which began in 1985, is fast approaching its 200th transplant. Performing more than 30 transplants each year, the lung and heart-lung transplant teams have earned a national reputation for excellence. Our world-renowned transplantation researchers have helped lead the way to improvements in care that, nationwide, have increased the long-term survival rate for lung transplantation by 50% over the past seven years. Among those improvements are new immunosuppressive agents, new antibiotics, refined surgical techniques, and a more comprehensive understanding of follow-up care.
It is the combination of basic research at the molecular cardiology level, biomaterial, surgical procedures and PUBLICATION of Cases and research results that found me in Dr. George’s territory as a renewed inspiration.
For Author’s training & experience @ MGH – Cardiac Floor – Ellison 11, BWH – CCU, Tower 3 – 12Fl, BIDMC – Acute Surgery, Farr 9, and Texas Heart Institute, Perfusion, Faulkner Hospital – ICU
Russo MJ, Chen JM, Sorabella RA, Martens TP, Garrido M, Davies RR, George I, Cheema FH, Mosca RS, Mital S, Ascheim DD, Argenziano M, Stewart AS, Oz MC, Naka Y.
Heart Failure and Dietary Sodium: Do we know as much as we think?
Samar Sheth,1 Alan B. Weder2 and Scott L. Hummel2,3; 1. Department of Internal Medicine, University of Michigan; 2. Division of Cardiovascular Medicine, Department of Medicine, University of Michigan Medical School; 3. Staff Cardiologist, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan
Depolarisation Reserve: A New Identification Concept of Responders to Biventricular Stimulation.
Philippe Chevalier and Alina Scridon; Centre de Référence des Troubles du Rythme Cardiaque Héréditaires, Hôpital Cardiologique Louis Pradel, Bron Cedex
Treatment Strategies – Cardiology is a print (on request) and online eBook publication that provides its readership with a collection of comprehensive and thought-provoking articles from the most respected key opinion leaders, leading doctors and authorities in the cardiology field. The series informs and educates clinicians on the latest therapeutic and technological advances. Published in line with the foremost cardiology congresses, the editorial content includes an unbiased, independent inbound supplement reviewing either the ESC or ACC congress. The review is dedicated to bringing readers the latest cardiology breaking news, exhibition highlights, awards and prizes and research developments from the key-note presentations at the congress.
Treatment Strategies – Cardiology (European and US edition) is available online as a free-to-view eBook providing its readers with an exciting interactive experience. Easily accessible, user friendly and free-to-print, the eBook can provide you with a wide range of dynamic features, including links to external websites, newsletters and email addresses to direct readers to your specialist products and services forming strong links with media partnerships. Importantly, an eBook can be sent out to clients worldwide in an organised and professional layout that allows a far-reaching distribution of your products. The eBook also offers you the opportunity to include, on any page, videos and podcasts of current events such as symposium proceedings that you may wish to highlight for the readership. The latest eBook also permits the advertiser to track statistical data for each page and publication; including the number of unique visits, click though pages, geographical location of the visitor and average time spent viewing.
Advisory Panel
Treatment Strategies – Cardiology is shaped by an advisory panel of world-renowned specialists from the leading associations and societies, including experts from:
Nicholas Antony Boon, Consultant Cardiologist, Royal Infirmary of Edinburgh, Honorary Reader, University of Edinburgh and former President of the British Cardiovascular Society (BCS)
Carl J. Pepine, Professor of Medicine, Division of Cardiovascular Medicine, University of Florida; Past-President, American College of Cardiology (ACC)
Bertram Pitt, University of Michigan Medical Center, William Beaumont Hospital, Ann Arbor, Michigan; President of the Michigan Chapter of American College of Cardiology, Chairman, Young Investigator’s Award Committee of the American College of Cardiology, Chairman of the Reveal Committee of the ACC
Treatment Strategies – CardiologyVolume 5 Issue 1 will include an unbiased, independent inbound supplement reviewing the ACC Congress, taking place in San Francisco in March. The inbound supplement will present the readers with the latest news, exhibition highlights, awards and prizes and research developments from the key-note presentations from the ACC. The publication will be published in April 2013.
