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Archive for the ‘Frontiers in Cardiology and Cardiovascular Disorders’ Category


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Stroke is a leading cause of death worldwide and the most common cause of long-term disability amongst adults, more particularly in patients with diabetes mellitus and arterial hypertension. Increasing evidence suggests that disordered physiological variables following acute ischaemic stroke, especially hyperglycaemia, adversely affect outcomes.

 

Post-stroke hyperglycaemia is common (up to 50% of patients) and may be rather prolonged, regardless of diabetes status. A substantial body of evidence has demonstrated that hyperglycaemia has a deleterious effect upon clinical and morphological stroke outcomes. Therefore, hyperglycaemia represents an attractive physiological target for acute stroke therapies.

 

However, whether intensive glycaemic manipulation positively influences the fate of ischaemic tissue remains unknown. One major adverse event of management of hyperglycaemia with insulin (either glucose-potassium-insulin infusions or intensive insulin therapy) is the occurrence of hypoglycaemia, which can also induce cerebral damage.

 

Doctors all over the world have debated whether intensive glucose management, which requires the use of IV insulin to bring blood sugar levels down to 80-130 mg/dL, or standard glucose control using insulin shots, which aims to get glucose below 180 mg/dL, lead to better outcomes after stroke.

 

A period of hyperglycemia is common, with elevated blood glucose in the periinfarct period consistently linked with poor outcome in patients with and without diabetes. The mechanisms that underlie this deleterious effect of dysglycemia on ischemic neuronal tissue remain to be established, although in vitro research, functional imaging, and animal work have provided clues.

 

While prompt correction of hyperglycemia can be achieved, trials of acute insulin administration in stroke and other critical care populations have been equivocal. Diabetes mellitus and hyperglycemia per se are associated with poor cerebrovascular health, both in terms of stroke risk and outcome thereafter.

 

Interventions to control blood sugar are available but evidence of cerebrovascular efficacy are lacking. In diabetes, glycemic control should be part of a global approach to vascular risk while in acute stroke, theoretical data suggest intervention to lower markedly elevated blood glucose may be of benefit, especially if thrombolysis is administered.

 

Both hypoglycaemia and hyperglycaemia may lead to further brain injury and clinical deterioration; that is the reason these conditions should be avoided after stroke. Yet, when correcting hyperglycaemia, great care should be taken not to switch the patient into hypoglycaemia, and subsequently aggressive insulin administration treatment should be avoided.

 

Early identification and prompt management of hyperglycaemia, especially in acute ischaemic stroke, is recommended. Although the appropriate level of blood glucose during acute stroke is still debated, a reasonable approach is to keep the patient in a mildly hyperglycaemic state, rather than risking hypoglycaemia, using continuous glucose monitoring.

 

The primary results from the Stroke Hyperglycemia Insulin Network Effort (SHINE) study, a large, multisite clinical study showed that intensive glucose management did not improve functional outcomes at 90 days after stroke compared to standard glucose therapy. In addition, intense glucose therapy increased the risk of very low blood glucose (hypoglycemia) and required a higher level of care such as increased supervision from nursing staff, compared to standard treatment.

 

References:

 

https://www.nih.gov/news-events/news-releases/nih-study-provides-answer-long-held-debate-blood-sugar-control-after-stroke

 

https://www.ncbi.nlm.nih.gov/pubmed/27873213

 

https://www.ncbi.nlm.nih.gov/pubmed/19342845

 

https://www.ncbi.nlm.nih.gov/pubmed/20491782

 

https://www.ncbi.nlm.nih.gov/pubmed/21211743

 

https://www.ncbi.nlm.nih.gov/pubmed/18690907

 

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Lesson 3 Cell Signaling & Motility: G Proteins, Signal Transduction: Curations and Articles of reference as supplemental information: #TUBiol3373

Curator: Stephen J. Williams, Ph.D.

