Hamer A, Peter T, Mandel W
Am Heart J. 1983 Apr;105(4):629-42. doi: 10.1016/0002-8703(83)90488-x.
Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.
14例复发性室上性心动过速(SVT)患者接受了电生理评估。结果显示,每位患者的折返均局限于房室(AV)结区域。在SVT稳定发作期间,给每位患者静脉注射0.075至0.15mg/kg维拉帕米,每次均导致心动过速终止。SVT的终止存在多种机制。9例患者表现为前传性房室结阻滞导致心动过速终止,在此之前,心动过速环路前传支的传导时间(Ae-H间期)增加,而后传支的传导时间(H-Ae间期)无变化。3例患者表现为环路后传支阻滞导致心动过速终止,在此之前,Ae-H间期和H-Ae间期均增加。还观察到了自发性室性早搏导致心动过速终止以及窦性心律篡夺的另外例子。共同特点是维拉帕米对房室结的前传和后传传导及不应期有显著影响。它延长了具有双前传房室结路径患者的快径路和慢径路的不应期,并且在对照研究中,即使在心室递增起搏期间心室房传导时间恒定的患者中,也观察到了对后传传导和不应期的明显影响。然而,根据对照研究中患者对心室起搏的反应以及在其SVT期间记录的维拉帕米效应,确定了三组不同的患者。对后一组发现的一种解释可能是,房室结部分对心室起搏的后传反应存在正常变异,并且一些患者对维拉帕米的反应存在变异性。