CARDIAC EFFECTS OF CALCIUM-ANTAGONISTS IN SYSTEMIC HYPERTENSION

The calcium antagonists are a class of heterogeneous drugs, with a wid e spectrum of direct and indirect cardiac effects that vary a great de al from one drug to another and depend upon formulation and duration o f action. Calcium antagonists act by decreasing total peripheral resis tance to lower arterial pressure. As a consequence, reflex tachycardia , increased cardiac output, and increased plasma catecholamine and pla sma renin activity are commonly seen, particularly with the initial do se and with short-acting dihydropyridines. The abrupt vasodilation can paradoxically elicit angina and even acute myocardial infarction. The se hemodynamic and neuroendocrine changes are less pronounced with the long-acting formulations. Most calcium antagonists diminish automatic ity of the sinus node, slow conduction in the atrioventricular node, a nd have little, if any, effect on the automaticity of the myocytes. Th e dihydropyridines generally have less effect on automaticity and card iac conduction than nondihydropyridines. The negative inotropic effect is most profound with nondihydropyridines and is greatly reduced or a bsent with newer dihydropyridines, such as isradipine, felodipine, aml odipine, and nisoldipine. Long-acting calcium antagonists generally im prove myocardial oxygenation by unloading the heart, increasing corona ry blood Flow, and reducing myocardial oxygen consumption. Thus, calci um antagonists have a variety of beneficial effects in patients with h ypertensive heart disease: they reduce left ventricular hypertrophy an d its sequelae, such as ventricular dysrhythmias, impaired filling and contractility, and myocardial ischemia. Ongoing studies should provid e a more conclusive answer regarding the efficacy and safety of calciu m antagonists. (C) 1997 by Excerpta Medico, Inc.