Lesson 3 Powerpoint (click link below):

cell signaling and motility 3 finalissima sjw

Four papers to choose from for your February 11 group presentation:

Structural studies of G protein Coupled receptor

Shapiro-2009-Annals_of_the_New_York_Academy_of_Sciences

G protein as target in neurodegerative disease

fish technique

 

 

Today’s lesson 3 explains how extracellular signals are transduced (transmitted) into the cell through receptors to produce an agonist-driven event (effect).  This lesson focused on signal transduction from agonist through G proteins (GTPases), and eventually to the effectors of the signal transduction process.  Agonists such as small molecules like neurotransmitters, hormones, nitric oxide were discussed however later lectures will discuss more in detail the large growth factor signalings which occur through receptor tyrosine kinases and the Ras family of G proteins as well as mechanosignaling through Rho and Rac family of G proteins.

Transducers: The Heterotrimeric G Proteins (GTPases)

An excellent review of heterotrimeric G Proteins found in the brain is given by

Heterotrimeric G Proteins by Eric J Nestler and Ronald S Duman.

 

 

from Seven-Transmembrane receptors – Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/Examples-of-heterotrimeric-G-protein-effectors_tbl1_11180073 [accessed 4 Feb, 2019] and see references within

 

 

See below for the G Protein Cycle

 

 

 

 

 

 

 

 

<a href=”https://www.researchgate.net/figure/32-The-G-protein-cycle-In-the-absence-of-agonist-A-GPCRs-are-mainly-in-the-low_fig2_47933733″><img src=”https://www.researchgate.net/profile/Veli_Pekka_Jaakola/publication/47933733/figure/fig2/AS:669499451781133@1536632516635/32-The-G-protein-cycle-In-the-absence-of-agonist-A-GPCRs-are-mainly-in-the-low.ppm&#8221; alt=”.3.2: The G protein cycle. In the absence of agonist (A), GPCRs are mainly in the low affinity state (R). After agonist binding, the receptor is activated in the high affinity state (R*), and the agonist-GPCR-G protein complex is formed. GTP replaces GDP in Gα. After that the G protein dissociates into the Gα subunit and the Gβγ heterodimer, which then activate several effector proteins. The built-in GTPase activity of the Gα subunit cleaves the terminal phosphate group of GTP, and the GDP bound Gα subunit reassociates with Gβγ heterodimer. This results in the deactivation of both Gα and Gβγ. The G protein cycle returns to the basal state. RGS, regulator of G protein signalling.”/></a>

 

From Citation: Review: A. M. Preininger, H. E. Hamm, G protein signaling: Insights from new structures. Sci. STKE2004, re3 (2004)

 

For a tutorial on G Protein coupled receptors (GPCR) see

https://www.khanacademy.org/test-prep/mcat/organ-systems/biosignaling/v/g-protein-coupled-receptors

 

 

 

cyclic AMP (cAMP) signaling to the effector Protein Kinase A (PKA)

from https://courses.washington.edu/conj/gprotein/cyclicamp.htm

Cyclic AMP is an important second messenger. It forms, as shown, when the membrane enzyme adenylyl cyclase is activated (as indicated, by the alpha subunit of a G protein).

 

The cyclic AMP then goes on the activate specific proteins. Some ion channels, for example, are gated by cyclic AMP. But an especially important protein activated by cyclic AMP is protein kinase A, which goes on the phosphorylate certain cellular proteins. The scheme below shows how cyclic AMP activates protein kinase A.

Additional information on Nitric Oxide as a Cellular Signal

Nitric oxide is actually a free radical and can react with other free radicals, resulting in a very short half life (only a few seconds) and so in the body is produced locally to its site of action (i.e. in endothelial cells surrounding the vascular smooth muscle, in nerve cells). In the late 1970s, Dr. Robert Furchgott observed that acetylcholine released a substance that produced vascular relaxation, but only when the endothelium was intact. This observation opened this field of research and eventually led to his receiving a Nobel prize. Initially, Furchgott called this substance endothelium-derived relaxing factor (EDRF), but by the mid-1980s he and others identified this substance as being NO.

