Hamada Takashi, Hiraki Tatsuro, Ikeda Hisao, Kubara Ichiro, Yoshida Teruhisa, Ohga Masanobu, Imaizumi Tsutomu
Department of Internal Medicine III and the Cardiovascular Research Institute, Kurume University School of Medicine, Japan.
J Cardiovasc Electrophysiol. 2002 Mar;13(3):223-9. doi: 10.1046/j.1540-8167.2002.00223.x.
Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs).
We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months).
The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.
阵发性心房颤动（PAF）在预激综合征（WPW）患者中频繁发生。为阐明PAF的机制，我们在消融旁路（AP）前后进行了电生理研究（EPS）。
我们研究了24例患有房室折返性心动过速且既往有PAF并成功消融AP的WPW综合征患者。在消融后第7天经EPS诱发心房颤动（AF）的患者被视为可诱发AF组（n = 14），而在消融后第7天经EPS未诱发AF的患者被视为不可诱发AF组（n = 10）。15例患有房室结折返性心动过速（AVNRT）但无PAF且接受慢房室结通路消融的患者作为对照组（AVNRT组）。在消融前后测量了作为心房易损性指标的最大心房传导延迟和传导延迟区。消融前，两个WPW综合征组的最大心房传导延迟和传导延迟区均显著大于AVNRT组（分别为P < 0.0001和P < 0.0001），表明伴有PAF的WPW综合征中心房易损性增加。消融后，可诱发AF组的这些参数未改变，而不可诱发AF组的这些参数显著降低（P < 0.0001）且与AVNRT组无差异，表明消融后不可诱发AF组的心房易损性恢复正常。前瞻性研究表明，在长期随访（17±7个月）期间，PAF仅在可诱发AF组复发。
本研究结果提示，WPW综合征患者中PAF有两种机制：一种机制是可逆的且依赖于AP的心房易损性，另一种是内在的且不依赖于AP的心房易损性。
