Reithmann Christopher, Hahnefeld Anton, Remp Thomas, Dorwarth Uwe, Dugas Martin, Steinbeck Gerhard, Hoffmann Ellen
Medizinische Klinik I, Klinikum Grosshadern, Universität München, München, Germany.
Pacing Clin Electrophysiol. 2003 Jun;26(6):1308-16. doi: 10.1046/j.1460-9592.2003.t01-1-00188.x.
Arrhythmogenic right ventricular dysplasia is a structural heart disease characterized by fibrofatty degeneration of right ventricular myocardium and arrhythmias of right ventricular origin. The aim of this study was to characterize endocardial right ventricular activation by electroanatomic mapping as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Electroanatomic mapping and entrainment procedures were performed in 5 patients with arrhythmogenic right ventricular dysplasia. Endocardial mapping during ventricular tachycardia demonstrated a focal activation pattern with radial spreading of activation from a site of earliest ventricular activation in all directions. Right ventricular activation time (127 +/- 34 ms) was markedly shorter than tachycardia cycle length (415 +/- 92 ms). The site of earliest ventricular activation was found in an aneurysmal outflow tract (n = 2), at the border of aneurysms near the tricuspid annulus (n = 2), and at the apex of the right ventricle (n = 1). Entrainment mapping criteria of these areas of earliest endocardial activity were consistent with exit sites of a reentrant circuit in an area of abnormal myocardium. Fractionated potentials were found 61 +/- 29 ms before the onset of the QRS complex at these sites. Catheter ablation rendered the "clinical" ventricular tachycardia noninducible in four patients but "nonclinical" faster ventricular tachycardias were inducible in three patients. During the follow-up of 7 +/- 3 months after ablation, the frequency of therapies in 4 patients with an implantable cardioverter defibrillator decreased from 49 +/- 61 episodes per month before ablation, to 0.3 +/- 0.5 episodes per month after ablation (P < 0.05). Electroanatomic mapping during ventricular tachycardia facilitates localization of exit sites in relation to aneurysms in diseased right ventricle and may guide catheter ablation in patients with arrhythmogenic right ventricular dysplasia.
致心律失常性右室发育不良是一种结构性心脏病，其特征为右室心肌纤维脂肪变性和起源于右室的心律失常。本研究的目的是通过电解剖标测来描述右室心内膜激动情况，以此作为致心律失常性右室发育不良患者导管消融的指导。对5例致心律失常性右室发育不良患者进行了电解剖标测和拖带程序。室性心动过速期间的心内膜标测显示为局灶性激动模式，激动从最早心室激动部位向各个方向呈放射状扩散。右室激动时间（127±34毫秒）明显短于心动过速周期长度（415±92毫秒）。最早心室激动部位见于动脉瘤样流出道（2例）、靠近三尖瓣环的动脉瘤边界处（2例）以及右室心尖部（1例）。这些最早心内膜活动区域的拖带标测标准与异常心肌区域折返环的出口部位一致。在这些部位，碎裂电位出现在QRS波群起始前61±29毫秒。导管消融使4例患者的“临床”室性心动过速不能被诱发，但3例患者可诱发“非临床”的更快室性心动过速。在消融后7±3个月的随访期间，4例植入式心律转复除颤器患者的治疗频率从消融前每月49±61次发作降至消融后每月0.3±0.5次发作（P<0.05）。室性心动过速期间的电解剖标测有助于确定病变右室中与动脉瘤相关的出口部位，可为致心律失常性右室发育不良患者的导管消融提供指导。
