The effect of molsidomine on hemodynamics and myocardial ischemia were studied in 48 patients with acute myocardial infarction. Between 8 and 12 mg of orally and intravenously administered molsidomine led to a significant reduction in left ventricular filling pressure. In response to 2 x 4 mg p.o., diastolic pulmonary arterial pressure fell from 12.1 to 8.8 mm Hg in patients with filling pressure below 20 mm Hg. Patients with left heart failure and left ventricular filling pressure above 20 mm Hg (Group 2) displayed a decline in filling pressure from 23.8 to 17.4 mm Hg following 12 mg i.v. In addition, right atrial pressure dropped significantly across the entire range of dosages. Although patients without left ventricular failure (Group I) showed a decline in cardiac output (5.7 to 4.7 l/min), this parameter remained unchanged in Group 2. Heart rate in Group 2 fell from 85 to 81 per min. Arterial blood pressure was reduced by a mean of only 10 mm Hg at high dosages and remained unchanged at lower dosages. No change was observed in peripheral resistance. The maximum effect was seen 30 min after oral administration. Three hours later, the effect was reduced by half. Only minimal activity could be observed after 8 h. The incidence of side effects was low, with transient headaches occurring in 8% of the patients. An intraindividual comparison with 1.6 mg of sublingually administered nitroglycerin demonstrated no significant difference in hemodynamic effectiveness (n = 11). Molsidomine, not unlike nitroglycerin, exerts a favorable effect on hemodynamics and myocardial ischemia. It acts primarily to reduce preload. The additional moderate effect on afterload with a slight decline in arterial pressure at high dosages may also be considered advantageous.