The aim of the study was to investigate the hemodynamic effects of a short-acting, potent, highly specific calcium antagonist, nisoldipine, in patients with acute myocardial infarction. Twenty-four patients were selected on the basis of an elevated wedge pressure and/or elevated blood pressure, less than 12 hours after the onset of symptoms. Patients were randomized to receive either placebo or low-dose nisoldipine (2 micrograms/kg) as a single intravenous injection over a 3-minute period. hemodynamic effects were monitored for 20 minutes, and thereafter patients were crossed over to the other agent after the preserved parameters had returned to baseline. An open-label study using double the dose of nisoldipine in 20 patients who had not reacted adversely to low-dose nisoldipine followed. Standard hemodynamic monitoring showed that peak effects of nisoldipine were reached at 5 minutes, with some residual effect at 20 minutes, and it took up to 60 minutes to return to baseline. Both doses of nisoldipine had similar effects: a fall in the systemic vascular resistance by about 600 units, variable tachycardia, little or no change in the wedge pressure, a decrease in the arterial pressure, an unchanged rate-pressure product, and an increase in ejection fraction. Tachycardia of more than 15 beats/min resulted in 5 of 24 patients with low-dose nisoldipine and 6 of 20 patients with high-dose nisoldipine. In view of the risk of tachycardia, nisoldipine seems unsuitable for use in the acute phase of myocardial infarction.