Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventricular premature stimulation in the Wolff-Parkinson-White syndrome.
Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventricular premature stimulation in the Wolff-Parkinson-White syndrome.
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逆行希氏浦肯野传导阻滞在沃尔夫-帕金森-怀特综合征室性早搏刺激引发室上性心动过速中的作用。
DOI：
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发表时间：
1981
影响因子：
15.9
通讯作者：
D. Schmidt
中科院分区：
文献类型：
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作者：
M. Akhtar;M. Shenasa;D. Schmidt
本文分析了14例Wolff-Parkinson-白色综合征患者在右室期前刺激（V（2）法）时诱发阵发性折返性室上性心动过速（PSVT）的确切机制。9例为左侧旁路，5例为右侧室房旁路。在基本周期长度（V（1）V（1））范围为550 - 900 ms（平均值，657.1+/-139.5）时，紧密耦合V（2）（平均V（1）V（2），357.3+/-59.2 ms，范围320-500）通过束支产生逆行希氏束（H（2））激动，通过AP产生逆行心房（A（2））激动。随着V（1）V（2）进一步缩短，V（2）在希氏浦肯野系统（HPS）内呈逆行阻滞，经AP传导至心房者9例。随后，在所有9例病例中，A（2）冲动在房室结-HPS上顺行传导，引发PSVT或心房回波反应。当V（2）通过束支产生逆行性H（2）激动时，没有患者发生由V（2）诱发的PSVT。然而，14例中有10例，由于HPS中的大折返，逆行H（2）之后是V（3）。在10例病例中，9例V3在HPS中逆行阻滞，同时通过AP产生A3，引发PSVT或心房回波反应。14例中13例因HPS内V2和/或V3的逆行阻滞而引发PSVT，而1例的确切机制尚不清楚。在这个系列中，没有一个患者的PSVT是由房室结的V2逆行阻滞引发的，伴或不伴经AP的A2逆行激动。我们得出结论，在测试的周期长度范围内，HPS中V（2）和/或V（3）的逆行阻滞是Wolff-Parkinson-白色综合征患者室性早搏刺激期间引发PSVT的最常见机制。
The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V(2) method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V(1)V(1)) ranging from 550 to 900 ms (mean, 657.1+/-139.5), closely coupled V(2) (mean V(1)V(2), 357.3+/-59.2 ms, range 320-500) produced retrograde His bundle (H(2)) activation via the bundle branches and retrograde atrial (A(2)) activation via the AP. As the V(1)V(2) were further shortened, the V(2) showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A(2) impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V(2) when the latter produced retrograde H(2) activation via the bundle branches. In 10 of 14 cases, however, the retrograde H(2) was followed by a V(3), due to macroreentry in the HPS. The V(3) in turn blocked retrogradely in the HPS while producing A(3) via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V(2) and/or V(3) in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none of the patients in this series was the PSVT initiated with a retrograde block of V(2) in the atrioventricular node with or without concomitant retrograde A(2) activation via the AP. We conclude that within the ranges of cycle lengths tested, a retrograde block of V(2) and/or V(3) in the HPS is the most common mechanism for initiation of PSVT during ventricular premature stimulation in patients with the Wolff-Parkinson-White Syndrome.