Nitric oxide is produced from metabolism of endogenous substances like L-arginine, catalyzed by one of three isoforms of nitric oxide synthase (for link to a good article see here) or release from exogenous compounds like drugs used to treat angina pectoris like amyl nitrate or drugs used for hypertension such as sodium nitroprusside.

The following articles are a great reference to the chemistry, and physiological and pathological Roles of Nitric Oxide:

46. The Molecular Biology of Renal Disorders: Nitric Oxide – Part III

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/11/26/the-molecular-biology-of-renal-disorders/

47. Nitric Oxide Function in Coagulation – Part II

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

https://pharmaceuticalintelligence.com/2012/11/26/nitric-oxide-function-in-coagulation/

48. Nitric Oxide, Platelets, Endothelium and Hemostasis

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/11/08/nitric-oxide-platelets-endothelium-and-hemostasis/

49. Interaction of Nitric Oxide and Prostacyclin in Vascular Endothelium

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/09/14/interaction-of-nitric-oxide-and-prostacyclin-in-vascular-endothelium/

50. Nitric Oxide and Immune Responses: Part 1

Curator and Author:  Aviral Vatsa PhD, MBBS

https://pharmaceuticalintelligence.com/2012/10/18/nitric-oxide-and-immune-responses-part-1/

51. Nitric Oxide and Immune Responses: Part 2

Curator and Author:  Aviral Vatsa PhD, MBBS

https://pharmaceuticalintelligence.com/2012/10/28/nitric-oxide-and-immune-responses-part-2/

56. Nitric Oxide and iNOS have Key Roles in Kidney Diseases – Part II

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/11/26/nitric-oxide-and-inos-have-key-roles-in-kidney-diseases/

57. New Insights on Nitric Oxide donors – Part IV

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/11/26/new-insights-on-no-donors/

59. Nitric Oxide has a ubiquitous role in the regulation of glycolysis -with a concomitant influence on mitochondrial function

Curator and Author: Larry H Bernstein, MD, FACP

https://pharmaceuticalintelligence.com/2012/09/16/nitric-oxide-has-a-ubiquitous-role-in-the-regulation-of-glycolysis-with-         a-concomitant-influence-on-mitochondrial-function/

Biochemistry of the Coagulation Cascade and Platelet Aggregation: Nitric Oxide: Platelets, Circulatory Disorders, and Coagulation Effects

Nitric Oxide Function in Coagulation – Part II

Nitric oxide is implicated in many pathologic processes as well.  Nitric oxide post translational modifications have been attributed to nitric oxide’s role in pathology however, although the general mechanism by which nitric oxide exerts its physiological effects is by stimulation of soluble guanylate cyclase to produce cGMP, these post translational modifications can act as a cellular signal as well.  For more information of NO pathologic effects and how NO induced post translational modifications can act as a cellular signal see the following:

Nitric Oxide Covalent Modifications: A Putative Therapeutic Target?

58. Crucial role of Nitric Oxide in Cancer

Curator and Author: Ritu Saxena, Ph.D.

https://pharmaceuticalintelligence.com/2012/10/16/crucial-role-of-nitric-oxide-in-cancer/

Note:  A more comprehensive ebook on Nitric Oxide and Disease Perspectives is found at

Cardiovascular Diseases, Volume One: Perspectives on Nitric Oxide in Disease Mechanisms

available on Kindle Store @ Amazon.com

http://www.amazon.com/dp/B00DINFFYC

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Hypertriglyceridemia: Evaluation and Treatment Guideline

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Severe and very severe hypertriglyceridemia increase the risk for pancreatitis, whereas mild or moderate hypertriglyceridemia may be a risk factor for cardiovascular disease. Individuals found to have any elevation of fasting triglycerides should be evaluated for secondary causes of hyperlipidemia including endocrine conditions and medications. Patients with primary hypertriglyceridemia must be assessed for other cardiovascular risk factors, such as central obesity, hypertension, abnormalities of glucose metabolism, and liver dysfunction. The aim of this study was to develop clinical practice guidelines on hypertriglyceridemia.

