Clinical impact of left ventricular paced conduction disturbance in cardiac resynchronization therapy

Myocardial scarring is associated with nonresponse to cardiac resynchronization therapy (CRT) and conduction delay. Little is known about the significance and cause of left ventricular (LV) paced conduction disturbance (LPCD).

The purpose of this study was to investigate the clinical impact of paced interlead electrical delay and the difference in each conduction time from LV pace to right ventricular (RV) sense (LVp-RVs) and from RV pace to LV sense (RVp-LVs) [(LVp-RVs) - (RVp-LVs)], in CRT.

Among 137 patients who underwent CRT implantation, LVp-RVs and RVp-LVs were measured intraoperatively. The relationships between [(LVp-RVs) - (RVp-LVs)] and perfusion defects on myocardial perfusion single photon emission computed tomography (SPECT) imaging or [(LVp-RVs) - (RVp-LVs)] and clinical outcomes were assessed.

After CRT implantation, 81 patients (59%) responded to CRT. [(LVp-RVs) - (RVp-LVs)] was significantly longer in nonresponders than in responders (9.7 ± 47.3 ms vs -4.5 ± 33.2 ms; P = .041). Patients with LPCD [(LVp-RVs) > (RVp-LVs)] had higher perfusion defects in the anterolateral region (2.7 ± 2.7 vs 1.1 ± 1.6; P = .0015) on SPECT. Multivariate analysis showed that LPCD was the independent predictor of nonresponse to CRT (odds ratio 0.40; 95% confidence interval [CI] 0.17-0.90; P = .026). During median follow-up of 2.3 years (interquartile range 1.3-5.5), LPCD was the independent predictor of cardiac death and/or heart failure hospitalization in multivariate analysis (hazard ratio 2.04; 95% CI 1.19-3.55; P = .010).

LPCD could predict nonresponse to CRT and poor outcome. Further intervention, such as adjustment of pacing timing or multipoint/site pacing, may be needed in such patients.