Saoudi N, Berland J, Cribier A, Letac B
Unité de soins intensifs, Hôpital Louis-Pradel, Lyon.
Arch Mal Coeur Vaiss. 1988 Apr;81(4):537-41.
A 42-year old man with non-obstructive myocardiopathy complicated by paroxysmal atrial fibrillation treated with amiodarone (200 mg per day) received flecainide in daily doses of 400 mg for undocumented palpitations. Ten syncopes and numerous malaises occurred during the following two months. Electrophysiological testing was performed, showing prolongation of HV to 80 ms and discreet widening of QRS to 100 ms. Programmed atrial stimulation failed to demonstrate a second degree subnodal block and to induce tachycardia. In contrast, ventricular stimulation elicited a critical SH delay (260 ms), always followed by a left delay-type complex preceded by His bundle deflection which suggested reentry within the His-Purkinje system. Three extrasystoles on imposed rhythm started sustained ventricular tachycardia with the same 270 ms cycle morphology and reproducing the symptoms. Each V wave was preceded by an H potential, with HV varying from 100 to 300 ms. Three weeks after flecainide was discontinued, HV was 60 ms, and no ventricular tachycardia could be triggered by programmed stimulation. The patient remained symptom-free throughout the 5-month follow-up. This case illustrates the proarrhythmic effect of the flecainide-amiodarone combination. The mechanism of provoked tachycardia probably involves ventricular reentry through the His bundle branches, induced by a critical depression of conduction below the His bundle.
一名42岁男性，患有非梗阻性心肌病并伴有阵发性心房颤动，接受胺碘酮治疗（每日200毫克），因不明原因的心悸接受了每日400毫克的氟卡尼治疗。在接下来的两个月内发生了十次晕厥和多次不适。进行了电生理检查，结果显示HV间期延长至80毫秒，QRS波群轻度增宽至100毫秒。程控心房刺激未能显示二度结下阻滞，也未能诱发心动过速。相反，心室刺激引发了临界性希氏束-心室（SH）延迟（260毫秒），随后总是出现一个左束支延迟型复合波，其前有希氏束波，提示希氏-浦肯野系统内存在折返。在诱发节律下的三个期前收缩引发了持续的室性心动过速，其形态为相同的270毫秒周期，且再现了症状。每个V波前都有一个H波，HV间期在100至300毫秒之间变化。停用氟卡尼三周后，HV间期为60毫秒，程控刺激未能诱发室性心动过速。在5个月的随访期间，患者一直无症状。该病例说明了氟卡尼-胺碘酮联合用药的促心律失常作用。诱发心动过速的机制可能涉及通过希氏束分支的室性折返，由希氏束以下传导的临界性抑制所诱发。