The diagnosis of hypertriglyceridemia should be based on fasting levels, that mild and moderate hypertriglyceridemia (triglycerides of 150–999 mg/dl) be diagnosed to aid in the evaluation of cardiovascular risk, and that severe and very severe hypertriglyceridemia (triglycerides of >1000 mg/dl) be considered a risk for pancreatitis. The patients with hypertriglyceridemia must be evaluated for secondary causes of hyperlipidemia and that subjects with primary hypertriglyceridemia be evaluated for family history of dyslipidemia and cardiovascular disease.

The treatment goal in patients with moderate hypertriglyceridemia should be a non-high-density lipoprotein cholesterol level in agreement with National Cholesterol Education Program Adult Treatment Panel guidelines. The initial treatment should be lifestyle therapy; a combination of diet modification, physical activity and drug therapy may also be considered. In patients with severe or very severe hypertriglyceridemia, a fibrate can be used as a first-line agent for reduction of triglycerides in patients at risk for triglyceride-induced pancreatitis.

Three drug classes (fibrates, niacin, n-3 fatty acids) alone or in combination with statins may be considered as treatment options in patients with moderate to severe triglyceride levels. Statins are not be used as monotherapy for severe or very severe hypertriglyceridemia. However, statins may be useful for the treatment of moderate hypertriglyceridemia when indicated to modify cardiovascular risk.

 

References:

 

https://www.medpagetoday.com/clinical-connection/cardio-endo/77242?xid=NL_CardioEndoConnection_2019-01-21

https://www.ncbi.nlm.nih.gov/pubmed/19307519

https://www.ncbi.nlm.nih.gov/pubmed/23009776

https://www.ncbi.nlm.nih.gov/pubmed/6827992

https://www.ncbi.nlm.nih.gov/pubmed/22463676

https://www.ncbi.nlm.nih.gov/pubmed/17635890

 

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Palmaz, Pinchuk, Schatz, Simpson and Yock are the 10th recipients of the Russ Prize for innovations leading to the widespread adoption of PCI at NAE Gala Ceremony, 2/20/2019, WashDC

 

Reporter: Aviva Lev-Ari, PhD, RN

 

National Academy of Engineering, Ohio University Award 2019 Russ Prize

Five interventional cardiologists awarded biennial $500,000 prize for innovations leading to the widespread adoption of PCI

National Academy of Engineering, Ohio University Award 2019 Russ Prize

January 3, 2019 — Ohio University and the National Academy of Engineering announced the 2019 Fritz J. and Dolores H. Russ Prize will be given to Julio Palmaz, Leonard Pinchuk, John Simpson, Richard Schatz and Paul Yock for innovations leading to the widespread adoption of percutaneous coronary intervention (PCI), also known as angioplasty with stent or coronary angioplasty. The $500,000 biennial prize, which recognizes a bioengineering achievement that significantly improves the human condition, cites PCI for “seminal contributions to coronary angioplasty, enabling minimally invasive treatment of advanced coronary artery disease.”

“The Russ Prize recipients personify engineering creations that advance health and healthcare every day,” said NAE President C. D. Mote, Jr.  “The PCI makes a remarkable contribution to patient well-being, helping millions afflicted with advanced coronary artery disease and significant angina. “

Ohio University alumnus and esteemed engineer Fritz Russ, BSEE ’42, HON ‘75, and his wife, Dolores Russ, established the biennial prize in 1999 with a multimillion dollar gift to Ohio University. They modeled it after the Nobel Prize, with the goal of recognizing bioengineering achievements worldwide that are in widespread use.

“This innovation — truly, sets of innovations — enables the treatment of coronary artery disease without the complexities, cost and risk of open heart surgery. Most of us have a friend or relative who has benefited greatly from angioplasty treatment,” said Russ College Dean Dennis Irwin. “These contributions have truly improved the human condition. Rewarding such innovations was the Russes’ intent.”

