Mechanisms of Cardiac Dysfunction in Heart Failure due to Myocardial Infarction

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.