Mechanisms of angina relief after nifedipine: A hemodynamic and myocardial metabolic study

Abstract

To elucidate the mechanisms of action of nifedipine in angina pectoris, 14 patients were studied before and after sublingual administration of 10 mg of nifedipine. Systemic and coronary hemodynamic and myocardial metabolic measurements were taken at rest and during pacing. At the pacing rate that induced pain in the control situation, no patient experienced angina after nifedipine administration. Lactate production during control turned into extraction after nifedipine administration (p < .05), and the double product was reduced (p < .001). Systemic and coronary vascular resistance were reduced by 26% (p < .001) and 19% (p < .005), respectively. Systolic blood pressure fell from 160 ± 29 to 127 ± 25 mm Hg (p < .001) and diastolic from 100 ± 14 to 79 ± 11 mm Hg (p < .001). Pulmonary artery diastolic blood pressure fell from 14 ± 4 to 10 ± 3 mm Hg (p < .01). When the pacing rate was further increased after nifedipine administration until pain developed, the double product and the degree of lactate production were the same as during pain before nifedipine was administered. The pacing rate was 131 ± 12 compared with 119 ± 13 during control (p < .001). Both the systolic and diastolic blood pressures were still significantly reduced compared with control pacing values, 131 ± 26 mm Hg (p < .01) and 84 ± 13 mm Hg (p < .01), respectively. Our data demonstrate that the antianginal efficiency can be partly explained by afterload reduction, which decreases myocardial oxygen consumption. The data also suggest additional mechanisms, possibly an increase in collateral flow, direct dilatation of stenotic parts of epicardial arteries, or a decrease in myocardial back pressure secondary to reduced left ventricular filling pressure.