[Calcium antagonists: effect on peripheral and coronary hemodynamics].

The effects of calcium channel blocking drugs, so-called calcium antagonists, on the human heart and circulation are a composite of various direct (cardiac) and indirect (peripheral vascular) actions. When injected into the coronary circulation, calcium antagonists produce a direct negative inotropic effect on the human myocardium that is characterized by a depression of DP/DT and left ventricular ejection fraction, an increase in end-diastolic pressure and a decrease in systolic pressure. When administered intravenously, sublingually or orally, all calcium antagonists cause a fall in systemic vascular resistance and a drop in systemic arterial pressure, but their actions on cardiac function are less uniform. In particular, a baroreceptor-mediated reflex increase in betaadrenergic tone that is triggered by the fall in blood pressure and depends in degree on the compound and the route of administration, may counterbalance or override the direct negative inotropic effect. As a result, myocardial contractility and ventricular performance can be depressed, unchanged, or even enhanced by calcium antagonists, depending on the underlying status of myocardial function. In the coronary circulation, calcium antagonists, whether administered directly or indirectly (systemically), elicit relaxation of vascular smooth muscle and vasodilatation that is associated with an increase in global coronary blood flow. In contrast to the effects of other vasodilating drugs, however, flow is found to be enhanced not only in myocardial regions supplied by normal coronaries but also in poststenotic areas, at rest as well as with rapid atrial pacing. Although not entirely understood, this latter phenomenon may be of particular interest for the treatment of patients with coronary disease and angina pectoris.