ELECTROPHYSIOLOGIC MECHANISMS UNDERLYING ARRHYTHMIAS DUE TO REPERFUSION OF ISCHEMIC MYOCARDIUM
ELECTROPHYSIOLOGIC MECHANISMS UNDERLYING ARRHYTHMIAS DUE TO REPERFUSION OF ISCHEMIC MYOCARDIUM
复制标题
DOI：
10.1161/01.cir.76.2.404
复制
发表时间：
1987-08-01
期刊：
影响因子：
37.8
通讯作者：
CORR, PB
中科院分区：
文献类型：
--
作者：
POGWIZD, SM;CORR, PB
用计算机三维标测系统，同时从232个双极部位进行8个水平的透壁记录，描绘了与缺血心肌再灌注相关的恶性室性心律失常的机制。在6只氯醛糖麻醉的猫中，通过闭塞冠状动脉左前降支诱导局部缺血10分钟，然后再灌注。在缺血后10分钟，就在再灌注前，窦性心律期间的总心室激动时间显著延迟（63 ± 1.5）min。8比25 +-。缺血前2毫秒，p <0.001）。再灌注后15秒内发生室性心动过速（VT），3只动物最终导致室颤。在75%的非持续性室性心动过速病例中，起始发生在再灌注区边缘的内膜下，通过不涉及折返的机制，如通过连续激动不明显和从窦性搏动结束到室性心动过速开始的时间（142 ± 100）确定的。14毫秒）与任何干预性去极化无关。在其余25%的非持续性室性心动过速病例中，室性心动过速的起始是由于邻近前一次窦性搏动的延迟中层心肌激活部位的内膜下壁内折返所致（总激活时间= 151 ± 100分钟）。9毫秒，p <0.001，与再灌注前相比）。这种折返机制类似于缺血无再灌注期间大多数VT病例的折返机制。再灌注期间维持室性心动过速发生的非折返机制以及壁内折返，与室性心动过速涉及两种机制的大多数情况下。导致室颤的室性心动过速由非折返机制在再灌注区边界的内膜下启动，并由非折返机制和折返机制维持，有时在同一搏动中组合。导致室颤的室性心动过速的第一次异位搏动的偶联间期与非持续性室性心动过速的第一次异位搏动的偶联间期无显著差异（199 . ±. 16比189 +-。9毫秒，p = NS）。然而，在从VT向心室纤颤的转变过程中，心内膜下和心外膜下出现的非折返性机制导致心动过速非常快速地加速到92 ± 1的偶联间期。2毫秒，导致增强的功能阻滞和进一步的传导延迟，过渡搏动的总激动时间超过心动过速的耦合间期。这随后导致了多个小折返回路和多个同时出现的室颤波前特征的发展。在非持续性室性心动过速的病例中，没有一个表现出心外膜的非折返性激动或周期长度小于120 msec。同样地，也没有发现内分泌的快速非折返性激活或室颤的发生。因此，缺血心肌再灌注期间室性心动过速最常见的是由非折返性机制引起的，尽管壁内折返也可能起作用。心室颤动是通过快速的非折返性加速心动过速发生的。这种非折返性兴奋的性质仍有待阐明，但可能涉及一种异常形式的自动性或触发活动。
The mechanisms responsible for malignant ventricular arrhythmias associated with reperfusion of ischemic myocardium were delineated with a computerized, three-dimensional mapping system, with simultaneous eight-level transmural recording from 232 bipolar sites. In six chloralose-anesthetized cats, regional ischemia was induced for 10 min by occlusion of the left anterior descending coronary artery, followed by reperfusion. At 10 min after ischemia, just before reperfusion, total ventricular activation time during sinus rhythm was significantly delayed (63 .+-. 8 vs 25 .+-. 2 msec before ischemia, p < .001). Ventricular tachycardia (VT) occurred within 15 sec after reperfusion and in three animals culminated in ventricular fibrillation. In 75% of cases of nonsustained VT, initiation occurred in the subendocardium at the border of the reperfused zone via a mechanism not involving reentry, as determined by the fact that continous activation was not apparent and the time from the end of the sinus beat to the beginning of VT (142 .+-. 14 msec) was not associated with any intervening depolarizations. In the remaining 25% of cases of nonsustained VT, initiation of the VT resulted from intramural reentry in the subendocardium adjacent to the site of delayed midmyocardial activation from the preceding sinus beat (total activation time = 151 .+-. 9 msec, p < .001 vs just before reperfusion). This reentrant mechanism was similar to that responsible for the majority of cases of VT during ischemia without reperfusion. Maintenance of VT during reperfusion occurred by nonreentrant mechanisms as well as by intramural reentry, with most cases of VT involving both mechanisms. Ventricular tachycardia leading to ventricular fibrillation was initiated in the subendocardium at the border of the reperfused zone by a nonreentrant mechanism was maintained by both nonreentrant and reentrant mechanisms, at times in combination in the same beat. The coupling interval of the first ectopic beat of VT leading to ventricular fibrillation was not significantly different from that of nonsustained VT (199 .+-. 16 vs 189 .+-. 9 msec, p = NS). However, during the transition from VT to ventricular fibrillation, nonreentrant mechanisms arising both in the subendocardium and subepicardium led to very rapid acceleration of the tachycardia to the coupling interval of 92 .+-. 2 msec, resulting in enhanced functional block and further conduction delay, with the total activation time of the transition beats exceeding the coupling interval of the tachycardia. This subsequently led to the development of multiple small reentrant circuits and multiple simultaneous wavefronts characteristics of ventricular fibrillation. In the cases of nonsustained VT, none demonstrated nonreentrant activation in the epicardium or a cycle length less than 120 msec. Likewise, no rapid nonreentrant activation of the endocardium or development of ventricular fibrillation was demonstrated. Thus, VT during reperfusion of ischemic myocardium is most commonly initiated by a nonreentrant mechanism, although intramural reentry can contribute. Ventricular fibrillation occurs through a rapid nonreentrant acceleration of the tachycardia. The nature of this nonreentrant excitation remains to be elucidated, but may involve an abnormal form of automaticity or triggered activity.