Percutaneous coronary intervention, also referred to as percutaneous transluminal coronary angioplasty (PTCA), is a minimally invasive procedure that uses a catheter to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup. PCI improves blood flow, thus decreasing heart-related chest pain, making patients feel better and increasing their ability to be active. Ten of millions of patients have benefited from PCI worldwide, and this procedure has replaced or significantly delayed the need for open heart coronary bypass surgery.

Julio C. Palmaz, inventor of the first U.S. Food and Drug Administration (FDA)-approved balloon-expandable vascular stent (1990), is Ashbel Smith Professor at the University of Texas Health Science Center in San Antonio and scientific adviser of Vactronix Scientific. The Palmaz stent is on display at the Smithsonian’s National Museum of American History in Washington, D.C. In 1994 he and Richard Schatz created a modified coronary stent — two Palmaz stents joined by a single connector — approved by the FDA as the first stent indicated for the treatment of failure of coronary balloon angioplasty. The Palmaz-Schatz stent became the gold standard for every subsequent stent submitted for FDA approval.

Leonard Pinchuk is an inventor and entrepreneur in biomedical engineering, with 128 U.S. patents and 90 publications. He has co-founded 10 companies where his major accomplishments include invention of the Nylon 12 angioplasty balloon, helical wire stent, modular stent-graft, a drug-eluting stent (Taxus), several biomaterials (Bionate and polystyrene-block-isobutylene-block-styrene [SIBS]), a novel glaucoma tube (InnFocus MicroShunt), and the next-generation intraocular lens. He is a Distinguished Research Professor of Biomedical Engineering at the University of Miami.

John Simpson has helped revolutionize the field of cardiology through innovations that fundamentally altered how physicians treat cardiovascular disease. In 1981 he created a new catheter system for coronary angioplasty with an independently steerable guidewire in the central lumen of the balloon catheter, patented as the over-the-wire balloon angioplasty catheter. He now focuses his efforts on the treatment of vascular disease through the development of new technologies combined with a new approach to optical imaging.

Read the related article “Requirements for Interventional Echocardiographers”

Richard Schatz is research director of cardiovascular interventions at the Scripps Heart, Lung and Vascular Center, and director of gene and stem cell therapy. He is a recognized international expert in interventional cardiology and has published and lectured extensively. His seminal work in coronary stents spurred a revolution in the treatment of coronary artery disease — over 2 million of them are placed annually worldwide, with an immeasurable impact on relieving mortality and morbidity, improving patients’ lives, and reducing healthcare costs.

Paul Yock is the Martha Meier Weiland Professor of Medicine and founding co-chair of Stanford’s Department of Bioengineering, with courtesy appointments in the Graduate School of Business and the Department of Mechanical Engineering. He is also founder and director of the Stanford Byers Center for Biodesign. He has authored over 300 peer-reviewed publications, chapters, and editorials and two textbooks, and holds over 50 U.S. patents. Yock is internationally known for his work in inventing, developing and testing new devices, including the Rapid Exchange stenting and balloon angioplasty system, which is now the primary system in use worldwide. He also invented the fundamental approach to intravascular ultrasound imaging and founded Cardiovascular Imaging Systems (CVIS), later acquired by Boston Scientific.

“Ohio University is honored to join the National Academy of Engineering in recognizing these accomplished individuals, who have contributed to a bioengineering advancement that has enabled better health for heart patients across the world,” said Ohio University President M. Duane Nellis. “Their multi-disciplinary collaboration that lead to the development of PCI, a technology that has revolutionized coronary health, truly embraces the vision that Fritz and Dolores Russ had when creating the Russ Prize.”

Palmaz, Pinchuk, Schatz, Simpson and Yock are the 10th recipients of the Russ Prize. They will receive the award at a National Academy of Engineering gala ceremony in Washington, D.C., on Feb. 20, 2019

For more information: www.nae.edu

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Changes in Levels of Sex Hormones and N-Terminal Pro–B-Type Natriuretic Peptide as Biomarker for Cardiovascular Diseases

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Considerable differences exist in the prevalence and manifestation of atherosclerotic cardiovascular disease (CVD) and heart failure (HF) between men and women. Premenopausal women have a lower risk of CVD and HF compared with men; however, this risk increases after menopause. Sex hormones, particularly androgens, are associated with CVD risk factors and events and have been postulated to mediate the observed sex differences in CVD.

