A remarkable medical story: benefits of angiotensin-converting enzyme inhibitors in cardiac patients

J Am Coll Cardiol. 2001 Jun 1;37(7):1757-64. doi: 10.1016/s0735-1097(01)01229-3.


The development of angiotensin-converting enzyme inhibitors (ACE inhibitors) has been one of the most remarkable stories in the treatment of cardiovascular diseases. Angiotensin converting enzyme inhibitors have several acute and sustained hemodynamic effects that are beneficial in the presence of left ventricular (LV) dysfunction. They increase cardiac output and stroke volume and reduce systemic vascular resistance as well as pulmonary capillary wedge pressure. The hemodynamic benefits are associated with improvement in the signs and symptoms of congestive heart failure (CHF) as well as decreased mortality, regardless of the severity of CHF. In patients with asymptomatic LV dysfunction, therapy with ACE inhibitors prevented the development of CHF and reduced hospitalization and cardiovascular death. They also increase survival when administered early after an acute myocardial infarction (MI). Most recently, ACE inhibition was associated with improved clinical outcomes in a broad spectrum of high-risk patients with preserved LV function. The mechanism of ACE inhibitors benefits is multifactorial and includes prevention of progressive LV remodeling, prevention of sudden death and arrhythmogenicity and structural stability of the atherosclerotic process. Evidence suggests that ACE inhibitors are underutilized in patients with cardiovascular diseases. Efforts should be directed to prescribe ACE inhibitors to appropriate patients in target doses. It is reasonable to believe that ACE inhibitors have a class effect in the management of LV dysfunction with or without CHF and acute MI. Whether the same is true for ACE inhibitors in the prevention of ischemic events is not known yet.

Publication types

  • Review

MeSH terms

  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use*
  • Forecasting
  • Heart Failure / drug therapy*
  • Heart Failure / physiopathology
  • Hemodynamics / drug effects
  • Humans
  • Myocardial Infarction / drug therapy*
  • Risk Factors
  • Ventricular Dysfunction / drug therapy*


  • Angiotensin-Converting Enzyme Inhibitors