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European Heart Journal 1995 16(Supplement N):103-106; doi:10.1093/eurheartj/16.suppl_N.103
Copyright © 1995 by the European Society of Cardiology.
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© 1995 The European Society of Cardiology

Aldosterone escape during ACE inhibitor therapy in chronic heart failure

A. D. Struthers

Department of Clinical Pharmacology, Ninewells Hospital and Medical School Dundee, UK

Correspondence: Prof Allan D. Struthers, Department of Clinical Pharmacology, Ninewells Hospital and Medical School, Dundee DD1 9SY, U K.

In the setting of chronic heart failure (CHF), therapy with angiotensin converting enzyme (ACE) inhibitors generally reduces serum aldosterone levels acutely. However, long-term ACE inhibition is associated with aldosterone suppression that is weak, variable, and unsustained, i e. aldosterone ‘escape’. Magnesium loss caused by aldosterone and by diuretics can contribute to coronary artery spasm and arrhythmias. Aldosterone can block noradrenaline uptake by the myocardiuin; extracellular catecholamines may lead to arrhythmias and ischaemia. Aldosterone has been shown to have an acute arrhythmogenic effect as well as a potential detrimental effect on baroreflex function, a marker of prognosis in CHF Both angiotensin II and aldosterone may stimulate myocardial fibrosis, which is associated with a higher incidence of malignant ventricular arrhythmias. ACE inhibition initiated early in the progression of CHF may prevent development of patchy myocardialflbrosis and its inherent arrhythmias and thus reduce the incidence of sudden death. Spironolactone therapy added to the regimen of an ACE inhibitor and diuretic can induce natriuresis and magnesium retention, increase myocardial noradrenaline uptake, and reduce the incidence of arrhythmias.

Key Words: Aldosterone escape • chronic heart failure • magnesium depletion • catecholamine potentiation • ventricular arrhythmias • baroreflex function • myocardial fibrosis • ACE inhibition • spironolactone


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