FUNCTIONAL-ROLE OF THE EPICARDIUM IN POSTINFARCTION VENTRICULAR-TACHYCARDIA - OBSERVATIONS DERIVED FROM COMPUTERIZED EPICARDIAL ACTIVATION MAPPING, ENTRAINMENT, AND EPICARDIAL LASER PHOTOABLATION
FUNCTIONAL-ROLE OF THE EPICARDIUM IN POSTINFARCTION VENTRICULAR-TACHYCARDIA - OBSERVATIONS DERIVED FROM COMPUTERIZED EPICARDIAL ACTIVATION MAPPING, ENTRAINMENT, AND EPICARDIAL LASER PHOTOABLATION
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DOI：
10.1161/01.cir.83.5.1577
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发表时间：
1991-05-01
期刊：
影响因子：
37.8
通讯作者：
COLAVITA, PG
中科院分区：
文献类型：
--
作者：
LITTMANN, L;SVENSON, RH;COLAVITA, PG
背景。 传统上，远端心肌梗塞患者的单形性持续性室性心动过速被认为起源于心内膜下。 在之前的一项研究中，我们证明室性心动过速期间的电激活模式偶尔表明心外膜下折返而不是心内膜下折返。方法和结果。 本研究通过复杂的术中技术前瞻性评估了心外膜在梗死后室性心动过速中的功能作用，包括计算机电激活映射、夹带、成功心外膜激光消融过程中激活模式变化的观察以及组织学研究。 接受术中计算机激活标测的 10 名连续患者中有 5 名有 10 种室性心动过速形态，显示心外膜舒张期激活。这 10 例“心外膜”室性心动过速揭示了以下整体激活模式：单区域扩散（2 例）、8 字形激活（5 例）和圆形宏观折返（3 例）。 使用心外膜刺激从舒张期慢传导区域成功地以四种心动过速形态夹带室性心动过速。 在夹带过程中，全局激活保持未受干扰，记录显示 QRS 间隔较长的刺激、QRS 形态未改变以及折返回路所有组件的起搏捕获。 在室性心动过速期间，将钕：钇铝石榴石激光光凝递送至假定折返的心外膜部位。 心外膜光消融终止了五个八字形心动过速中的五个，三个圆形大折返心动过速中的两个，但不能终止单区域心动过速。心外膜激光光凝期间的电生理记录表明室性心动过速周期长度逐渐延长，并且假定的折返回路明显中断。折返区域（三名患者）的组织学评估显示心外膜表面下存在存活心肌的边缘。结论。 这项研究表明：1) 慢性梗死后室性心动过速可能由心外膜下宏观折返引起，2) 折返回路内的慢传导可以通过计算机测绘和心外膜夹带来定位，3) 激光光凝引起的室性心动过速中断是由于折返通路关键元件内的传导延迟和阻滞造成的。 存活的心外膜下肌纤维可能构成潜在的病理。
Background. Conventionally, monomorphic sustained ventricular tachycardia in patients with remote myocardial infarction is believed to originate from the subendocardium. In a previous study, we demonstrated that electrical activation patterns during ventricular tachycardia occasionally suggest a subepicardial rather than subendocardial reentry.Methods and Results. This study prospectively evaluated the functional role of the epicardium in postinfarction ventricular tachycardia with complex intraoperative techniques including computerized electrical activation mapping, entrainment, observation of changes in activation pattern during successful epicardial laser photoablation, and histological study. Five of 10 consecutive patients undergoing intraoperative computerized activation mapping had 10 ventricular tachycardia morphologies displaying epicardial diastolic activation. These 10 "epicardial" ventricular tachycardias revealed the following global activation patterns: monoregional spread (two), figure-eight activation (five), and circular macroreentry (three). Entrainment of ventricular tachycardia using epicardial stimulation was successfully performed from an area of slow diastolic conduction in four tachycardia morphologies. During entrainment, global activation remained undisturbed with recordings showing a long stimulus to QRS interval, unchanged QRS morphology, and pacing capture of all components of the reentry circuit. Neodymium:yttrium aluminum garnet laser photocoagulation was delivered during ventricular tachycardia to epicardial sites of presumed reentry. Epicardial photoablation terminated five of five figure-eight tachycardias, two of three circular macroreentry tachycardias but not the monoregional tachycardias. Electrophysiological recordings during epicardial laser photocoagulation demonstrated progressive prolongation of ventricular tachycardia cycle length and apparent interruption of the presumed reentrant circuit. Histological evaluation of the reentrant region (three patients) showed a rim of surviving myocardium under the epicardial surface.Conclusions. This study suggests that 1) chronic postinfarction ventricular tachycardia may result from subepicardial macroreentry, 2) slow conduction within the reentry circuit can be localized by computerized mapping and epicardial entrainment, and 3) ventricular tachycardia interruption by laser photocoagulation results from conduction delay and block within critical elements of the reentrant pathway. Viable subepicardial muscle fibers may constitute the underlying pathology.