Mehdirad A A, Nelson S D, Love C J, Schaal S F, Tchou P J
Ohio State University School of Medicine, Department of Medicine, Columbus, USA.
Pacing Clin Electrophysiol. 1998 Aug;21(8):1589-94. doi: 10.1111/j.1540-8159.1998.tb00247.x.
Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation of RV and LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 +/- 8 ms with mean HV interval of 40 +/- 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RV apex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 +/- 7, 87 +/- 8 and 88 +/- 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 +/- 8, 146 +/- 12 and 157 +/- 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.
希氏 - 浦肯野系统（HPS）的顺向激动导致右心室（RV）和左心室内膜的同步激动，形成正常、窄QRS波时限（QRSD）。据报道，间隔激动和跨间隔传导时间的改变是束支传导阻滞时QRSD增宽的原因。然而，右心室和左心室内膜激动同步性降低作为QRSD增宽的另一种潜在机制尚未得到系统研究。连续15例患者接受射频消融（RFA）治疗室上性心动过速。RFA后，正常窦性心律时的平均QRSD为86±8毫秒，平均HV间期为40±5毫秒。进行了右心房（RA）、冠状窦（CS）、同步（S）RA - CS、右心室心尖（RVA）、左心室心尖（LVA）以及SRVA - LVA起搏。RA、CS、SRA - CS起搏时的平均QRSD与正常窦性心律相似（分别为87±7、87±8和88±8毫秒）。与正常窦性心律相比，单独进行SRVA - LVA起搏以及单独进行RVA或LVA起搏时，平均QRSD显著更长（分别为106±8、146±12和157±13毫秒）。然而，与单独进行RVA或LVA起搏相比，SRVA - LVA起搏时的QRSD显著更短（P < 0.0001）。我们得出结论，与单独进行RVA或LVA起搏相比，SRVA - LVA起搏时QRSD更短是由于消除了跨间隔传导延迟；与窦性或心房起搏心律相比，SRVA - LVA起搏时QRSD更长是由于冲动异位进入HPS网络导致心内膜激动同步性降低，且无法利用HPS的分支结构。因此，除了跨间隔传导延迟外，心内膜激动同步性降低是QRSD增宽的另一种潜在机制。
