Timmis A D, Griffin B, Crick J C, Nelson D J, Sowton E
Department of Cardiology, Guy's Hospital, London.
Br Heart J. 1987 Oct;58(4):345-51. doi: 10.1136/hrt.58.4.345.
The effects of early spontaneous coronary patency on the evolution of myocardial infarction were evaluated in 41 patients. They had coronary arteriography (mean (SEM)) 3.1 (0.2) hours after the onset of chest pain with repeat studies 90 minutes and three days later. In 12 (29%) patients the infarct related coronary artery was patent at the first arteriogram (group 1). A further 10 patients, nine of whom received thrombolytic treatment, showed early recanalisation of the infarct related coronary artery within 90 minutes of treatment (group 2). In the remainder the infarct related coronary artery was persistently occluded (group 3). Baseline values for infarct location, the sum of ST elevation in all leads, QRS scores, and serum creatine kinase activity did not permit discrimination between the groups. Nevertheless, patterns of ST segment change and enzyme release in group 1 were closely similar to those that occurred in response to thrombolysis in group 2. Thus compared with group 3, groups 1 and 2 showed earlier 50% reduction in the sum of peak ST elevation in all leads and earlier peaking of serum creatine kinase activity. Importantly, creatine kinase release was significantly attenuated in group 1, rising to a peak serum activity (mean (SEM)) of only 1242 (415) IU/1. Analysis of angiographic left ventricular ejection fractions at three days indicated limitation of infarct size in groups 1 and 2 compared with group 3. Mean (SEM) ejection fraction, however, was best preserved in group 1 (62(6)%) and in this group the frequency of non-Q wave infarction was higher than in groups 2 and 3. Thus in patients who present with a patent infarct related coronary artery early during infarction: (a) there is a reduction in the pattern of infarct size as reflected by attenuation of release of creatine kinase, preservation of left ventricular ejection fraction, and a relatively high frequency of non-Q wave infarction; (b) patterns of ST segment change and creatine kinase release resemble those that occur after successful thrombolytic treatment, suggesting that early coronary patency is the result of spontaneous recanalisation of a previously occluded artery.
在41例患者中评估了早期自发性冠状动脉再通对心肌梗死演变的影响。他们在胸痛发作后3.1（0.2）小时进行了冠状动脉造影（均值（标准误）），并在90分钟和三天后重复检查。在12例（29%）患者中，梗死相关冠状动脉在首次血管造影时通畅（第1组）。另有10例患者，其中9例接受了溶栓治疗，在治疗后90分钟内梗死相关冠状动脉出现早期再通（第2组）。其余患者梗死相关冠状动脉持续闭塞（第3组）。梗死部位、所有导联ST段抬高总和、QRS评分以及血清肌酸激酶活性的基线值无法区分这些组。然而，第1组的ST段变化模式和酶释放与第2组溶栓后的情况非常相似。因此，与第3组相比，第1组和第2组所有导联峰值ST段抬高总和降低50%的时间更早，血清肌酸激酶活性达到峰值的时间更早。重要的是，第1组肌酸激酶释放明显减弱，血清活性峰值（均值（标准误））仅为1242（415）IU/1。三天时血管造影左心室射血分数分析表明，与第3组相比，第1组和第2组梗死面积受限。然而，平均（标准误）射血分数在第1组中保存最好（62（6）%），且该组非Q波梗死的发生率高于第2组和第3组。因此，在梗死早期梗死相关冠状动脉通畅的患者中：（a）肌酸激酶释放减弱、左心室射血分数保存以及非Q波梗死频率相对较高反映出梗死面积减小；（b）ST段变化模式和肌酸激酶释放类似于成功溶栓治疗后的情况，提示早期冠状动脉再通是先前闭塞动脉自发再通的结果。
