Littmann L, Svenson R H, Gallagher J J, Selle J G, Zimmern S H, Fedor J M, Colavita P G
Sanger Clinic, Charlotte, N.C.
Circulation. 1991 May;83(5):1577-91. doi: 10.1161/01.cir.83.5.1577.
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.
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 photoblation, 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.
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.
传统观点认为，陈旧性心肌梗死患者的单形性持续性室性心动过速起源于心内膜下。在先前的一项研究中，我们证明室性心动过速期间的电激活模式偶尔提示是心外膜而非心内膜下折返。
本研究采用包括计算机化电激活标测、拖带、观察成功的心外膜激光光凝期间激活模式的变化以及组织学研究等复杂的术中技术，前瞻性评估心外膜在心肌梗死后室性心动过速中的功能作用。连续10例接受术中计算机化激活标测的患者中有5例出现10种显示心外膜舒张期激活的室性心动过速形态。这10种“心外膜”室性心动过速呈现以下整体激活模式：单区域传播（2种）、8字形激活（5种）和环形大折返（3种）。在4种心动过速形态中，利用心外膜刺激成功地从舒张期缓慢传导区域对室性心动过速进行了拖带。拖带期间，整体激活未受干扰，记录显示刺激至QRS间期延长、QRS形态不变以及折返环所有成分的起搏夺获。在室性心动过速期间对推测的折返心外膜部位进行钕：钇铝石榴石激光光凝。心外膜光凝终止了5种8字形心动过速中的5种、3种环形大折返心动过速中的2种，但未终止单区域心动过速。心外膜激光光凝期间的电生理记录显示室性心动过速周期长度逐渐延长以及推测的折返环明显中断。对折返区域（3例患者）的组织学评估显示心外膜表面下有一层存活的心肌。
本研究提示：1）心肌梗死后慢性室性心动过速可能由心外膜大折返引起；2）折返环内的缓慢传导可通过计算机化标测和心外膜拖带定位；3）激光光凝中断室性心动过速是由于折返途径关键部位的传导延迟和阻滞。存活的心外膜肌纤维可能构成潜在病变。