 

B-type natriuretic peptides (BNPs) are secreted from cardiomyocytes in response to myocardial wall stress. BNP plays an important role in cardiovascular remodelling and volume homeostasis. It exerts numerous cardioprotective effects by promoting vasodilation, natriuresis, and ventricular relaxation and by antagonizing fibrosis and the effects of the renin-angiotensin-aldosterone system. Although the physiological role of BNP is cardioprotective, pathologically elevated N-terminal pro–BNP (NT-proBNP) levels are used clinically to indicate left ventricular hypertrophy, dysfunction, and myocardial ischemia. Higher NT-proBNP levels among individuals free of clinical CVD are associated with an increased risk of incident CVD, HF, and cardiovascular mortality.

 

BNP and NT-proBNP levels are higher in women than men in the general population. Several studies have proposed the use of sex- and age-specific reference ranges for BNP and NT-proBNP levels, in which reference limits are higher for women and older individuals. The etiology behind this sex difference has not been fully elucidated, but prior studies have demonstrated an association between sex hormones and NT-proBNP levels. Recent studies measuring endogenous sex hormones have suggested that androgens may play a larger role in BNP regulation by inhibiting its production.

 

Data were collected from a large, multiethnic community-based cohort of individuals free of CVD and HF at baseline to analyze both the cross-sectional and longitudinal associations between sex hormones [total testosterone (T), bioavailable T, freeT, dehydroepiandrosterone (DHEA), SHBG, and estradiol] and NT-proBNP, separately for women and men. It was found that a more androgenic pattern of sex hormones was independently associated with lower NT-proBNP levels in cross-sectional analyses in men and postmenopausal women.

 

This association may help explain sex differences in the distribution of NT-proBNP and may contribute to the NP deficiency in men relative to women. In longitudinal analyses, a more androgenic pattern of sex hormones was associated with a greater increase in NT-proBNP levels in both sexes, with a more robust association among women. This relationship may reflect a mechanism for the increased risk of CVD and HF seen in women after menopause.

 

Additional research is needed to further explore whether longitudinal changes in NT-proBNP levels seen in our study are correlated with longitudinal changes in sex hormones. The impact of menopause on changes in NT-proBNP levels over time should also be explored. Furthermore, future studies should aim to determine whether sex hormones directly play a role in biological pathways of BNP synthesis and clearance in a causal fashion. Lastly, the dual role of NTproBNP as both

  • a cardioprotective hormone and
  • a biomarker of CVD and HF, as well as
  • the role of sex hormones in delineating these processes,

should be further explored. This would provide a step toward improved clinical CVD risk stratification and prognostication based on

  • sex hormone and
  • NT-proBNP levels.

 

References:

 

https://www.medpagetoday.com/clinical-connection/cardio-endo/76480?xid=NL_CardioEndoConnection_2018-12-27

 

https://www.ncbi.nlm.nih.gov/pubmed/30137406

 

https://www.ncbi.nlm.nih.gov/pubmed/22064958

 

https://www.ncbi.nlm.nih.gov/pubmed/24036936

 

https://www.ncbi.nlm.nih.gov/pubmed/19854731

 

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2019 Trends in Cardiology

Reporter: Aviva Lev-Ari, PhD, RN

 

BLOG | DAVE FORNELL, DAIC EDITORDECEMBER 11, 2018

A 40,000 Foot View of Trends in Cardiology

A 40,000 Foot View of Trends in Cardiology

 

I was recently asked about my thoughts on the big picture, over arching trends effecting cardiology. Here is the outline I gave them.