European Edition
Treatment Strategies – Cardiology Volume 5 Issue 2will include an independently written review of the ESC congress taking place in Amsterdam in August. The review is dedicated to bringing readers the latest cardiology news, exhibition highlights, awards and prizes and research developments from the key-note presentations at the congress. Please click on the image (below) to view the media pack as an eBook. Volume 5 Issue 2 will be published in September 2013.
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
The evaluation of coronary artery disease (blocked arterial blood supply to heart muscle) by stress tests is functional: is there enough blockage to starve a region of muscle when demand is high? By starvation we mean ischemia – insufficient supply to meet metabolic demands as expressed by consequent functional impairment, e.g., metabolic, electric, mechanical. In the catheterization laboratory, the evaluation is primarily anatomic – is there a bite missing in the silhouette of a coronary artery consistent with a significant impediment to blood delivery beyond the lesion? Half of all heart attacks are due to such lesions. The other half derive from non-obstructive but unstable lesions that may crack, bleed into the vessel wall, and suddenly clot, blocking the blood flow. Coronary lesions that restrict blood delivery sufficient to cause demand ischemia (insufficient blood supply to meet high demands) cause angina pectoris.
The focus of flow reserve is to add an assessment of functional significance to anatomic lesions observed at catheterization. The widespread practice of deciding on intervention based on percent diameter reduction imposed by a lesion is obviously flawed. The flow limitation imposed by a lesion depends on its length and shape (entrance and exit effects on flow pattern), not merely the diameter reduction expressed as a percent, that is currently deemed the decision-making “degree of stenosis.” In the midst of a medical emergency heart attack, the target of intervention is the culprit lesion, the one that best explains why a region of muscle is dying. In that case, timely intervention is potentially life saving and does not depend on or wait for measurements. In the non-emergent setting, it is much harder to establish benefit from intervention. If a lesion is flow limiting and explanatory for angina pectoris, then intervention to relieve obstruction offers pain relief and may improve exertion tolerance. In relatively rare circumstances (3-vessel obstruction, left main obstruction) intervention may avoid heart attack and extend life expectancy, but with as good or better outcomes from bypass surgery. Most elective catheter interventions (balloon angioplasty, stent placement) have failed to establish improved life expectancy or even superiority over medication. Furthermore, stent placement obligates use of strong anti-platelet medications (e.g., aspirin plus clopidogrel) that elevate risk of serious bleeding and stroke. Therefore it is reasonable to require further evidence that a coronary lesion is obstructive and consequential that just percent stenosis (narrowing) as indication for intervention. Fractional flow reserve offers such confirmation of lesion significance.
The use of FFR is relatively widespread in Europe, while its usage is beginning to catch up in the US. But for what reasons? Drs Roxana Mehran,Justin Davies, and Ron Waksman gathered recently to share their thoughts on the role of functional assessment in the cath lab, to evaluate FFR and its alternatives, and discuss what testing the future might hold for the optimal detection of culprit lesions.
Host
Roxana Mehran MD
Professor of Medicine, Divisions of Cardiology and Health Evidence and Policy
Director, Interventional Cardiovascular Research and Clinical Trials
The Zena and Michael A Wiener Cardiovascular Institute Icahn School of Medicine at Mount Sinai
New York, NY
Dr Mehran has served as an advisor or consultant for AstraZeneca Pharmaceuticals, Regado Biosciences, Abbott Cardiovascular Systems, Janssen (Johnson & Johnson), Merck, and Maya Medical. She has received grants for clinical research from Bristol-Myers Squibb, Sanofi, the Medicines Company, and Lilly/DSI.
Guests
Justin Davies MBBS PhD
Consultant Interventional Cardiologist
Hammersmith Hospital
Imperial College
London, United Kingdom
Dr Davies has served as an advisor or consultant for Volcano and Medtronic. He has served as a speaker or a member of a speakers’ bureau for Medtronic and has received grants for clinical research from Volcano, Medtronic, and Abbott.
