Pogwizd S M, Hoyt R H, Saffitz J E, Corr P B, Cox J L, Cain M E
Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
Circulation. 1992 Dec;86(6):1872-87. doi: 10.1161/01.cir.86.6.1872.
To determine the mechanisms of ventricular tachycardia (VT) in humans, three-dimensional intraoperative mapping of up to 156 intramural sites was performed in 13 patients with healed myocardial infarction and refractory VT.
Mapping was of sufficient density to define the mechanism of 10 VTs in eight patients. In five of 10 cases, sustained VT was initiated in the subendocardium or epicardium by intramural reentry with marked conduction delay as well as functional and anatomic block most prominent in the subendocardium and midmyocardium. The initiating beats of reentrant VT induced by programmed electrical stimulation arose in the endocardium or midmyocardium by progressive slowing of conduction leading to unidirectional block. Multiple simultaneous reentrant circuits can be present. In contrast, five of the 10 sustained VTs were initiated by a focal mechanism as defined by the absence of electrical activity between the termination of one beat and the initiation of the next despite the presence of multiple intervening intramural electrode recording sites. Comparisons of the mapping data with results of histopathological analysis of tissue demonstrated that the location of infarction as well as that of adjacent fibrotic muscle determined sites of both fixed and functional conduction block during macroreentrant VT and that slowing of conduction occurred in a direction transverse rather than longitudinal to fiber orientation.
Both intramural reentry and a focal mechanism underlie sustained VT in patients with healed myocardial infarction.
为了确定人类室性心动过速（VT）的机制，对13例陈旧性心肌梗死合并难治性VT患者进行了多达156个壁内位点的三维术中标测。
标测密度足以确定8例患者中10次室性心动过速的机制。在10例中的5例中，持续性室性心动过速由壁内折返在心内膜下或心外膜起始，伴有明显的传导延迟以及在心内膜下和心肌中层最显著的功能性和解剖性阻滞。程序性电刺激诱发的折返性室性心动过速的起始搏动通过传导逐渐减慢导致单向阻滞而在心内膜或心肌中层产生。可能存在多个同时存在的折返环。相比之下，10次持续性室性心动过速中的5次由局灶机制起始，其定义为尽管存在多个壁内电极记录位点，但在一次搏动终止与下一次搏动起始之间无电活动。将标测数据与组织病理分析结果进行比较表明，梗死部位以及相邻纤维化心肌的位置决定了大折返性室性心动过速期间固定性和功能性传导阻滞的部位，并且传导减慢沿与纤维方向垂直而非平行的方向发生。
壁内折返和局灶机制均是陈旧性心肌梗死患者持续性室性心动过速的基础。
