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European Heart Journal 1991 12(Supplement F):18-24; doi:10.1093/eurheartj/12.suppl_F.18
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Calcium channel blockers and ischaemic heart disease: theoretical expectations and clinical experience

R. Ferrari and O. Visioli

Cattedra di Cardiologia, Universita' degli Studi di Brescia Brescia, Italia

Correspondence: Prof. Roberto Ferrari, Cattedra di Cardiologia, Universita' degli Studi, c/o Spedali Civili, P.le Spedali Civili 1, 25123 Brescia, Italia

There are several reasons for using calcium antagonists to protect ischaemic and reperfused myocytes and to treat coronary artery disease (CAD) patients. At the molecular level, calcium antagonists induce: coronary dilatation and improvement of the supply of oxygen and substrate to the area at risk; energy sparing secondary to dilatation of the peripheral vasculature and, at least in the case of phenylalkylamines and benzothiazepines, a reduction in contractility and heart rate; attenuation of reperfusion-induced arrhythmias; inhibition of platelet aggregation (only at high concentration); reduction of loss of adenosine precursor; reduction of the release of lysosomal enzymes; a direct protective effect on the sarcolemma (for the phenylalkylamines); a protective effect of the mitochondria and specific reduction of mitochondrial calcium transport (for benzothiazepines and some phenylalkylamines; attenuation of the ischaemia-reperfusion-induced displacement of endogenous noradrenaline (for the phenylalkylamines). Evidence of a protective role has been obtained in a variety of experiments provided the calcium antagonists were introduced prior to ischaemia. It is believed that this protective effect is an indirect consequence of the ability to modulate the function of the calcium channels and the energy-sparing effect is of major importance. Conversely, protection has not been obtained when calcium antagonists are added after ischaemia or during reperfusion. Thus is not surprising that when administered after the signs of human myocardial infarction, calcium antagonists do not reduce infarct size or avoid subsequent complications or decrease mortality. Diltiazem and verapamil, however, are two recent exceptions to this general tendency.

Key Words: Myocardial ischaemia • calcium antagonist • verapamil • nifedipine • diltiazem • ischaemic heart disease


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