article = {JICOA-2019-4-112}
title = {Mechanisms of Cardiac Dysfunction in Heart Failure due to Myocardial Infarction}
journal = {Journal of Integrative Cardiology Open Access}
year = {2019}
issn = {2674-2489}
doi = {http://dx.doi.org/10.31487/j.JICOA.2019.04.12}
url = {https://www.sciencerepository.org/mechanisms-of-cardiac-dysfunction-in-heart-failure_JICOA-2019-4-112 
author = {Anureet K. Shah,Mohamad Nusier,Naranjan S. Dhalla,Vijayan Elimban,}
keywords = {Myocardial infarction, ventricular arrhythmias, cardiac hypertrophy, heart failure, vasoactive hormones, oxidative stress, Ca2+- handling abnormalities}
abstract ={Acute myocardial infarction (MI) is associated with marked elevation of plasma vasoactive
hormones, ventricular arrhythmias, scar formation in the ischemic portion of left ventricle (LV) and
hypertrophy of the viable LV as well as the right ventricle (RV). Particularly, elevated levels of
plasma catecholamines and angiotensin II activate their membrane receptors and stimulate different
signal transduction systems for producing cardiac hypertrophy, augmenting the activities of
subcellular organelles and increasing cardiac function. While marked arrhythmias due to acute MI
produce 30 to 40% mortality, hypertrophic alterations in the viable LV as well as RV are
compensatory for maintaining hemodynamic homeostasis due to loss of cardiomyocytes. On the other
hand, prolonged elevation of plasma vasoactive hormones in chronic MI produce deleterious effects
on the hypertrophied heart by promoting the formation of oxyradicals, inducing Ca2+
- handling
abnormalities in subcellular organelles, depressing cardiac gene expression, activating different
proteases and resulting in the development of cardiac dysfunction. Thus, in view of the complexities
of mechanisms for both acute and chronic effects of MI, there is a real challenge of developing new
interventions for preventing the transition of cardiac hypertrophy to heart failure as well as
progression of the MI-induced cardiovascular abnormalities.}