BACKGROUND: Cardiac resynchronization therapy (CRT) was shown to improve heart failure (HF) prognosis. But many patients do not benefit from CRT. Optimization of left ventricular (LV) lead position to the latest activated LV area is important to increase CRT response. We aimed to detect the relationship between LV lead sensing delay and echocardiographic and electrocardiographic response to CRT treatment. METHODS: We prospectively included 156 consecutive patients with HF diagnosis, QRS ≥ 120 ms, left bundle branch block, New York Heart Association II-IV, LV ejection fraction (LVEF) < 35%, and scheduled for CRT (100 male, 56 female; mean age 65.8 ± 10.06 years). Echocardiographic CRT response was defined as ≥15% reduction in LV end-systolic volume (LVESV). LV lead sensing delay was calculated as the time interval from the onset of surface QRS wave to the onset of depolarization wave recorded from the LV lead by using the LV pacing lead as a bipolar electrode. RESULTS: LVESV reduction was associated with baseline QRS width (r = 0.292, P = 001), QRS narrowing (r = 0.332, P < 001), and LV lead sensing delay (r = 0.454, P < 001) in bivariate analysis. In logistic regression analysis, LV lead sensing delay was found to be the only independent parameter for predicting significant LVESV reduction (β = 0.423, P < 0.001). LV lead sensing delay was also found to be significantly associated with LVEF increase (r = 0.320, P < 0.001) and QRS narrowing (r = 0.345, P < 0.001). CONCLUSION: LV lead sensing delay is the only independent predictor for significant reduction in LVESV and was found to be significantly associated with LVEF increase and QRS narrowing after CRT treatment. We suggest that LV lead sensing delay may be used as a marker to predict the favorable response to CRT.
BACKGROUND: Cardiac resynchronization therapy (CRT) was shown to improve heart failure (HF) prognosis. But many patients do not benefit from CRT. Optimization of left ventricular (LV) lead position to the latest activated LV area is important to increase CRT response. We aimed to detect the relationship between LV lead sensing delay and echocardiographic and electrocardiographic response to CRT treatment. METHODS: We prospectively included 156 consecutive patients with HF diagnosis, QRS ≥ 120 ms, left bundle branch block, New York Heart Association II-IV, LV ejection fraction (LVEF) < 35%, and scheduled for CRT (100 male, 56 female; mean age 65.8 ± 10.06 years). Echocardiographic CRT response was defined as ≥15% reduction in LV end-systolic volume (LVESV). LV lead sensing delay was calculated as the time interval from the onset of surface QRS wave to the onset of depolarization wave recorded from the LV lead by using the LV pacing lead as a bipolar electrode. RESULTS: LVESV reduction was associated with baseline QRS width (r = 0.292, P = 001), QRS narrowing (r = 0.332, P < 001), and LV lead sensing delay (r = 0.454, P < 001) in bivariate analysis. In logistic regression analysis, LV lead sensing delay was found to be the only independent parameter for predicting significant LVESV reduction (β = 0.423, P < 0.001). LV lead sensing delay was also found to be significantly associated with LVEF increase (r = 0.320, P < 0.001) and QRS narrowing (r = 0.345, P < 0.001). CONCLUSION: LV lead sensing delay is the only independent predictor for significant reduction in LVESV and was found to be significantly associated with LVEF increase and QRS narrowing after CRT treatment. We suggest that LV lead sensing delay may be used as a marker to predict the favorable response to CRT.