Pogwizd S M, Corr P B
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Circ Res. 1990 Mar;66(3):672-95. doi: 10.1161/01.res.66.3.672.
The mechanisms underlying the development of ventricular fibrillation (VF) during early myocardial ischemia were assessed by use of a computerized three-dimensional mapping system capable of recording simultaneously from 232 intramural recording sites throughout the entire feline heart in vivo. Occlusion of the proximal left anterior descending coronary artery led to ventricular tachycardia (VT), which degenerated to VF in 1-5 minutes in four of 15 animals. Normal sinus beats immediately preceding the initiation of VT leading to VF demonstrated delayed activation (total activation time 133 +/- 14 msec), which was not significantly different from the activation time for normal sinus beats immediately preceding nonsustained VT (149 +/- 7 msec). Most of the conduction delay occurred in the subendocardial and midmyocardial regions in both groups. Initiation of VT leading to VF occurred by intramural reentry in three of the four cases. In one case, a mechanism responsible for the initiation of VT could not be assigned. The coupling interval of the initiating beats of VT ultimately leading to VF (210 +/- 15 msec) did not differ from that of nonsustained VT. Maintenance of the VT that led to VF was due primarily to intramural reentry (84% of cases) involving multiple activation sites in and around the border region of the ischemic zone. Nonreentrant mechanisms, arising in the subendocardium and subepicardium, also contributed to the maintenance of VT before development of VT. The transition from VT to VF was due exclusively to intramural reentry with initiation of the reentrant beats in the subendocardium and, occasionally, the subepicardium. Acceleration of the tachycardia by intramural reentry, along with very rapid and inhomogeneous recovery of excitability (as low as 50-60 msec), led to increased functional block and conduction delay. As a result, the total activation time for a given beat exceeded the coupling interval for that beat and led to the multiple reentrant circuits and multiple simultaneous activations characteristic of VF. Thus, the initiation and maintenance of VT leading to VF during early ischemia is due to intramural reentry, although nonreentrant mechanisms also contribute. However, the development of VF is due to continued intramural reentry and rapid recovery of excitability.
利用一种计算机三维标测系统评估早期心肌缺血期间室颤（VF）发生的机制，该系统能够在体内同时记录猫整个心脏232个壁内记录位点的情况。左前降支冠状动脉近端闭塞导致室性心动过速（VT），15只动物中有4只在1 - 5分钟内恶化为VF。导致VF的VT发作前的正常窦性搏动表现为激动延迟（总激动时间133±14毫秒），这与非持续性VT发作前正常窦性搏动的激动时间（149±7毫秒）无显著差异。两组中大部分传导延迟发生在心肌内膜下和中层心肌区域。导致VF的VT发作在4例中有3例是由壁内折返引起。在1例中，无法确定导致VT发作的机制。最终导致VF的VT起始搏动的联律间期（210±15毫秒）与非持续性VT的联律间期无差异。导致VF的VT维持主要是由于壁内折返（84%的病例），涉及缺血区边界区域及其周围的多个激动位点。起源于心内膜下和心外膜下的非折返机制在VT发生前也有助于VT的维持。从VT到VF的转变完全是由于壁内折返，折返搏动起始于心内膜下，偶尔也起始于心外膜下。壁内折返导致心动过速加速，同时兴奋性恢复非常迅速且不均匀（低至50 - 60毫秒），导致功能性阻滞和传导延迟增加。结果，给定搏动的总激动时间超过该搏动的联律间期，导致多个折返环和VF特有的多个同时激动。因此，早期缺血期间导致VF的VT的起始和维持是由于壁内折返，尽管非折返机制也有作用。然而，VF的发生是由于持续的壁内折返和兴奋性的快速恢复。
