Frishman W H, Lazar E J
Department of Medicine, Jack D. Weiler Hospital, Albert Einstein College of Medicine-Montefiore Medical Center, Bronx, New York.
Am J Cardiol. 1990 Nov 6;66(16):66G-70G. doi: 10.1016/0002-9149(90)90401-l.
Beta-adrenergic blockers have been shown definitely to reduce the incidence of total mortality, cardiovascular mortality, sudden death and nonfatal reinfarction in survivors of an acute myocardial infarction. The mechanisms to explain this protective action of beta blockers have never been elucidated conclusively, and include the antiarrhythmic and myocardial oxygen demand-reducing effects of the drugs. An antithrombotic mechanism has also been suggested. However, beta blockers have relatively weak antiplatelet activity, suggesting that their antithrombotic effects may be related to prevention of coronary artery plaque rupture and the subsequent propagation of an occlusive arterial thrombus rather than direct anticoagulant action. The therapeutic ability of beta blockers to attenuate the hemodynamic consequences of catecholamine surges, may protect a vulnerable atherosclerotic plaque from fracture, thereby reducing risk of coronary thrombosis, myocardial infarction and death.
β-肾上腺素能阻滞剂已被明确证明可降低急性心肌梗死幸存者的总死亡率、心血管死亡率、猝死率和非致命性再梗死发生率。解释β受体阻滞剂这种保护作用的机制尚未得到最终阐明，包括药物的抗心律失常和降低心肌需氧量的作用。也有人提出了抗血栓形成机制。然而，β受体阻滞剂的抗血小板活性相对较弱，这表明它们的抗血栓作用可能与预防冠状动脉斑块破裂及随后闭塞性动脉血栓的形成有关，而非直接的抗凝作用。β受体阻滞剂减弱儿茶酚胺激增对血流动力学影响的治疗能力，可能会保护易损的动脉粥样硬化斑块不发生破裂，从而降低冠状动脉血栓形成、心肌梗死和死亡的风险。
