Effects of verapamil on myocardial performance in coronary disease.

Abstract

Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.

An Overview of Slow Channel Blocking Drugs: Pharmacological Basis for Therapeutic Applications

“…These overall data, which arc in substantial agreement with the subsequent report of Ferlinz et al [40]. clearly indicate that the negative inotropic action of verapamil is substantially mini mized by its effect on aflerload so that car diac index is not reduced by the drug in patients with cardiac disease.…”

Effect of Doxorubicin and Verapamil on Circulatory System in Rabbits

“…The morphological Findings after DXR administration clearly indicate that this is due 49 to the destructive changes in the myocardium after DXR [6,21], Both negative and positive hemodynamic effects of Vp were reported [22][23][24], Thus, a decrease of cardiac output or an increase of the ejection fraction and SV was observed by some authors [22,24,25], Marked reduction in blood pressure and systemic vascular resis tance is the typical response to intravenous administration of Vp in animals and humans [5,23,24,26,27], It should be stressed that we did not ob serve any negative effect of DXR upon Cl and SI in rabbits pretreated with Vp or DXR plus Vp. This effect seems to result from the reduc tion in TPR.…”

“…Kerr et al [31] found an elevated DXR plasma concen tration in patients receiving DXR with Vp, while Formelli et al [32] suggested that Vp did not modify the pharmacokinetics of this anthracycline. Calcium overload of myocar dial cells after DXR treatment has been pro posed as an important factor in the develop ment of cardiomyopathy [21], It is suggested that Vp may protect the heart from this un wanted effect [5,24], Peroxidation of the myocardial cell membranes is considered an important mechanism of anthracycline car diotoxicity. Sridhay et al [33] found that Vp effectively inhibits DXR-mediated lipid per oxidation in vivo.…”

Calcium Antagonists

“…Ve rapamil and diltiazem have variable effects on cardiac output, although the general ten dency is towards a small increase. All of these agents can improve left ventricular wall mo tion in certain patients [15]. Nifedipine may lower left ventricular end-diastolic pressure minimally, secondary to decreases in both vascular loading and the diastolic filling pe riod as heart rate increases.…”