Morady F, Kadish A H, DiCarlo L, Kou W H, Winston S, deBuitlier M, Calkins H, Rosenheck S, Sousa J
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0022.
Circulation. 1990 Dec;82(6):2093-9. doi: 10.1161/01.cir.82.6.2093.
Ten consecutive patients with recurrent episodes of symptomatic, idiopathic, sustained monomorphic ventricular tachycardia (VT) originating in the right ventricle underwent an attempt at catheter ablation of the ventricular tachycardia. There were seven women and three men, with a mean age of 39 +/- 14 years (+/- SD). None of the patients had any evidence of structural heart disease. The VT had a left bundle branch block configuration and an inferior axis in each patient, and the mean cycle length was 313 +/- 75 msec. Based on the methods of induction of the VT and the response of the VT to verapamil, the VT mechanism was presumed to be reentry in six patients, triggered activity in three patients, and catecholamine-sensitive automaticity in one patient. Sites for ablation were guided by pace mapping, and an appropriate target site was identified in the right ventricular outflow tract in each patient. From one to three shocks of 100-360 J (mean total, 336 +/- 195 J) were delivered from a defibrillator between the tip of the ablation catheter (cathode) and a patch electrode on the anterior chest (anode). An electrophysiology test 7-9 days after ablation demonstrated that VT was still inducible in only one patient, who was treated with amiodarone. One other patient had a recurrence of VT 3 weeks after ablation and was treated with verapamil. Eight of 10 patients were not treated with antiarrhythmic medications and have had no episodes of symptomatic VT during 15-68 months of follow-up (mean follow-up, 33 +/- 18 months). There were no acute or long-term complications.(ABSTRACT TRUNCATED AT 250 WORDS)
十名连续出现症状性、特发性、持续性单形性室性心动过速（VT）复发且起源于右心室的患者接受了室性心动过速的导管消融尝试。其中有七名女性和三名男性，平均年龄为39±14岁（±标准差）。所有患者均无结构性心脏病证据。每位患者的室性心动过速均呈左束支传导阻滞形态且电轴向下，平均心动周期长度为313±75毫秒。根据室性心动过速的诱发方法及对维拉帕米的反应，推测六名患者的室性心动过速机制为折返，三名患者为触发活动，一名患者为儿茶酚胺敏感性自律性。消融部位通过起搏标测引导，每位患者均在右心室流出道确定了合适的靶点。从除颤器在消融导管尖端（阴极）与前胸贴片电极（阳极）之间施加1至3次100 - 360焦耳的电击（平均总量为336±195焦耳）。消融后7 - 9天的电生理检查显示，仅一名患者仍可诱发室性心动过速，该患者接受了胺碘酮治疗。另一名患者在消融后3周室性心动过速复发，接受了维拉帕米治疗。10名患者中有8名未接受抗心律失常药物治疗，在15 - 68个月的随访期间（平均随访33±18个月）未出现症状性室性心动过速发作。无急性或长期并发症。（摘要截断于250字）
