QRS DURATION WIDENING - REDUCED SYNCHRONIZATION OF ENDOCARDIAL ACTIVATION OR TRANSSEPTAL CONDUCTION TIME

Antegrade activation of the His-Purkinje system (HPS) results in synch ronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alterat ion in septal activation and transseptal conduction time have been rep orted to be the causes for QRSD widening seen with bundle branch block . However, reduced synchronization of activation of RV and LV endocard ia as another potential mechanism for QRSD widening has not been syste matically studied. Fifteen consecutive patients underwent radiofrequen cy ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 +/- 8 ms with mean HV in terval of 40 +/- 5 ms. Right atrial (RA), coronary sinus (CS), simulta neous (S) RA-CS, RV apex (RVA), LV apex (LVA), and SRVA-LVA pacing wer e performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to norma l sinus rhythm (87 +/- 7, 87 8 and 88 +/- 8 ms respectively). Mean QRS D was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 +/- 8, 146 +/- 12 and 257 /- 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 eith er RVA or LVA pacing alone is due to elimination of transseptal conduc tion delay; longer QRSD with SRVA-LVA pacing compared to sinus or atri al paced rhythm is due to reduced synchronization of endocardial activ ation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. The refore, in addition to transseptal conduction delay, reduced synchroni zation of endocardial activation is another potential mechanism for QR SD widening.