The afterload reduction and myocardial oxygen sparing that results after administration of calcium antagonists suggests a possible role for these drugs in intervention after onset of acute myocardial infarction, but their use in this setting is limited by the possibility that left ventricular failure will develop. Tiapamil is a new verapamil congener. The hemodynamic effects of this drug (1 mg/kg followed by 25 ,ug/kg/min over 36 hr) were studied in 30 patients randomly assigned in a double-blind manner to a tiapamil or control group within 12 hr of the onset of acute myocardial infarction as diagnosed by Swan-Ganz catheterization and gated blood pool scans. Tiapamil reduced heart rate from 83 ± 20 beats/min (mean SD) before to 74 + 19 beats/min after drug (over an average 36 hr), arterial pressure from 128 22/87 ± 14 to 118 16/74 ± 11 mm Hg, rate-pressure product from 10,695 ± 3492 to 8800 ± 2550 units, and systemic vascular resistance from 1732 ± 351 to 1400 + 350 dynes.sec.cm-5. Tiapamil also increased stroke volume index from 34.7 ± 12.1 to 41.6 ± 12.0 ml/m2, left ventricular ejection fraction from 50.1 ± 14.8% to 56.4 ± 17.4% (at 24 hr), left ventricular end-diastolic volume index from 71.3 + 23.1 to 80.5 ± 23.7 ml/m2, and peak diastolic filling rate (an index of diastolic relaxation) from 2.1 0.9 to 2.6 ± 0.8 end-diastolic volumes/sec (p < .05 for all changes). Cardiac index, wedge pressure, left ventricular end-systolic volume, and PR interval remained unchanged. Without precipitating left ventricular failure, tiapamil reduced afterload and heart rate and maintained cardiac index while apparently improving diastolic compliance. Circulation 71, No. 4, 779-786, 1985. IN 1971 proposed that pharmacologic interventions that reduce myocardial oxygen consumption (MVO2) and/or increase blood supply to ischemic myocardium during the very first hours after onset of infarction should reduce infarct size. Clinical studies have supported this principle of early intervention, showing beneficial effects of early ,8-receptor blockade on the indexes of infarct size.2 Although /3-blockers effectively reduce MVO2 (mainly by reducing heart rate), their cardiodepressive effects may result in heart failure, especially in patients with large infarcts. There is also concern that /3-blockers, particularly noncardioselective compounds, might give rise to vasoconstriction of coronary arteries.3