Reentrant and Nonreentrant Mechanisms Contribute to Arrhythmogenesis During Early Myocardial Ischemia: Results Using Three‐Dimensional Mapping
Reentrant and Nonreentrant Mechanisms Contribute to Arrhythmogenesis During Early Myocardial Ischemia: Results Using Three‐Dimensional Mapping
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折返和非折返机制导致早期心肌缺血期间的心律失常：使用三维映射的结果
作者：
S. Pogwizd;P. Corr
本研究采用一种独特的计算机标测系统，能够同时记录232个单独的壁内部位，评估了早期缺血期间室性早搏（PVC）和室性心动过速（VT）的发生和维持机制。在氯醛糖麻醉的猫中，在缺血前的正常窦性心律期间，心室激动迅速，总激动时间为25 ± 2 msec。左前降支（LAD）冠状动脉闭塞后5分钟，窦性心律期间激活延迟（64 ± 6 msec）（与对照组相比p<0.001），其特征为同一平面内传导缓慢，同一平面和心内膜-心外膜方向传导阻滞。在76%的病例（21例中的16例）中，单次PVC和VT的第一次搏动发生在壁内折返。在所有情况下，但一个，启动发生在subendocardium，相邻的网站延迟subendocardium和midmyocardial激活的前一个窦性搏动。PVC或VT之前的窦性搏动的激动时间显著延长（149 ± 7 msec，p<0.001，与未发生PVC或VT的缺血期间的窦性搏动相比），大部分延迟活动发生在内膜下和心肌中层，这一发现单独通过心外膜标测并不明显。折返径的长度为1.8-3.0 cm。明显延迟是发生折返的必要条件，但不是充分条件，因为在某些情况下，在没有开始折返或发生非折返性PVC或VT的情况下发现延迟长达220 msec。室性心动过速的室壁内折返维持发生在心内膜下或心外膜下，主要取决于持续存在明显的透壁延迟（159 ± 8 msec）。相比之下，在24%的病例（5/21）中，VT的第一次搏动起始于心内膜下或心外膜下，通过除折返以外的机制发生，如前一次窦性搏动结束与异位搏动起始之间缺乏干预电活动所证明。前一个窦性心搏的特征是延迟（129 ± 12 msec），与折返性异位心搏前的窦性心搏（p = NS）相当，但显著延迟远离非折返性起始部位。室性心动过速可由一种机制（折返性或非折返性）启动，并由另一种机制维持或终止。这两种机制也可能发生在同一心跳的开始和同一心动过速期间。因此，室性心动过速在早期缺血的启动和维持是由于壁内折返和非折返机制。治疗干预旨在抑制与早期缺血相关的恶性心律失常，因此，人类猝死可能需要证明不仅对折返机制，而且对非折返机制的疗效。
The present study assessed the mechanisms responsible for the initiation and maintenance of premature ventricular complexes (PVCs) and ventricular tachycardia (VT) during early ischemia using a unique computerized mapping system capable of recording simultaneously from 232 individual intramural sites. In the chloralose-anesthetized cat, during normal sinus rhythm prior to ischemia, ventricular activation was rapid with a total activation time of 25 ± 2 msec. Five minutes after occlusion of the left anterior descending (LAD) coronary artery, activation was delayed during sinus rhythm (64 ± 6 msec) (p<0.001 vs. control) and was characterized by slow conduction in the same plane and block in both the same plane and in the endocardial-to-epicardial direction. In 76% of cases (16 of 21), initiation of single PVCs and the first beat of VT occurred through intramural reentry. In all but one case, initiation occurred in the subendocardium, adjacent to the site of delayed subendocardial and midmyocardial activation of the preceding sinus beat. The activation time of the sinus beat preceding the PVC or VT was significantly prolonged (149 ± 7 msec, p<0.001 vs. sinus beats during ischemia not followed by a PVC or VT) with most of the delayed activity occurring in the subendocardium and midmyocardium, a finding that would not have been apparent by epicardial mapping alone. The length of the reentrant pathway ranged from 1.8–3.0 cm. Marked delay was a necessary, but not a sufficient, condition for reentry to occur since, in some cases, delays as large as 220 msec was found without initiation of reentry or the occurrence of nonreentrant PVCs or VT. Maintenance of VT by intramural reentry arose in either the subendocardium or the subepicardium and was primarily dependent on the continued presence of marked transmural delay (159 ± 8 msec). In contrast, in 24% of cases (5 of 21), initiation of the first beat of VT arose in either the subendocardium or subepicardium by a mechanism other than reentry as evidenced by the lack of intervening electrical activity between the end of the preceding sinus beat and the initiation of the ectopic beat. The preceding sinus beat was characterized by delay (129 ± 12 msec) comparable to that of sinus beats preceding reentrant ectopic beats (p = NS), but the marked delay was distant from the site of nonreentrant initiation. Ventricular tachycardia could be initiated by one mechanism (reentrant or nonreentrant) and maintained or terminated by another mechanism. Both mechanisms could also occur during the initiation of the same beat and during the same tachycardia. Thus, the initiation and maintenance of VT during early ischemia is due to both intramural reentry and nonreentrant mechanisms. Therapeutic interventions designed to inhibit the malignant arrhythmias associated with early ischemia and, hence, sudden death in man will likely require demonstration of efficacy against not only the reentrant but also nonreentrant mechanisms.
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影响因子：
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