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1Division of Cardiology, St Louis University School of Medicine, MO 63110.
Insights
Angiotensin-converting enzyme (ACE) inhibitors significantly improve survival in congestive heart failure (CHF) patients across various New York Heart Association classes. ACE inhibitors also reduce cardiovascular events in post-myocardial infarction patients with left ventricular dysfunction.
Area of Science:
- Cardiology
- Pharmacology
Background:
- The traditional stepped-care approach for congestive heart failure (CHF) is outdated.
- Improved understanding of CHF pathophysiology necessitates revised treatment strategies.
Purpose of the Study:
- To evaluate the efficacy of angiotensin-converting enzyme (ACE) inhibitors in improving survival and reducing cardiovascular events in CHF patients.
- To assess the role of ACE inhibitors in post-myocardial infarction patients with left ventricular dysfunction.
Main Methods:
- Review of evidence supporting the use of vasodilators, specifically ACE inhibitors, in CHF management.
- Analysis of studies on long-term captopril administration in post-myocardial infarction patients.
Main Results:
- ACE inhibitors improve survival in New York Heart Association classes II-IV CHF compared to placebo or direct-acting vasodilators.
- Long-term captopril use enhances survival and reduces morbidity/mortality from cardiovascular events in asymptomatic post-MI patients with left ventricular dysfunction.
- Preventive therapy with ACE inhibitors should be considered for post-MI patients with asymptomatic left ventricular dysfunction (ejection fraction ≤40%).
Conclusions:
- ACE inhibitors are the preferred vasodilators for improving survival in congestive heart failure.
- Early intervention with ACE inhibitors in post-myocardial infarction patients with left ventricular dysfunction is recommended.
- Further research is needed to define the role of newer vasodilators and beta-blockers in CHF management.
Abstract:
As understanding of the mechanisms of congestive heart failure (CHF) has improved, it has become apparent that the previously applied stepped-care approach (ie, diuretic, digitalis, then vasodilator) is no longer valid. There is compelling evidence that use of vasodilators increases survival in CHF, and angiotensin-converting enzyme (ACE) inhibitors are the vasodilators of choice. Use of an ACE inhibitor in patients with New York Heart Association classes II, III, and IV CHF improves survival over that achieved with use of placebo or direct-acting vasodilators. In patients with asymptomatic left ventricular dysfunction after myocardial infarction, long-term administration of captopril improved survival and reduced morbidity and mortality from major cardiovascular events. Using an ACE inhibitor as preventive therapy in post-myocardial infarction patients without overt CHF but with evidence of muscle dysfunction (ie, left ventricular ejection fraction 40% or less) should be considered. The role of a newer vasodilator (eg, amlodipine besylate [Norvasc]) as an adjunct to therapy remains to be defined. If current theories on the pathophysiology of CHF are correct, continued interest in beta blockers is justified, especially in newer agents that have actual vasodilatory action in addition to their other beneficial properties.
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