Ron Waksman MD
Director, Clinical Research and Advanced Education
MedStar Cardiovascular Research Network/Cleveland Clinic Heart and Vascular Institute
Clinical Professor of Medicine (Cardiology)
Georgetown University
Washington, DC
Dr Waksman has served as a speaker or a member of a speakers’ bureau for AstraZeneca Pharmaceuticals, Boston Scientific, and Medtronic.
Roxana Mehran, MD: Hello. My name is Roxana Mehran from Mount Sinai
School of Medicine in New York. It’s my pleasure to welcome you to this editorial
program in which we will look into how FFR usage differs in Europe vs the United
States.
I’m joined by my colleagues Justin Davies from Imperial College London and, of
There has been increasing interest on the so-called cardiorenal syndrome (CRS), defined as
a complex pathophysiological disorder of the heart and kidneys where by acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other.
In this review, we contend that there is lack of evidence warranting the adoption of a specific clinical construct such as the CRS within the heart failure (HF) syndrome by demonstrating that:
(a) the approaches and tools regarding the definition of kidney involvement in HF are suboptimal;
(b) development of renal failure in HF is often confounded by age, hypertension, and diabetes;
(c) worsening of renal function (WRF) in HF may be largely independent of alterations in cardiac function;
(d) the bidirectional association between HF and renal failure is not unique and represents one of the several such associations encountered in HF; and
(e) inflammation is a common denominator for HF and associated noncardiac morbidities.
Based on these arguments, we believe that
dissecting one of the multiple bidirectional associations in HF and
constructing the so-called cardiorenal syndrome is not justified pathophysiologically.
Fully understanding of all morbid associations and not only the cardiorenal, that is of great significance for the clinician who is caring for the patient with HF.
Bart et al. (Dec. 13 issue)1 report the results of the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF). They state that ultrafiltration was inferior to a strategy of stepped pharmacologic therapy with respect to the
It is unclear at first sight why renal function should be different at 96 hours only when serum creatinine concentrations are used as a marker of renal function,
but not when the level of cystatin C or the glomerular filtration rate are used.
How can this discrepancy be explained?
According to the study Ultrafiltration in Decompensated Heart Failure with Cardiorenal Syndrome
Ultrafiltration is an alternative strategy to diuretic therapy for the treatment of patients with acute decompensated heart failure.
Little is known about the efficacy and safety of ultrafiltration in patients with acute decompensated heart failure
complicated by persistent congestion and worsened renal function.
Ultrafiltration was inferior to pharmacologic therapy with respect to the bivariate end point of
the change in the serum creatinine level and body weight 96 hours after enrollment (P=0.003),
owing primarily to an increase in the creatinine level in the ultrafiltration group.
At 96 hours, the mean change in the creatinine level was −0.04±0.53 mg per deciliter (−3.5±46.9 μmol per liter) in the pharmacologic-therapy group,
as compared with +0.23±0.70 mg per deciliter (20.3±61.9 μmol per liter) in the ultrafiltration group (P=0.003).
A higher percentage of patients in the ultrafiltration group than in the pharmacologic-therapy group had a serious adverse event (72% vs. 57%, P=0.03).
In a randomized trial involving patients hospitalized for acute decompensated heart failure,
worsened renal function, and
persistent congestion,
the use of a stepped pharmacologic-therapy algorithm was superior to a strategy of ultrafiltration for
the preservation of renal function at 96 hours,
with a similar amount of weight loss with the two approaches.
What is Acute Heart Failure? (Photo credit: Novartis AG)
English: Physiology of Nephron (Photo credit: Wikipedia)
Forrester-classification for classification of Congestive heart failure ; Forrester-Klassifikation zur Einteilung einer akuten Herzinsuffizienz (Photo credit: Wikipedia)
AIMS: We examined the prognostic importance of cardiac troponin I (cTnI) in a cohort of patients enrolled in the ASCEND-HF study of nesiritide in acute decompensated heart failure (ADHF). Circulating troponins are a prognostic marker in patients with ADHF. Contemporary assays with greater sensitivity require reassessment of the significance of troponin elevation in HF.
