几年来,急性心肌梗塞(AMI)的实验模型显示,β-阻滞剂对 AMI 发展起防御作用。其主要作用似乎是β_1-受体的阻滞,从而减轻心脏总的工作负荷和心肌缺血的严重度。后一作用在临床上可使疼痛减轻,室性异位搏动减少及抬高的 ST 段降低。这些观察结果促使人们去研究心肌梗塞后应用β-阻滞剂治疗能否降低总的病死率。有安慰剂作对照的研究一致显示,β-阻滞剂治疗的病人与安慰剂相比,其病死率降低至25%。随着更多经验的积累,清楚地表明,β- For several years, experimental models of acute myocardial infarction (AMI) have shown that beta-blockers play a defensive role in the development of AMI. Its main effect appears to be block of β 1 -receptors, thereby reducing the overall cardiac workload and the severity of myocardial ischemia. The latter effect clinically reduces pain, decreases in ventricular ectopic beats and increases in ST-segment. These observations prompted people to study whether beta-blocker therapy after myocardial infarction can reduce overall mortality. A placebo-controlled study consistently showed that patients treated with beta-blocker had a 25% lower case fatality rate than placebo. As more experience accumulates, it is clear that β-