Cardiovascular effects of aldosterone and post-acute myocardial infarction pathophysiology

Abstract

Aldosterone is an important mediator of the renin-angiotensin-aldosterone system (RAAS) that plays a major role in the pathophysiology of cardiovascular disease as well as regulation of extracellular fluid volume and potassium. In experimental models, aldosterone has been shown to promote endothelial dysfunction; induce vascular inflammation, myocardial ischemia, and necrosis; increase collagen synthesis in cardiac fibroblasts; contribute to plasminogen activator inhibitor-1 regulation; decrease baroreceptor sensitivity and reflex function; block myocardial uptake of norepinephrine; increase oxidative stress; and stimulate cardiomyocyte apoptosis. A review of animal and human studies with aldosterone blockers reveals improvement in, and in some cases complete reversal of, these pathophysiologic effects of aldosterone on the cardiovascular system.