METHODS: Cardiac troponin I was measured in a core laboratory in 808 ADHF patients enrolled in the ASCEND-HF biomarkers substudy using a sensitive assay (VITROS Trop I ES, Ortho Clinical Diagnostics) with a lower limit of detection of 0.012 ng/mL and a 99th percentile upper reference limit (URL) of 0.034 ng/mL. Patients with clinical evidence of acute coronary syndrome or troponin >5× the URL were excluded. Multivariable modelling was used to assess the relationship between log(cTnI) and in-hospital and post-discharge outcomes.
RESULTS:
Baseline cTnI was undetectable in 22% and
elevated above the 99th percentile URL in 50% of subjects.
cTnI levels did not differ based on HF etiology. After multivariable adjustment, higher cTnI was associated with worsened in-hospital outcomes such as
length of stay (P = 0.01) and
worsening HF during the index hospitalization (P = 0.01), but
was not associated with worsened post-discharge outcomes at 30 or 180 days.
The relationship between cTnI and outcomes was generally linear and
there was no evidence of a threshold effect at any particular level of cTnI.
CONCLUSION:
cTnI is elevated above the 99th percentile URL in 50% of ADHF patients and
predicts in-hospital outcome, but
is not an independent predictor of long-term outcomes.
This reviewer finds the results quite interesting, and the study was done with care. The Ortho Diagnostics method of cTnI is high-sensitivity assay, so that the lowest measureable level at < 10% CV is manyfold lower than the 4th generation assay.
AMI did occur below the ROC cutoff in both cases, but the reasons for elevations other than AMI were determined to be CRF, and this was more accurate (a small probability with the cTnT between 0.085 and 0.1 ng/ml.
However, the findings in this study did indeed exclude symptomatic ACS, or cTnI at the level not > 5x ULN. [0.17 ng/ml] with the hs-TnI. The hs-cTnI assay opened up the identification of non-ACS elevation related to cardiomyocyte damage unrelated to plaque rupture, but related to a persistent coronary ischemia, possibly related to cardiomegaly and/or vascular rigidity.
Test Limitations
Troponins are not normally present in serum, so any amount present in serum (measured at the 99th percentile of the upper limit of normal at a 10% imprecision) indicates structural damage to the heart, although not necessarily AMI.
Both troponin I (TnI) and troponin T (TnT) are affected by renal insufficiency, but TnT is to a greater extent
100% of TnT is excreted in urine, but 70% of TnI is degraded by vascular endothelium; this means that minor elevations of troponins have to be considered in the context of comorbidities, especially renal impairment, and risk factors
Among heart failure patients, the objective parameter of NT-proBNP seems more useful to delineate the “cardiorenal syndrome” than the previous criteria of a clinical diagnosis of heart failure
However, the NT-proBNP is best interpreted by using the log(NT-proBNP)/eGFR with an adjustment.
These investigators used the log(cTnI), which I would not have thought of in this case, but it is important to do because the distribution of the peptide levels in the study population would be nonparametric. The median values at the time points are not given. Actually, there are presumably, not definitely, two populations – if you were to infer short- and long-term outcomes measured as 30-days, and 180-days. That a baseline cTNI was undetectable in 22% of patients is actually not so different than would be found in a random selection from patients presenting to the emergency department. It should not be a surprise that the test as a single predictor, did not meet the requirement for long-term prediction of outcome, despite agreement with the in-hospital outcome. This is consistent with the absence of ACS.