 

Cardiology Cost Drivers

Reimbursements from Centers for Medicare and Medicaid Services (CMS) and insurance providers drive trends for the adoption of new technologies. However, new technologies that can show empirical evidence for being able to improve outcomes at lower costs are being moved up for better payments. CMS and other insurers are also using a carrot and stick approach with increased use of CMS bundled payments. These give a flat fee for diagnosing and treating a heart attack or heart failure, rather than hospitals being paid for all the tests and procedures they did. This approach makes the hospitals want to find new ways to be more cost effective to increase their bottom lines to capture more of the bundled payment as revenue.

 

Heart failure makes up about a third or more of the costs to Medicare. This has caused CMS to look closely at what is driving costs, and really high readmission rates are mainly to blame. There are penalties or no reimbursements for patients who come back for repeat treatments because they were not managed properly the first time. New technologies to address heart failure and other chronic diseases are of major interest to DAIC readers. Many of these include information technology (IT) solutions, rather than treatment device technologies.

 

Other conditions like atrial fibrillation (AF) also drive up costs, so vendors are attempting to find better ways to diagnose and treat this condition. Current treatments are only effective in the first attempt in about 60 percent of patients.

 

Consolidation of Hospitals and Outside Physicians

This is a continuing trend where single hospitals or smaller hospital systems are being bought up by bigger fish to create economy of scale with larger healthcare systems. These often cover specific geographic areas and often cast a wide net to include some luminary hospitals, smaller community hospitals, immediate care centers and minute clinics inside drug partner pharmacies. Duplicate staff and services are sometimes eliminated after mergers and consolidation. Outside physicians, including cardiologists and radiologists, are also being brought into the fold as employees of the health systems, rather than the old model as outside contractors who have access to the hospital’s amenities.

 

While there is fear about consolidation, it can also offer advantages in many cases. This includes faster access to the newest technologies and devices through the system’s luminary hospitals, which can train staff at other hospitals, and more complex cases can be referred to the larger hospital. Read about this in more detail in the article “Hospital Consolidation May Increase Access to TAVR, New Cardiac Technologies.”
Trends in Cardiovascular Technologies

Any techniques and technologies that can improve outcomes, cut costs, reduce hospital length of stay or prevent readmissions can capture hospital and cardiologist attention in today’s healthcare environment. There has been a massive movement over the past two decades away from traditional open heart or vascular surgical procedures to catheter-based interventional procedures. This includes improvements in the durability and complexity of percutaneous coronary intervention (PCI), reopening chronic total occlusions (CTOs)endovascular aortic repair (EVAR), expanded interest in treating peripheral artery disease (PAD), and structural heart cases that used to be the realm of the cardiac surgeon.

 

There is a major revolution and rapid uptake in transcatheter valve technologies to replace open heart surgery. Structural heart procedures to repair or replace failing heart valves have had positive clinical trial after positive trial over the last several years. Several key cardiac surgeons in the field say catheter based interventions will likely be the way of the future and surgical case volumes will see stead declines over the next decade.

 

The Role of Information Technology and AI in Cardiology

IT solutions are now increasingly being leveraged in more sophisticated ways since most hospitals have converted to integrated electronic medical records (EMRs) over the past decade. These allow all patient and departmental data to be accessible in one location. Analytics software is now being used to mine this data to identify workflow inefficiencies and areas to cut costs or improve charge capture. Clinical decision support (CDS) software to help hospitals and doctors better meet guideline-based care in all specialties is being introduced to help clinicians make better care decisions. This includes choosing appropriate tests and procedures in an effort to reduce costs or avoid tests that will not be reimbursed.

 

Artificial intelligence (AI) will be taking over many of the manual tasks for monitoring data and to answer questions more quickly. AI will also be used to alert administrators or doctors when it autonomously identifies a problem. Applications to watch also include AI to monitor population health in the background. This can identify patients at risk for various cardiovascular diseases before they present with any symptoms. The software also can identify patients who need extra care and counseling because of the high likelihood they will not be compliant with discharge orders and be readmitted. AI also will offer a second set of eyes on cardiac imaging to help identify anomalies or greatly reduce time by performing all the measurements automatically without human intervention.

