What question did this study set out to answer?

To examine the presence of an intrinsic cardiac renin-angiotensin system and evaluate the therapeutic effects of converting enzyme inhibition on myocardial ischemia and cardiac hypertrophy.

January 1, 1989Journal of Cardiovascular Pharmacology

Pharmacological Interference with the Cardiac Renin-Angiotensin System

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Why the study?

Does converting enzyme inhibition prevent ischemia-reperfusion injury and cardiac hypertrophy in preclinical models?

Population

Preclinical models including nephrectomized animals, isolated working rat hearts subjected to transient…

Comparison

Converting enzyme inhibitors and/or bradykinin… vs Pure vasodilation or untreated controls.

Design

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Authors

RBR. H. A. BeckerHospital zum Heiligen Geist WLWolfgang LinzOntario Brain Institute BSBernward A. SchölkensGoethe University Frankfurt

Discussion

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Implication

Supports local ACE inhibitor effects in preclinical models; hypothesis-generating for BP-independent benefits in human HF and ischemia.

Key Points

To examine the presence of an intrinsic cardiac renin-angiotensin system and evaluate the therapeutic effects of converting enzyme inhibition on myocardial ischemia and cardiac hypertrophy.
Measured local cardiac angiotensin II generation following oral converting enzyme inhibitor administration in nephrectomized animal models.
Tested arrhythmia severity, energy status, and biomarker release in isolated working rat hearts and anesthetized dogs exposed to transient ischemia-reperfusion with bradykinin or converting enzyme inhibitors.
Administered the converting enzyme inhibitor ramipril versus non-specific vasodilators in rats with aortic constriction to evaluate cardiac hypertrophy and blood pressure changes.
Converting enzyme inhibition and bradykinin perfusion prevented angiotensin-induced arrhythmia aggravation, preserved myocardial energy status, and reduced enzyme and lactate release during ischemia-reperfusion.
Oral ramipril both prevented and reversed aortic constriction-induced cardiac hypertrophy at doses that did not reduce elevated blood pressure, whereas pure vasodilators lowered blood pressure without resolving hypertrophy.
The clinical benefits of converting enzyme inhibitors in cardiac hypertrophy and myocardial ischemia stem from intracardiac suppression of angiotensin II production and inhibition of bradykinin degradation rather than afterload reduction alone.

Structured PICO

Does converting enzyme inhibition prevent ischemia-reperfusion injury and cardiac hypertrophy in preclinical models?

Population

Preclinical models including nephrectomized animals, isolated working rat hearts subjected to transient regional ischemia and reperfusion, anesthetized dogs, and rats with aortic constriction.

Intervention

Converting enzyme (CE) inhibitors (e.g., oral ramipril) and/or bradykinin perfusion/infusion.

Comparator

Pure vasodilation (in the hypertrophy model) or untreated controls.

Outcome

Cardiac angiotensin II formation, ischemia-reperfusion injury (arrhythmias, energy status, enzyme and lactate release), and cardiac hypertrophy.surrogate

The efficacy of ACE inhibitors in congestive heart failure and myocardial ischemia may be partly explained by local intracardiac suppression of angiotensin II generation and bradykinin degradation, independent of systemic hemodynamic effects.

Cite This Study

Becker et al. (1989) studied this question.

synapsesocial.com/papers/6a9818b448723bb28e367eb1 https://doi.org/10.1097/00005344-198906144-00004

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Pharmacological Interference with the Cardiac Renin-Angiotensin System

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Pharmacological Interference with the Cardiac Renin-Angiotensin System

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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