三磷酸腺苷对宽QRS性心动过速治疗效果的评价

Therapeutic effects of adenosine triphosphate on the wide QRS tachycardia

目的 探讨三磷酸腺苷 (ATP)对宽QRS性心动过速的治疗效果。方法 18例患儿均存在宽QRS性心动过速 (QRS时限≥ 12 0ms,HR≥ 15 0次 /min) ,按 0 .2 5mg/kg静脉推注ATP。心肌电生理检查以评价心动过速发生的机制。结果 18例患儿中经ATP治疗后 9例伴宽QRS的室上性心动过速 (SVT)中有 8例终止 ,1例无效 ,其中 3例在心动过速终止后出现Ⅰ度房室传导阻滞 ,食道电生理显示有效病例其SVT发生是由房室或房室结折返所致。ATP对 3例房颤及房扑无明显疗效。 6例室性心动过速 (VT) 3例有效 ,3例失败 ,心脏电生理研究显示有效的 3例系由触发的自律性增高所致 ,而失败 3例由折返引起。结论 ATP可终止由房室或房室结折返所致的宽QRS性SVT和可能是由于触发的自律性增高所致的宽QRS的VT ,但对于由于折返机制所致的VT以及房颤和房扑则无疗效。

Objective Adenosine is highly effective in blocking atrioventricular nodal conduction, and has little effect on the inotropic as well as the haemodynamics, and works with a very short half life. Adenosine has been used safely for treating the patients with supraventricular tachycardia. It was reported that adenosine could terminate the triggered activity induced idiopathic ventricular tachycardia, but the observed cases were limited. The effect of adenosine triphosphate (ATP) on wide QRS tachycardia was not clarified. This study aimed at evaluaning the therapeutic effects of ATP in wide QRS tachycardia. Methods Eighteen patients with wide QRS tachycardia (QRS≥120 ms, HR≥150 bpm) were included. ATP (0.25 mg/kg) was administered intravenously. The electrophysiological study was performed in all patients for elucidating the tachycardia mechanism. All antiarrhythmic agents were discontinued for at least five half lives before the observation. Four quadripolar electrode catheters were inserted percutaneously and advanced under fluoroscopic guidance to the high right atrium, coronary sinus, right ventricular apex, and atrio ventricular junction for recording of the His bundle electrogram. If sustained ventricular tachycardia could not be induced during programmed stimulation, the stimulation protocol was repeated plus the infusion of isoproterenol (1～3 μg/kg). Intravenous ATP was injected via a central vein during sustained ventricular tachycardia to assess the effect of the termination. Results ATP could terminate the tachycardia due to atrio ventricular nodal and atrio ventricular reentry in 8 of 9 patients with supraventricular tachycardia (SVT). ATP had no effect on the preexcited atrial fibrillation and pre excited atrial flutter in 3 patients. Ventricular tachycardia(VT) was terminated by ATP in 3 of 6 patients and failed in 3 patients. The electrophysiological detection revealed that ATP could terminate VT due to triggered elevation of autonomy. No entrainment phenomenon was demonstrated in the stress test or isoproterenol infusion. ATP could not terminate VT due to atrio ventricular reentry tachycardia which presented with the entrainment phenomenon in the electrophysiological study. Conclusion ATP could terminate SVT with wide QRS and VT due to triggered autonomy. ATP showed no effect on pre excited atrial fibrillation, flutter, and VT due to a reentry mechanism.