Angiotensin as local modulating factor in ventricular dysfunction and failure due to coronary artery disease
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V J Dzau1, R Pratt, G H Gibbons
1Division of Cardiovascular Medicine, Falk Cardiovascular Research Center, Stanford University Medical Center, California.
Insights
Angiotensin converting enzyme (ACE) inhibitors may protect the heart by inhibiting local angiotensin II formation, potentially preventing heart failure progression. This offers cardioprotective effects against cardiovascular disorders.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Congestive heart failure results from progressive myocardial damage.
- Neurohormonal systems activate during left ventricular dysfunction and decompensated heart failure.
- Autocrine/paracrine modulators, including the renin-angiotensin system, are implicated in preclinical heart failure stages.
Purpose of the Study:
- To explore the role of locally generated angiotensin II in cardiovascular pathophysiology.
- To investigate the cardioprotective potential of angiotensin converting enzyme (ACE) inhibitors.
Main Methods:
- Review of recent studies on neurohormonal systems in heart failure.
- Analysis of the impact of renin-angiotensin system activation on cardiovascular structure.
- Evaluation of ACE inhibitors' effects on preventing heart failure progression.
Main Results:
- Locally generated angiotensin II contributes to cardiac hypertrophy, remodeling, coronary artery disease, and atherosclerosis.
- Inhibition of angiotensin formation via ACE inhibitors shows cardioprotective effects.
- ACE inhibitors demonstrate efficacy in preventing asymptomatic left ventricular dysfunction from progressing to overt heart failure.
Conclusions:
- Targeting local angiotensin formation with ACE inhibitors may offer significant cardioprotection.
- ACE inhibitors are effective in managing cardiovascular disorders and preventing heart failure progression.
Abstract:
Congestive heart failure is the end product of a progressive series of events resulting from acute myocardial damage. Circulatory neurohormonal systems are activated during the acute phase of left ventricular dysfunction resulting from initial myocardial damage and again in the latter phase of decompensated heart failure. However, these neurohormonal mechanisms return to normal during the compensated stage of heart failure. Recent studies have suggested that autocrine/paracrine modulators of cardiovascular function are activated in the preclinical phase preceding the development of overt heart failure. The renin-angiotensin system in particular has been shown to modulate many of the chronic processes involved in the pathophysiology of cardiovascular disorders. Recent studies suggest that locally generated angiotensin II may contribute to the secondary structural changes seen in cardiovascular disorders, such as cardiac hypertrophy and remodelling, coronary artery disease, and atherosclerosis. Thus, inhibition of angiotensin formation with angiotensin converting enzyme (ACE) inhibitors, particularly at the tissue level, may provide valuable cardioprotective effects. Additional evidence points to the efficacy of ACE inhibitors in preventing the progression of asymptomatic left ventricular dysfunction to overt heart failure.