 

This use of IT also includes patient portals to engage with patients and allow better access to their records and care. This is already starting to filter down to apps on smart phones to improve care, compliance with doctor’s orders and to aid diagnosis of conditions before they become problematic, such as heart failure and AF.

 

Cardiac Imaging Trends

Cardiac ultrasound (echo) remains the No.1 imaging modality in cardiology because of its broad availability, low cost and no radiation. However, computed tomography (CT) is poised to become the front-line imaging test for acute chest pain patients in the emergency department. It is also the gold standard for structural heart procedure planning, and the number of these cases is rapidly rising. CT fractional flow reserve (CT-FFR) technology is widely expected to become the main test for chest pain in the next decade, since it has the potential to save both time and money. CT-FFR also will become the primary gate-keeper to the cath lab to significantly lower, or possibly eliminate, the need for diagnostic catheter angiograms.

 

Cardiac MRI has seen numerous advances in recent years that cut imaging times by 50 percent and automate quantification, cutting the time to read and process these exams. MRI is expected to see and increase for cardiac exams in the coming years. MRI and CT-FFR may greatly reduce the number of nuclear exams, which are currently the gold standard for cardiac perfusion imaging.

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Paraoxonase 2 (PON2) appears to play a cardioprotective role in both human and experimental heart failure: Cardiologist Wai Hong Wilson Tang, MD, Director of Cleveland Clinic Lerner Research Institute’s Center for Clinical Genomics.

Reporter: Aviva Lev-Ari, PhD, RN

Enzyme Protects Heart Against Stress and Could Potentially Lead to New Heart Failure Treatments

https://consultqd.clevelandclinic.org/enzyme-protects-heart-against-stress-and-could-potentially-lead-to-new-heart-failure-treatments/amp/?__twitter_impression=true

Original Study:
 2018 Jun;121:117-126. doi: 10.1016/j.freeradbiomed.2018.04.583. Epub 2018 May 2.

Paraoxonase 2 prevents the development of heart failure.

Abstract

BACKGROUND:

Mitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression.

METHODS AND RESULTS:

Using qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression. To determine the cardiac-specific function of PON2, we performed heart transplantations in which PON2-def and wild type (WT) donor hearts were implanted into WT recipient mice. Beating scores of the donor hearts, assessed at 4 weeks post-transplantation, were significantly decreased in PON2-def hearts when compared to WT donor hearts. By using a transverse aortic constriction (TAC) model, we found PON2 deficiency significantly exacerbated left ventricular remodeling and cardiac fibrosis post-TAC. We further demonstrated PON2 deficiency significantly enhanced ROS generation in heart tissues post-TAC. ROS generation was measured through dihydroethidium (DHE) using high-pressure liquid chromatography (HPLC) with a fluorescent detector. By using neonatal cardiomyocytes treated with CoCl2 to mimic hypoxia, we found PON2 deficiency dramatically increased ROS generation in the cardiomyocytes upon CoCl2 treatment. In response to a short CoCl2 exposure, cell viability and succinate dehydrogenase (SDH) activity assessed by MTT assay were significantly diminished in PON2-def cardiomyocytes compared to those in WT cardiomyocytes. PON2-def cardiomyocytes also had lower baseline SDH activity. By using adult mouse cardiomyocytes and mitochondrial ToxGlo assay, we found impaired cellular ATP generation in PON2-def cells compared to that in WT cells, suggesting that PON2 is necessary for proper mitochondrial function.

CONCLUSION:

Our study suggests a cardioprotective role for PON2 in both experimental and human heart failure, which may be associated with the ability of PON2 to improve mitochondrial function and diminish ROS generation.

KEYWORDS:

Cardiomyopathy; Heart failure; Paraoxonase 2

PMID:
29729330
PMCID:
PMC5971153
 [Available on 2019-06-01]
DOI:
10.1016/j.freeradbiomed.2018.04.583

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