Niraj Varma1, Ping Jia, Yoram Rudy. 1. Cardiac Bioelectricity Research Department, Case Western Reserve University, Cleveland, OH, USA. nivarma@lumc.edu
Abstract
BACKGROUND: Cardiac resynchronization therapy (CRT) for patients with left bundle branch block (LBBB) and left ventricular (LV) dysfunction has variable responses. We hypothesized that conduction delays in intrinsic rhythm and responses to pacing may be influenced by electrophysiologic substrate. To determine this, we used electrocardiographic imaging (ECGI), which maps epicardial ventricular excitation noninvasively. METHODS AND RESULTS: Electrocardiographic imaging was conducted in 8 patients undergoing CRT. During intrinsic conduction with LBBB (6 patients), ventricular activation was heterogeneous, with regions of delayed and/or absent conduction, reflecting varied LV pathology. Latest LV activation occurred in the lateral LV base in 3 patients but variably in the remainder. The anterior LV was susceptible to block and slow conduction. Cardiac resynchronization therapy usually improved interventricular electrical synchrony, but this did not correlate with changes in QRS duration. In some patients, during CRT, regions of slow conduction appeared in the LV in response to pacing, indicating functional electrical characteristics of local tissue. CONCLUSION: In LBBB and LV dysfunction, LV activation is heterogenous and unpredictable, with areas of slow and/or absent conduction. Functional lines of block generate complex barriers and may interfere with paced wave fronts. Thus, patient-specific electrophysiologic substrate properties may determine outcome of CRT.
BACKGROUND: Cardiac resynchronization therapy (CRT) for patients with left bundle branch block (LBBB) and left ventricular (LV) dysfunction has variable responses. We hypothesized that conduction delays in intrinsic rhythm and responses to pacing may be influenced by electrophysiologic substrate. To determine this, we used electrocardiographic imaging (ECGI), which maps epicardial ventricular excitation noninvasively. METHODS AND RESULTS: Electrocardiographic imaging was conducted in 8 patients undergoing CRT. During intrinsic conduction with LBBB (6 patients), ventricular activation was heterogeneous, with regions of delayed and/or absent conduction, reflecting varied LV pathology. Latest LV activation occurred in the lateral LV base in 3 patients but variably in the remainder. The anterior LV was susceptible to block and slow conduction. Cardiac resynchronization therapy usually improved interventricular electrical synchrony, but this did not correlate with changes in QRS duration. In some patients, during CRT, regions of slow conduction appeared in the LV in response to pacing, indicating functional electrical characteristics of local tissue. CONCLUSION: In LBBB and LV dysfunction, LV activation is heterogenous and unpredictable, with areas of slow and/or absent conduction. Functional lines of block generate complex barriers and may interfere with paced wave fronts. Thus, patient-specific electrophysiologic substrate properties may determine outcome of CRT.
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