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Converting-enzyme inhibition in the management of severe chronic congestive heart failure: physiologic concepts
1Department of Medicine, Mount Sinai School of Medicine, City University of New York, New York.
Insights
Converting-enzyme inhibitors effectively treat heart failure by addressing both vasoconstriction and neurohormonal imbalances. These drugs improve circulation, symptoms, and survival in heart failure patients.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Heart failure involves excessive vasoconstriction and neurohormonal responses.
- Targeting only vasoconstriction can worsen neurohormonal issues, limiting treatment benefits.
Purpose of the Study:
- To evaluate the efficacy of converting-enzyme inhibitors in managing severe chronic heart failure.
- To assess the impact of these inhibitors on patient survival.
Main Methods:
- Review of experimental and clinical laboratory evidence.
- Analysis of controlled clinical trials comparing converting-enzyme inhibitors to placebo and other vasodilators.
- Inclusion of data from a large-scale, multicenter, placebo-controlled trial on survival benefits.
Main Results:
- Converting-enzyme inhibitors effectively counteract both vasoconstriction and neurohormonal imbalances.
- These agents demonstrate consistent circulatory and symptomatic improvement in heart failure patients.
- Evidence confirms improved survival rates in patients treated with converting-enzyme inhibitors.
Conclusions:
- Converting-enzyme inhibitors are a key therapeutic option for severe chronic heart failure, offering benefits beyond other vasodilators.
- While effective, potential adverse effects like hypotension and renal issues require monitoring due to angiotensin II pathway interference.
Abstract:
Evidence from the experimental and clinical laboratory suggests that the heart failure state is characterized not only by an excessive degree of systemic vasoconstriction but also by an exaggerated neurohormonal response to the decline in cardiac performance. Therapeutic interventions directed only at the first abnormality may serve to exacerbate the second, and thus may fail to produce long-term hemodynamic and clinical benefits. Converting-enzyme inhibitors successfully antagonize both homeostatic malfunctions, and thus are among the few vasodilators that have been shown to produce consistent circulatory and symptomatic improvement in patients with severe chronic heart failure in controlled clinical trials; the responses to treatment with these agents have been superior to those seen during therapy with placebo or other vasodilator drugs. Furthermore, experimental and clinical evidence suggests that converting-enzyme inhibitors exert favorable effects on the survival of patients with severe heart failure; this potential has now been confirmed in a large-scale, multicenter, placebo-controlled trial. Despite its benefits, converting-enzyme inhibition may be accompanied by adverse circulatory and metabolic reactions (symptomatic hypotension, renal insufficiency, and potassium retention), which are predictable consequences of interference with the homeostatic role of angiotensin II in low-output states.