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Pathophysiology of heart failure following myocardial infarction

Abstract

The structural and functional abnormalities that lead to cardiac death are coronary artery disease and left ventricular abnormalities related to remodelling (left ventricular hypertrophy, left ventricular systolic dysfunction, and left ventricular fibrosis). Aldosterone adversely affects all of these processes. It produces both a vasculopathy and left ventricular dysfunction and fibrosis. Endothelial dysfunction in the coronary arteries can lead to acute coronary events. Left ventricular dysfunction will cause the progression of heart failure, and left ventricular fibrosis and dysfunction provide an arrhythmic substrate. The combination of acute coronary events and arrhythmias can lead to sudden cardiac deaths, while acceleration of the heart failure disease process can lead to deaths from progressive heart failure. The increased understanding of the mechanistic role of aldosterone in cardiovascular disease provides a rationale for the positive results that have been seen in clinical trials of aldosterone blockade.

  • ACE, angiotensin converting enzyme
  • COX-2, cyclo-oxygenase- 2
  • L-NMMA, N-monomethyl-L-arginine
  • MI, myocardial infarction
  • PIII NP, procollagen type III amino terminal peptide
  • VCAM-1, vascular cell adhesion molecule-1
  • aldosterone
  • heart failure
  • myocardial infarction

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