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Development and prevention of congestive heart failure following myocardial infarction
M A Pfeffer1, J M Pfeffer, G A Lamas
1Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115.
Insights
Ischemic heart disease often leads to heart failure. Angiotensin converting enzyme inhibitors may reduce ventricular enlargement after myocardial infarction, potentially improving survival and preventing heart failure.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Ischemic heart disease is a primary cause of congestive heart failure.
- Acute myocardial infarction significantly increases mortality and heart failure risk, especially with extensive infarction and depressed ventricular function.
Purpose of the Study:
- To investigate the potential of angiotensin converting enzyme inhibitors in attenuating progressive ventricular enlargement post-myocardial infarction.
- To assess if this therapy improves survival and prevents congestive heart failure.
Main Methods:
- Review of experimental studies in rats and early clinical trials involving angiotensin converting enzyme inhibitors.
- Ongoing definitive clinical trials to evaluate long-term outcomes.
Main Results:
- Ventricular enlargement post-myocardial infarction is a progressive process linked to adverse outcomes.
- Early studies suggest chronic angiotensin converting enzyme inhibitor therapy may attenuate this enlargement.
Conclusions:
- Angiotensin converting enzyme inhibitors show promise in managing post-myocardial infarction ventricular remodeling.
- Combined with atherosclerosis prevention and infarct size limitation, this therapy could significantly reduce congestive heart failure incidence.
Abstract:
Ischemic heart disease is the major etiology for the development of congestive heart failure. Patients with acute myocardial infarction have a greatly increased risk for mortality and for manifesting symptomatic heart failure. This risk is not a uniform one but is greatly augmented in patients with a more extensive infarction and, consequently, a more depressed global ventricular function. An important concept that was derived from studies in rats with myocardial infarction and has been confirmed in patients is that ventricular enlargement, which has been shown to be a marker for an adverse outcome, can be a progressive process that leads to further deterioration of ventricular performance. Both experimental and early clinical studies have indicated that chronic therapy with an angiotensin converting enzyme inhibitor may attenuate this progressive ventricular enlargement. More definitive clinical trials are currently under way to determine whether this form of therapy, which may diminish the extent of ventricular enlargement over time, will result in an improvement in survival and in the prevention of the development of congestive heart failure. The addition of this pharmacological therapy to that of the primary prevention of atherosclerosis and that of the limitation of infarct size should make a substantial impact on the reduction of the incidence of congestive heart failure.