Myocardial electrical dyssynchrony following right ventricular pacing in patients with proximal left bundle branch block after transcatheter aortic valve implantation: data from noninvasive cardiac activation mapping

Objective. To compare characteristics of myocardial electrical dyssynchrony in patients with long-term right ventricular pacing and iatrogenic left bundle branch block (LBBB) following transcatheter aortic valve implantation (TAVI) using non-invasive activation cardiac mapping (NIAM); to evaluate the effect of pacing electrode location on cardiac activation maps. Material and methods. The study included 50 patients. The main group consisted of 30 patients with implanted pacemakers and right ventricular pacing (RVCP) rate of 100%. The control group consisted of 20 patients with LBBB after TAVI (TAVI-LBBB group). All patients underwent NIAM to construct isochronous maps. We assessed ventricular endo- and epicardium activation time (AT), activation time difference (ATD), localization of late activation points (LAPs), and conduction block lines (CBLs). In the RVCP group, additional analysis of activation map formation was performed with different stimulating electrode positions (apical, middle third of interventricular septum, basal). Results. The RVCP group was characterized by more severe electrical dyssynchrony: QRS duration 157 versus 140 ms (p=0.001), interventricular activation delay on the epicardium 17.8 versus 12 ms (p<0.001). Ventricular myocardial activation maps in the RVCP group were highly variable. LAP zone typical for LBBB was detected in only 30% of patients (versus 90% in the TAVI-LBBB group), and conduction block line was absent in 20% of cases. Full compliance with LBBB criteria according to NIAM data was found in only 10% of patients with RVCP. Within the RVCP group, electrode position did not affect topography of LAP and CBL. However, apical pacing resulted in the shortest endocardial interventricular activation delay (18 ms) compared to basal and mid-positions (41 ms and 50 ms; p=0.035, respectively). Conclusion. Ventricular electrical activation during cardiac pacing is not equivalent to that in LBBB after TAVI. These processes are characterized by more severe electrical dyssynchrony and variability of activation maps. Apical electrode position, despite small endocardial conduction delay, creates effect of “pseudosynchrony of onset” followed by significant slowing of impulse propagation across the epicardium. These differences indicate that ventricular pacing forms independent pathophysiological model of ventricular myocardial electrical dyssynchrony distinct from that in proximal LBBB after TAVI.