Garcia Fermin C, Bazan Victor, Zado Erica S, Ren Jian-Fang, Marchlinski Francis E
Cardiovascular Division, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, USA.
Circulation. 2009 Aug 4;120(5):366-75. doi: 10.1161/CIRCULATIONAHA.108.834903. Epub 2009 Jul 20.
Efficacy of endocardial ventricular tachycardia (VT) ablation in arrhythmogenic right ventricular cardiomyopathy/dysplasia may be limited by epicardial VT, right ventricular thickening, or both. We sought to characterize the endocardial versus epicardial substrate, measure right ventricular free wall thickness, and determine epicardial ablation efficacy in patients with right ventricular cardiomyopathy/dysplasia.
Thirteen consecutive patients (3 female; aged 43+/-15 years; range, 17 to 70 years) undergoing endocardial and epicardial sinus rhythm voltage mapping and epicardial VT ablation after failed endocardial VT ablation were included. In each patient, the low bipolar voltage area (<1.0 mV for epicardium and <1.5 mV for endocardium) was more extensive on the epicardium (95+/-47 versus 38+/-32 cm(2); P<0.001) and was uniformly marked by multicomponent and late electrograms. The basal right ventricular thickness assessed by electroanatomic map was >10 mm in 6 of 13 patients compared with 5 to 10 mm in 4 reference patients without structural disease. Twenty-seven VTs were targeted on the epicardium with the use of activation, entrainment, or pace mapping with focal/linear ablation and targeting of late potentials. Epicardial VTs were targeted opposite normal endocardium in 10 patients (77%) and/or opposite ineffective endocardial ablation sites in 11 patients (85%). During 18+/-13 months, 10 of the 13 patients (77%) had no VT, with 2 patients having only a single VT at 2 and 38 months, respectively.
Patients with right ventricular cardiomyopathy/dysplasia and VT after endocardial ablation have a more extensive epicardial area of electrogram abnormalities and frequently have basal right ventricular wall thickening. Epicardial substrate and VT mapping identifies targets, and ablation results in VT control.
在致心律失常性右室心肌病/发育不良中，心内膜室性心动过速（VT）消融的疗效可能受到心外膜VT、右室增厚或两者的限制。我们试图对心内膜与心外膜基质进行特征分析，测量右室游离壁厚度，并确定右室心肌病/发育不良患者的心外膜消融疗效。
纳入13例连续患者（3例女性；年龄43±15岁；范围17至70岁），这些患者在心内膜VT消融失败后接受心内膜和心外膜窦性心律电压标测以及心外膜VT消融。在每位患者中，心外膜上的低双极电压区域（心外膜<1.0 mV，心内膜<1.5 mV）范围更广（95±47对38±32 cm²；P<0.001），且均表现为多成分和延迟电图。通过电解剖图评估，13例患者中有6例的右室基底厚度>10 mm，而4例无结构疾病的对照患者的右室基底厚度为5至10 mm。使用激动标测、拖带标测或起搏标测结合局灶性/线性消融以及对延迟电位进行标测，在心外膜上针对27个VT进行消融。10例患者（77%）的心外膜VT位于正常心内膜的对侧，和/或11例患者（85%）的心外膜VT位于心内膜无效消融部位的对侧。在18±13个月期间，13例患者中有10例（77%）无VT发作，2例患者分别在2个月和38个月时仅发作过一次VT。
心内膜消融后发生VT的右室心肌病/发育不良患者的心外膜电图异常区域更广泛，且常伴有右室基底壁增厚。心外膜基质和VT标测可确定消融靶点，消融可控制VT发作。
