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QRS Duration Widening: Reduced Synchronization of Endocardial Activation or Transseptal Conduction Time?

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 ofRVand 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, RVapex (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 t 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.