[1] Troponins (Cardiac-specific Troponin I and Troponin T). LH Bernstein. http://PathologyOutlines.com/Chemistry
[2] Effect of renal function loss on NT-proBNP level variations. LH Bernstein, MY Zions, SA Haq, S Zarich, J Rucinski, B Seamonds, et al. Clin Biochem 2009; 42(10-11):1091-1098. ICID: 937529 http://dx.doi.org/10.1016/j.clinbiochem.2009.02.027. [3] Enhancing the diagnostic performance of troponins in the acute care setting. SA Haq, M Tavakol, S Silber, L Bernstein, J Kneifati-Hayek, M Schleffer, et al. J Emerg Med 2008; x:x ICID: 937619 http://www.nymethodistemergencymedicine.com/program/research.html [4] Comparison of test characteristics of cardiac troponin T in patients with normal renal function and chronic renal failure evaluated in the emergency department. S Silber, L Melniker, E Haines, LH Bernstein. Academic Emergency Medicine 2006; 13(5):S1186-187. ICID: 939943 http://www.nymethodistemergencymedicine.com/program/research.html [5} The ACC/ESC Recommendation for 99th Percentile of the Reference Normal Troponin I Overestimates the Risk of an Acute Myocardial Infarction: a novel enhancement in the diagnostic performance of troponins. “6th Scientific Forum on Quality of Care and Outcomes Research in Cardiovascular Disease and Stroke.” S Haq, M Tavakol, LH Bernstein, J Kneifati-Hayek, M Schlefer, S Silber, T Sacchi, J Pima. Circulation 2005; 111(20):e313-313. ICID: 939931 http://pt.wkhealth.com/pt/re/circ/toc.00003017-200505240-00000.htm [6] Minor elevations in troponin T values enhance risk assessment in emergency department patients with suspected myocardial ischemia: analysis of novel troponin T cut-off values. SW Zarich, K Bradley, ID Mayall, LH Bernstein.
Clin Chim Acta 2004; 343(1-2):223-229. ICID: 825515 http://www.ncbi.nlm.nih.gov/pubmed/15115700
[7] GOLDmineR: improving models for classifying patients with chest pain. L Bernstein, K Bradley, SW Zarich. Yale J Biol Med 2002; 75(4):183-198. ICID: 825624 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588788/
Other related articles published on this Open Access Online Scientific Journal, include the following:
High-Sensitivity Cardiac Troponin Assays- Preparing the United States for High-Sensitivity Cardiac Troponin Assays
refer to: Cardiac ischemia in patients with septic shock randomized to vasopressin or norepinephrine
Mehta S, Granton J, Gordon AC, Cook DJ, et al.
Critical Care 2013, 17:R117 http://dx.doi.org/10.1186/cc12789
Troponin and CK levels, and rates of ischemic ECG changes were similar in the VP and NE groups. In multivariable analysis
only APACHE II was associated with 28-day mortality (OR 1.07, 95% CI 1.01-1.14, p=0.033).
What is Acute Heart Failure? (Photo credit: Novartis AG)
Troponin activation. Troponin C (red) binds Ca2+, which stabilizes the activated state, where troponin I (yellow) is no longer bound to actin. Troponin T (blue) anchors the complex on tropomyosin. (Photo credit: Wikipedia)
Vasoplegia or vasoplegic syndrome (VS) is thought to be due to
dysregulation of endothelial homeostasis and subsequent endothelial dysfunction
secondary to direct and indirect effects of multiple inflammatory mediators.
Vasoplegia has been observed in all age groups and in various clinical settings, such as anaphylaxis (including protamine reaction), sepsis, hemorrhagic shock, hemodialysis, and cardiac surgery. Among mechanisms thought to be contributory to VS, the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway appears to play a prominent role.
Methylene blue (MB),
an inhibitor of nitric oxide synthase (NOS) and guanylate cyclase (GC),
has been found to improve
the refractory hypotension associated with endothelial dysfunction of VS.
METHODS: We reviewed peri-operative data from 311 consecutive adult patients who underwent OHT between January 2003 and June 2008.
Vasoplegia was defined as
persistent low systemic vascular resistance,
despite multiple intravenous pressor drugs at high dose,
between 6 and 48 hours after surgery.
RESULTS: In our cohort of 311 patients, 35 (11%) patients developed vasoplegia syndrome; these patients were more likely to be UNOS Status 1A, with
a higher body surface area (1.8 ± 0.25 vs 1.63 ± 0.36, p = 0.0007),
greater history of thyroid disease (38.2% vs 18.5%, p = 0.0075) and
a higher rate of previous cardiothoracic surgery (79% vs 48%, p = 0.0006).
