Obesity and Cardiomyopathy

2021 ◽  
Author(s):  
Willis K. Samson ◽  
Gina L. C. Yosten ◽  
Carol Ann Remme
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Coronary Artery Disease ◽  
Oxygen Species ◽  
Comprehensive Review ◽  
Novel Approaches ◽  
Obesity Cardiomyopathy ◽  
Artery Disease ◽  
Diabetic Syndrome

While much has been written about the syndrome of diabetic cardiomyopathy, clinicians and research scientists are now beginning to realize that an entirely unique syndrome exists, albeit with several commonalities to the diabetic syndrome, that being obesity cardiomyopathy. This syndrome develops independent of such comorbidities as hypertension, myocardial infarction and coronary artery disease; and it is characterized by specific alterations in adipose tissue function, inflammation and metabolism. Recent insights into the etiology of the syndrome and its consequences have focused on the roles played by altered intracellular calcium homeostasis, reactive oxygen species, and mitochondrial dysfunction. A timely and comprehensive review by Ren, Wu, Wang, Sowers and Zhang (1) identifies unique mechanisms underlying this syndrome, its relationship to heart failure and the recently identified incidence of COVID-19-related cardiovascular mortality. Importantly, the review concludes by advancing recommendations for novel approaches to the clinical management of this dangerous form of cardiomyopathy.

Abstract P380: Coronary Artery Disease Extent is Predictive of Heart Failure Incidence After Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Yariv Gerber ◽  
Susan A Weston ◽  
Maurice E Sarano ◽  
Sheila M Manemann ◽  
Alanna M Chamberlain ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Proportional Hazards ◽  
Incidence Rates ◽  
Cox Proportional Hazards ◽  
Disease Extent ◽  
Increased Risk ◽  
Artery Disease

Background: Little is known about the association between coronary artery disease (CAD) and the risk of heart failure (HF) after myocardial infarction (MI), and whether it differs by reduced (HFrEF) or preserved (HFpEF) ejection fraction (EF) has yet to be determined. Subjects and Methods: Olmsted County, Minnesota residents (n=1,924; mean age, 64 years; 66% male) with first MI diagnosed in 1990-2010 and no prior HF were followed through 2013. Framingham Heart Study criteria were used to define HF, which was further classified according to EF (applying a 50% cutoff). The extent of angiographic CAD was defined at index MI according to the number of major epicardial coronary arteries with ≥50% lumen diameter obstruction. Fine & Gray and Cox proportional hazards regression models were used to assess the association of CAD categories with incidence of HF, and multiple imputation methodology was applied to account for the 19% with missing EF data. Results: During a mean (SD) follow-up of 6.7 (5.9) years, 594 patients developed HF. Adjusted for age and sex, with death considered a competing risk, the cumulative incidence rates of HF among patients with 1- (n=581), 2- (n=622), and 3-vessel disease (n=721) were 11.2%, 14.6% and 20.5% at 30 days; and 18.1%, 22.3% and 29.4% at 5 years after MI, respectively. The increased risk of HF with greater number of occluded vessels was only modestly attenuated after further adjustment for patient and MI characteristics, and did not differ materially by EF (Table). Conclusions: The extent of angiographic CAD expressed by the number of diseased vessels is independently associated with HF incidence after MI. The association is evident promptly after MI and applies to both HFrEF and HFpEF.

scholarly journals Aldosterone, mortality, and acute ischaemic events in coronary artery disease patients outside the setting of acute myocardial infarction or heart failure

2011 ◽  
Vol 33 (2) ◽  
pp. 191-202 ◽  
Author(s):  
Fabrice Ivanes ◽  
Sophie Susen ◽  
Frédéric Mouquet ◽  
Pascal Pigny ◽  
François Cuilleret ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Artery Disease

scholarly journals Endostatin attenuates heart failure via inhibiting reactive oxygen species in myocardial infarction rats

2020 ◽  
Author(s):  
Xuguang Xu ◽  
Tingbo Jiang ◽  
Yong Li ◽  
Liusha Kong
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Cardiac Function ◽  
Cardiac Fibrosis ◽  
Smooth Muscle Actin ◽  
Reactive Oxygen ◽  
Tissue Growth ◽  
Oxygen Species ◽  
Collagen Iii

The purpose of the present study was to evaluate whether endostatin overexpression could improve cardiac function, hemodynamics, and fibrosis in heart failure (HF) via inhibiting reactive oxygen species (ROS). The HF models were established by inducing ischemia myocardial infarction (MI) through ligation of the left anterior descending (LAD) artery in Sprague-Dawley (SD) rats. Endostatin level in serum was increased in MI rats. The decreases of cardiac function and hemodynamics in MI rats were enhanced by endostatin overexpression. Endostatin overexpression inhibited the increases of collagen I, collagen III, α-smooth muscle actin (SMA), connective tissue growth factor (CTGF), matrix metalloproteinase (MMP)-2 and MMP9 in the heart of MI rats. MI-induced cardiac hypertrophy was reduced by endostatin overexpression. The increased levels of malondialdehyde (MDA), superoxide anions, the promoted NAD(P)H oxidase (Nox) activity, and the reduced superoxide dismutase (SOD) activity in MI rats were reversed by endostatin overexpression. Nox4 overexpression inhibited the cardiac protective effects of endostatin. These results demonstrated that endostatin improved cardiac dysfunction and hemodynamics, and attenuated cardiac fibrosis and hypertrophy via inhibiting oxidative stress in MI-induced HF rats.

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