Studies in experimental and clinical myocardial infarction support the idea that sympathetic activity and myocardial noradrenaline release play a significant role in the development of myocardial ischemic damage. Betablockade has been shown to limit infarct size and lower the incidence of ventricular fibrillation in experimental models. Betablockade to patients (pts) with acute myocardial infarction (AMI) has been shown to reduce ischemia reflected as reduction of ischemic chest pain, decrease ST-segment elevation and increase lactate extraction. Whether this treatment in the clinical situation can prevent development of infarction, reduce infarct size and early mortality in man remains to be proven. In Gøteborg a double-blind study on metoprolol and placebo was started four and a half years ago. Inclusion of pts. in the study has been terminated and survival data will be available on May 1, 1981. 1395 pts. were included of whom 800 developed AMI. Metoprolol 15 mg was given IV followed by a total daily dose of 200 mg/day. The tolerance for betablockade was generally good. Analysis of serum enzyme estimations of maximal LD I + II showed a significant reduction by metoprolol when the treatment was given within 12 hours of onset of pain. In a subgroup consisting of 103 pts. with AMI metoprolol had no clearcut effects on the ventricular arrhythmias during the first 24 hours in hospital. The betablockade resulted in a 15% reduction in heart rate. The main objective of this study, the mortality during three months of blind treatment will be published late in 1981.