Akhtar M, Shenasa M, Schmidt D H
J Clin Invest. 1981 Apr;67(4):1047-55. doi: 10.1172/jci110116.
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.
对14例预激综合征患者在逆行不应期研究中可诱发阵发性室上性心动过速(PSVT)时右心室早搏刺激(V(2)法)引发PSVT的精确机制进行了分析。这14例患者中,9例有左侧旁路,其余5例有右侧室房(VA)旁路。在基础周期长度(V(1)V(1))为550至900毫秒(平均657.1±139.5毫秒)时,紧密耦合的V(2)(平均V(1)V(2)为357.3±59.2毫秒,范围320 - 500毫秒)通过束支产生逆行希氏束(H(2))激动,并通过旁路产生逆行心房(A(2))激动。随着V(1)V(2)进一步缩短,14例中有9例V(2)在希氏 - 浦肯野系统(HPS)中出现逆行阻滞,并通过旁路传导至心房。随后,在所有9例中,A(2)冲动经房室结 - HPS前传引发PSVT或心房回波反应。当V(2)通过束支产生逆行H(2)激动时,无一例患者由V(2)诱发PSVT。然而,14例中有10例,由于HPS中的大折返,逆行H(2)后出现V(3)。V(3)继而在HPS中逆行阻滞,同时通过旁路产生A(3),在10例中有9例引发PSVT或心房回波反应。14例中有13例HPS中V(2)和/或V(3)的逆行阻滞导致PSVT发作,而其余1例的确切机制尚不清楚。在本系列患者中,无一例PSVT是由V(2)在房室结逆行阻滞伴或不伴通过旁路的逆行A(2)激动引发的。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)的逆行阻滞是预激综合征患者室性早搏刺激时引发PSVT最常见的机制。