Bolooki H
Am J Cardiol. 1975 Sep;36(3):395-406. doi: 10.1016/0002-9149(75)90494-4.
The purpose of this study was (1) to establish the maximal interval between the onset of ischemia and reperfusion that would permit a decrease in the size of infarction, and (2) to evaluate the relation between changes in infarct size and preservation of cardiac function. Studies were carried out in 19 dogs of which 13 had temporary (1 to 3 hours) occlusion of the left anterior descending coronary artery. The hospital course of 15 patients of whom 13 underwent myocardial revascularization within 8 hours of acute infarction was also reviewed. In dogs, the eventual pathologic infarct size was significantly reduced if reperfusion was performed within 2 hours of ischemia. After 2 hours of ischemia, the revascularized segment remained dyskinetic on angiographic assessment and cardiac function was depressed. After 3 hours of ischemia, in spite of a patent coronary artery, the extent of infarct and dykinesia was greater than during ligation of the left anterior descending coronary artery. In patients, small infarcts developed with revascularization performed more than 4 hours after infarction but with revascularization of the left anterior descending coronary artery the size of the dyskinetic area (as assessed with angiography) was similar to that in patients with a closed graft to the left anterior descending coronary artery but with a patent graft to its diagonal branch. In all patients after revascularization the extent of the left ventricular dyskinetic area was smaller and cardiac function was significantly better than in patient who did not receive revascularization for complete occlusion of the left anterior descending coronary artery. In spite of successful revascularization, electrocardiographic evidence of transmural infarction persisted postoperatively. It is concluded that reperfusion of an area of myocardium that has been ischemic for less than 2 hours in dogs or less than 4 hours in man may lead to a significant reduction in the extent of infarction as well as improvement in cardiac function. However, the revascularized area remains angiographically dyskinetic and electrocardiographically abnormal.
(1)确定缺血发作与再灌注之间能使梗死面积减小的最大间隔时间;(2)评估梗死面积变化与心功能保留之间的关系。对19只犬进行了研究,其中13只犬的左前降支冠状动脉被暂时阻断(1至3小时)。还回顾了15例患者的住院病程,其中13例在急性梗死8小时内接受了心肌血运重建。在犬中,如果在缺血2小时内进行再灌注,最终的病理梗死面积会显著减小。缺血2小时后,血管造影评估显示再灌注节段仍运动障碍,心功能降低。缺血3小时后,尽管冠状动脉通畅,但梗死范围和运动障碍程度比左前降支冠状动脉结扎时更大。在患者中,梗死发生4小时后进行血运重建会形成小梗死灶,但左前降支冠状动脉血运重建时,运动障碍区域大小(血管造影评估)与左前降支冠状动脉移植闭塞但对角支移植通畅的患者相似。在所有血运重建后的患者中,左心室运动障碍区域范围比未接受血运重建治疗左前降支冠状动脉完全闭塞的患者小,心功能明显更好。尽管血运重建成功,但术后仍有透壁梗死的心电图证据。结论是,犬缺血少于2小时或人缺血少于4小时的心肌区域再灌注可能会导致梗死范围显著减小以及心功能改善。然而在血管造影上,再灌注区域仍运动障碍,心电图仍异常。