Angiotensin-converting enzyme inhibitors in patients with coronary atherosclerosis

Am Heart J. 1994 Dec;128(6 Pt 2):1328-32. doi: 10.1016/0002-8703(94)90255-0.


Activation of the renin-angiotensin-aldosterone system has been shown to be an independent risk factor for myocardial infarction (MI). The importance of this risk factor has been confirmed by the finding that patients with a DD genotype for the angiotensin-converting enzyme (ACE) gene, which is associated with increased serum ACE levels, have a higher incidence of MI than do patients without this genotype. ACE inhibitors have been shown to significantly reduce the incidence of recurrent MI in patients with left ventricular dysfunction. The mechanism by which activation of the renin-angiotensin-aldosterone system leads to MI has not been ascertained, but it may be related to the effect of angiotensin II or aldosterone on the development of atherosclerosis, endothelial dysfunction, plaque rupture, or thrombosis after plaque rupture. Experimental data suggest that each of these mechanisms may be of importance. Several prospective randomized studies are under way to determine the effect of ACE inhibitors on recurrent ischemic events and the progression of atherosclerosis in patients without left ventricular dysfunction. If these studies yield positive results, ACE inhibitors might assume an important role in the secondary and possibly primary prevention of ischemic heart disease.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / pharmacology
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Clinical Trials as Topic
  • Coronary Artery Disease / drug therapy*
  • Coronary Artery Disease / etiology
  • Coronary Artery Disease / physiopathology
  • Humans
  • Myocardial Infarction / prevention & control
  • Renin-Angiotensin System / drug effects


  • Angiotensin-Converting Enzyme Inhibitors