Nifedipine and acute myocardial infarction

In consideration of the results of experimental studies indicating that nifedipine, a vasodilating calcium antagonist with little inotropic or electrophysiological effects, increases coronary flow to both normal and ischemic zones potentially rendering protection of ischemic myocardium as well as the results of clinical studies in patients with angina pectoris, this pilot study was carried out in patients with acute myocardial infarction to evaluate the clinical, hemodynamic and electrophysiological responses. Nifedipine was administered sublingually in a dosage of 10 mg initially, after an interval of 1 to 1.5 hours and thereafter to maintain the pressure at the level prevailing after three hours. As compared with a control group, the frequency of ventricular dysrhythmia as well as the frequency of complex dysrhythmias in the 17 treated patients were similar (mean 313 vs. 325 PVCs/24 hours; and 5.9 vs. 3.6 episodes respectively in treated and controls). No patient developed evidence of second or third degree AV block. Systemic vascular resistance fell from 1661 to 1283 dyne . s . cm-5 and cardiac index increased from 3.2 to 3.59 l/min/m2 at one hour. Arterial pressure decreased from 146/93 to 131/88 mm Hg. Pulmonary artery pressure remained unchanged in five patients and decreased by more than 3 mm Hg in four. Thus, in patients with acute myocardial infarction nifedipine decreases systemic resistance and, provided preload is not substantially reduced, increases cardiac output. Neither an exacerbation of chest pain nor an increase in ventricular dysrhythmia was observed. Extensive clinical investigation will be needed to definitively characterize effects of nifedipine on infarct size, coronary flow and prognosis of patients with acute myocardial infarction.