Little W C
Curr Probl Cardiol. 1983 Dec;8(9):1-47. doi: 10.1016/0146-2806(83)90045-2.
Thrombotic coronary artery occlusion is now recognized as the usual cause of acute myocardial infarction. The thrombus usually forms at the site of intimal disruption over an atherosclerotic plaque. Following coronary occlusion, myocardial necrosis begins within 40 minutes in the subendocardium and progresses outward toward the epicardium over the next several hours. The intracoronary infusion of streptokinase will produce lysis of the occluding thrombus in up to 80% of patients. It appears that reperfusion with streptokinase in the first few hours following the onset of the myocardial infarction produces a small increase in late left ventricular function, though ECG and enzyme evidence of acute myocardial infarction are not prevented. The improvement in left ventricular function is variable from patient to patient and has not been demonstrated in all the randomized studies to date. The time limit for myocardial salvage may not be the same in all patients. The greatest benefit is probably achieved with reperfusion in the first 4-6 hours, although some benefit may occur as late as 18 hours after the onset of infarction. Many patients who receive intracoronary infusion of streptokinase develop a systemic lytic state, though serious bleeding complications in carefully selected patients are infrequent. High-dose IV streptokinase is easier, cheaper, and quicker to initiate than intracoronary streptokinase but is probably less effective than the intracoronary route in producing rapid lysis of the occluding coronary thrombus. The optimal dose and rate of administration of IV streptokinase have not been determined. The final role and ultimate benefit of thrombolytic therapy of myocardial infarction have not yet been determined, but some of the issues may be clarified by the larger randomized trials now under way. It appears, at present, that the use of intracoronary streptokinase may have a role in the treatment of selected patients with acute myocardial infarctions in institutions with the facilities and the personnel necessary to perform this procedure safely. In the future, thrombolytic therapy may also have a place in the treatment of selected patients with unstable angina and post-myocardial infarction angina. The future availability of more selective thrombolytic agents may make the early IV therapy of myocardial infarction a safer, more effective option and expand the indications for thrombolytic therapy.
血栓形成性冠状动脉闭塞现被认为是急性心肌梗死的常见病因。血栓通常形成于动脉粥样硬化斑块上内膜破损处。冠状动脉闭塞后,心内膜下心肌坏死在40分钟内开始,并在接下来的数小时内向外膜方向发展。冠状动脉内输注链激酶可使高达80%的患者闭塞血栓溶解。心肌梗死发作后的最初数小时内用链激酶进行再灌注,虽然不能防止急性心肌梗死的心电图和酶学表现,但似乎能使晚期左心室功能略有增加。左心室功能的改善在患者之间存在差异,且迄今为止并非在所有随机研究中都得到证实。心肌挽救的时间限制在所有患者中可能并不相同。在发病后的最初4至6小时内进行再灌注可能获得最大益处,尽管在梗死发作后18小时进行再灌注也可能有一些益处。许多接受冠状动脉内输注链激酶的患者会出现全身溶解状态,不过在精心挑选的患者中严重出血并发症并不常见。大剂量静脉注射链激酶比冠状动脉内链激酶更容易启动、成本更低且速度更快,但在使闭塞冠状动脉血栓快速溶解方面可能不如冠状动脉途径有效。静脉注射链激酶的最佳剂量和给药速率尚未确定。心肌梗死溶栓治疗的最终作用和最终益处尚未确定,但目前正在进行的更大规模随机试验可能会阐明一些问题。目前看来,在具备安全实施该操作所需设施和人员的机构中,冠状动脉内链激酶的使用可能在治疗某些急性心肌梗死患者中发挥作用。未来,溶栓治疗在治疗某些不稳定型心绞痛和心肌梗死后心绞痛患者中可能也会有一席之地。未来更具选择性的溶栓药物的出现可能会使心肌梗死的早期静脉治疗成为更安全、更有效的选择,并扩大溶栓治疗的适应证。