Short- and long-term influence of beta-adrenergic antagonists after acute myocardial infarction

After coronary arterial occlusion, catecholamines are released from storage depots in the left ventricle and injured myocardial cells are exposed to relatively high concentrations of catecholamines during the evolutionary period in which cell injury is becoming progressively more severe. In addition, in experimental animal models, there is a substantial increase in beta-adrenergic receptor density without any alteration in affinity within 1 hour of permanent coronary arterial occlusion. Recent data suggest that alpha-adrenergic receptor density increases within 30 to 60 minutes after coronary arterial occlusion in experimental animal models. The administration of catecholamines during the early phases of evolving myocardial injury can result in heightened adrenergic biochemical responses in severely injured compared with normally perfused tissue in the hearts of experimental animals. Thus, there is adequate rationale for anticipating that beta-adrenergic antagonists would protect ischemic myocardium and potentially reduce the incidence of life-threatening arrhythmias in individuals with evolving acute myocardial infarction (AMI). Studies in animal models demonstrate that the administration of beta-adrenergic antagonists in the first few minutes after coronary artery occlusion may reduce the ultimate extent of myocardial necrosis. Clinical data from several different trials in which beta-adrenergic antagonists were administered to (1) protect ischemic myocardium and preserve ventricular function and (2) reduce the severity of serious ventricular arrhythmias in patients with AMI are reviewed. The effects of longer-term administration of beta-adrenergic antagonists in patients after AMI in prolonging life and reducing risk of reinfarction are presented.