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Immediate converting-enzyme inhibition with intravenous enalapril in chronic congestive heart failure
Insights
Intravenous enalapril rapidly and completely blocks the converting enzyme in patients with severe congestive heart failure (CHF). This effective blockade improves cardiac index and reduces systemic vascular resistance, aiding in renin-angiotensin system assessment.
Area of Science:
- Cardiology
- Pharmacology
- Renal Physiology
Background:
- Severe congestive heart failure (CHF) is often associated with an activated renin-angiotensin system (RAS).
- Accurate assessment of the RAS is crucial for understanding and managing CHF.
- Pharmacologic probes can offer insights into complex physiological systems.
Purpose of the Study:
- To evaluate intravenous enalapril as a pharmacologic probe for assessing the renin-angiotensin system in severe CHF.
- To determine the efficacy and time course of enalapril's blockade of angiotensin-converting enzyme (ACE).
Main Methods:
- Intravenous enalapril was administered to 9 patients with severe CHF.
- Plasma renin activity, aldosterone, angiotensin II, systemic vascular resistance, and cardiac index were measured.
- Hemodynamic parameters and hormonal levels were monitored over time.
Main Results:
- Enalapril caused rapid and complete blockade of converting enzyme, peaking at 30 minutes.
- Significant increases in plasma renin activity and decreases in plasma aldosterone were observed (p < 0.05).
- Marked reduction in systemic vascular resistance and improvement in cardiac index were noted (p < 0.05).
Conclusions:
- Intravenous enalapril effectively and rapidly inhibits converting enzyme in severe CHF patients.
- Enalapril serves as a valuable tool for assessing angiotensin II-mediated vasoconstriction.
- The study highlights the utility of enalapril in evaluating the RAS in critical cardiovascular conditions.
Abstract:
To test the hypothesis that intravenous enalapril is a useful pharmacologic probe of the renin angiotensin system, intravenous enalapril was administered to 9 patients with severe congestive heart failure (CHF). This produced abrupt and complete blockade of converting enzyme, with peak effect occurring at 30 minutes, as reflected by increases of plasma renin activity (from 16.8 +/- 6 to 86.6 +/- 23 ng/ml/hour) and decreases of plasma aldosterone levels (from 46 +/- 14 to 25 +/- 6 ng%) (both p less than 0.05). With reduction of angiotensin II--mediated vasoconstriction, systemic vascular resistance decreased markedly (from 1,974 +/- 233 to 1,400 +/- 136 dyne s cm-5) and cardiac index was improved (from 1.88 +/- 0.9 to 2.20 +/- 0.21 liters/min/m2) (both p less than 0.05). The time course of angiotensin II levels suggested that the lack of a cumulative effect from additive doses of intravenous enalapril was a reflection of complete inhibition of converting enzyme. One patient did not respond to enalapril; despite comparable hemodynamic severity of CHF, the renin-angiotensin system was not activated in this patient. Thus, intravenous enalapril is capable of rapid and complete inhibition of converting enzyme for the accurate assessment of angiotensin II--mediated vasoconstriction in patients with severe CHF.