Della Bella P, Carbucicchio C, Tondo C, Riva S
Istituto di Cardiologia, Università degli Studi, Milan, Italy.
J Am Coll Cardiol. 1995 Jan;25(1):39-46. doi: 10.1016/0735-1097(94)00315-h.
We hypothesized that modulation of atrioventricular (AV) node conduction, allowing a reduction in ventricular rate during atrial fibrillation or flutter without affecting AV conduction during sinus rhythm, might be achieved through ablation of the "slow" AV node pathway.
In patients with atrial fibrillation or flutter not amenable to a direct atrial approach, ablation of the His bundle is performed to induce complete AV block. This procedure causes pacemaker dependence.
Fourteen patients with drug-refractory paroxysmal atrial flutter or fibrillation underwent ablation of the slow AV node pathway. Radiofrequency current was delivered in six patients during sinus rhythm, in six during atrial flutter and in two during atrial fibrillation.
The anterograde effective refractory period of the AV node was prolonged from 270 +/- 50 (mean +/- SD) to 390 +/- 87 ms (p = 0.005) and the Wenckebach cycle from 346 +/- 33 to 458 +/- 75 ms (p = 0.004) in six patients during sinus rhythm. Mean AV ratio increased from 1.6 +/- 0.5 to 3.0 +/- 0.6 (p = 0.02) in six patients with atrial flutter. Mean ventricular rate decreased from 157 +/- 38 to 67 +/- 10 beats/min in two patients with atrial fibrillation. Complete AV block was induced in two patients (transient in one, permanent in one). During a follow-up period of 5.8 +/- 3.5 months, 11 patients experienced a recurrence of atrial fibrillation at 60 to 95 beats/min. No patient had progression to any degree of AV block.
Ablation of the slow AV node pathway allows reduction of ventricular rate during atrial fibrillation or flutter while maintaining intact AV conduction during sinus rhythm. Modulation of AV node conduction is effective in most patients as an alternative to His bundle ablation for control of ventricular rate in paroxysmal atrial fibrillation or flutter.
我们假设通过消融“慢”房室结通路,或许能够实现对房室(AV)结传导的调节,从而在心房颤动或心房扑动期间降低心室率,同时在窦性心律期间不影响房室传导。
对于无法采用直接心房途径治疗的心房颤动或心房扑动患者,会进行希氏束消融以诱发完全性房室传导阻滞。该操作会导致起搏器依赖。
14例药物难治性阵发性心房扑动或心房颤动患者接受了慢房室结通路消融。6例患者在窦性心律时进行射频电流消融,6例在心房扑动时进行,2例在心房颤动时进行。
6例窦性心律患者的房室结前向有效不应期从270±50(均值±标准差)毫秒延长至390±87毫秒(p = 0.005),文氏周期从346±33毫秒延长至458±75毫秒(p = 0.004)。6例心房扑动患者的平均房室传导比例从1.6±0.5增至3.0±0.6(p = 0.02)。2例心房颤动患者的平均心室率从157±38次/分钟降至67±10次/分钟。2例患者诱发了完全性房室传导阻滞(1例为暂时性,1例为永久性)。在5.8±3.5个月的随访期内,11例患者心房颤动复发,心室率为60至95次/分钟。无患者进展为任何程度的房室传导阻滞。
消融慢房室结通路可在心房颤动或心房扑动期间降低心室率,同时在窦性心律期间保持房室传导完整。对于阵发性心房颤动或心房扑动患者,调节房室结传导作为控制心室率的一种替代希氏束消融的方法,在大多数患者中是有效的。