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Renal hemodynamic consequences of angiotensin-converting enzyme inhibition in congestive heart failure
1Department of Medicine, Baylor College of Medicine, Houston.
Insights
Shorter-acting angiotensin-converting enzyme (ACE) inhibitors may be preferable for heart failure patients experiencing renal function decline. Predisposing factors include hormonal and hemodynamic changes that can be exacerbated by longer-acting ACE inhibitors.
Area of Science:
- Cardiology
- Nephrology
- Pharmacology
Background:
- Angiotensin-converting enzyme (ACE) inhibitors are crucial in managing heart failure.
- Some studies indicate a higher incidence of renal function decline with longer-acting ACE inhibitors like enalapril maleate compared to shorter-acting ones like captopril.
Purpose of the Study:
- To investigate the factors contributing to renal function decline in heart failure patients treated with ACE inhibitors.
- To compare the effects of different ACE inhibitor durations on renal function.
Main Methods:
- Review of existing studies examining renal function changes in heart failure patients on ACE inhibitors.
- Analysis of predisposing hormonal and hemodynamic factors associated with renal impairment.
Main Results:
- Renal function decline was more frequent with enalapril maleate than captopril.
- Predisposing factors included sustained hypotension, low cardiac output, high enalapril dose, low systemic arterial pressure, volume depletion, and activated renin-angiotensin system.
- ACE inhibitors reduce angiotensin II, potentially decreasing glomerular filtration rate, especially with inadequate cardiac output or pre-existing renal issues.
Conclusions:
- Long-acting ACE inhibitors may prolong detrimental effects on renal function.
- Shorter-acting ACE inhibitors might be a safer option for heart failure patients with deteriorating renal function.
Abstract:
Angiotensin-converting enzyme (ACE) inhibitors are of benefit in the management of heart failure. In some studies in patients with heart failure, a decline in renal function occurred more frequently in patients treated with enalapril maleate, a longer-acting agent, than in those treated with captopril, a shorter-acting drug. Patients experiencing a decline in renal function had a number of predisposing hormonal and hemodynamic factors. In one report, these factors included an initial fall in blood pressure that was sustained, lower cardiac output, and a relatively high fixed dose of enalapril that contributed to renal impairment. In a second study, the decline in renal function was most severe in patients with a lower systemic arterial pressure in whom glomerular filtration may have been dependent on angiotensin II. In a third study, intravascular volume depletion and an activated renin-angiotensin system led to reduced renal function. Reduction of angiotensin II level in plasma and tissues by ACE inhibitors decreases systemic vascular resistance and efferent arteriolar tone, which tends to decrease glomerular filtration rate. If compensatory increases in cardiac output are inadequate or preexisting renal impairment or volume depletion is present, renal function will deteriorate. Long-acting ACE inhibitors prolong the decreased efferent arteriolar tone and may compromise cardiac muscle response to catecholamines. The use of shorter-acting agents in patients who exhibit deterioration in renal function may be preferable.