Pre-operatively,
they were more frequently treated with aspirin (73% vs 48%, p = 0.005) and
mechanical assist devices (ventricular assist devices [VADs]: 45% vs 17%, p < 0.0001;
total artificial hearts: 8.6% vs 0%, p < 0.0001), and
less treated with milrinone (14.7% vs 45.8%, p = 0.0005).
Bypass time (118 ± 37 vs 142 ± 39 minutes, p = 0.0002) and
donor heart ischemic time (191 ± 46 vs 219 ± 51 minutes, p = 0.002) were longer, with
higher mortality (3.2% vs 17.1%, p = 0.0003) and morbidity in the first 30 days after transplant.
In the multivariate analysis, history of thyroid disease(odds ratio [OR] = 2.7, 95% CI 1.0 to 7.0, p = 0.04) and VAD prior to transplant (OR = 2.8, 95% CI 1.07 to 7.4, p = 0.03)
were independent risk factors for development of vasoplegia syndrome.
CONCLUSIONS:
High body mass index,
long cardiopulmonary bypass time,
prior cardiothoracic surgery,
mechanical support,
use of aspirin, and
thyroid disease
are risk factors associated with development of vasoplegia syndrome.
Space-filling model of the cyclic guanosine monophosphate molecule, also known as cGMP, a nucleotide. This image shows the anionic (negatively charged) form. Colour code (click to show) : Black: Carbon, C : White: Hydrogen, H : Red: Oxygen, O : Blue: Nitrogen, N : Orange: Phosphorus, P (Photo credit: Wikipedia)
Ball-and-stick model of the cyclic guanosine monophosphate molecule, also known as cGMP, a nucleotide. This image shows the anionic (negatively charged) form. Colour code (click to show) : Black: Carbon, C : White: Hydrogen, H : Red: Oxygen, O : Blue: Nitrogen, N : Orange: Phosphorus, P (Photo credit: Wikipedia)
English: Drawing showing targets of cGMP in cells (Photo credit: Wikipedia)
“When heart failure (HF) progresses to an advanced stage, difficult decisions must be made,” the AHA says on its website. “Do I want to receive aggressive treatment? Is quality of life more important than living as long as possible? How do I feel about resuscitation?”
LVADs can take over the pumping function of a failing heart, but they also present some of the most expensive implantable-device surgeries. An article in the peer-reviewed journal JACC: Heart Failure reported last year that the average total cost to implant an LVAD in Medicare beneficiaries was $175,000, more than double the cost of a heart transplant.
Amador said between 5,000 and 5,500 Americans will have LVAD implants this year. That compares with 2,200 adult heart transplants that happen annually in the U.S., according to the JACC article.
For patients with advanced heart failure, outcomes are good after heart transplantation, but not enough donor hearts are available. Fortunately, mechanical circulatory assist devices have become an excellent option and should be considered either as a bridge to transplantation or as “destination therapy.” Current mechanical circulatory assist devices improve quality of life in patients who are candidates.
For some patients, conventional treatments are inadequate to relieve the effects of heart failure. Under these circumstances, mechanical circulatory support is considered. There are now a variety of devices capable of pumping blood to restore circulation of vital organs, even temporarily replacing the function of the native heart.
The ABIOMED AB5000™ Circulatory Support System is a short-term mechanical system that can provide left, right, or biventricular support for patients whose hearts have failed but have the potential for recovery. The AB5000™ can be used to support the heart, giving it time to rest – and potentially recover native heart function. The device can also be used as a bridge to definitive therapy.
What is Acute Heart Failure? (Photo credit: Novartis AG)
English: The CardioWest™ temporary Total Artificial Heart (Photo credit: Wikipedia)
English: Graph showing the correlation between BNP serum level and mortality. Source: Inder S. Anand, Lloyd D. Fisher, Yann-Tong Chiang, Roberto Latini, Serge Masson,Aldo P. Maggioni, Robert D. Glazer, Gianni Tognoni, Jay N. Cohn (24th Feb 2003). Changes in Brain Natriuretic Peptide and Norepinephrine Over Time and Mortality and Morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 107: 1278-83. DOI: 10.1161/01.CIR.0000054164.99881.00 (Photo credit: Wikipedia)