RV electrical activation in heart failure during right, left, and biventricular pacing.

OBJECTIVES: To compare right ventricular (RV) activation during intrinsic conduction or pacing in heart failure (HF) patients.

BACKGROUND: RV activation during intrinsic conduction or pacing in patients with left ventricular (LV) dysfunction is unclear but may affect the prognosis. In cardiac resynchronization therapy (CRT), timed LV pacing (CRT-LV) may be superior to biventricular pacing (CRT-BiV), and is hypothesized to be due to the merging of LV-paced and right bundle branch-mediated wavefronts, thus avoiding perturbation of RV electrical activation.

METHODS: Epicardial RV activation duration (RVAD) (onset to end of free wall activation) was evaluated noninvasively by electrocardiographic imaging in healthy control subjects (n = 7) and compared with that of HF patients (LV ejection fraction 23 +/- 10%, n = 14). RVAD in HF was contrasted during RV pacing, CRT-BiV, and CRT-LV at optimized AV intervals.

RESULTS: During intrinsic conduction in HF (n = 12), the durations of QRS and precordial lead rS complexes were 158 +/- 24 and 77 +/- 17 ms, respectively, indicating delayed total ventricular depolarization but rapid initial myocardial activation. Echocardiography demonstrated no significant RV disease. RV epicardial voltage, activation patterns, and RVAD in HF did not differ from normal (RVAD 32 +/- 15 vs. 28 +/- 3 ms, respectively, p = 0.42). In HF, RV pacing generated variable areas of slow conduction and prolonged RVAD (78 +/- 33 ms, p < 0.001). RVAD remained delayed during CRT-BiV at optimized atrioventricular intervals (76 +/- 32 ms, p = 0.87). In contrast, CRT-LV reduced RVAD to 40 +/- 26 ms (p < 0.016), comparable to intrinsic conduction (p = 0.39) but not when atrioventricular conduction was poor or absent.

CONCLUSIONS: In HF patients without RV dysfunction treated with CRT, normal RV free wall activation in intrinsic rhythm indicated normal right bundle branch-mediated depolarization. However, the RV was vulnerable to the development of activation delays during RV pacing, whether alone or with CRT-BiV. These were avoided by CRT-LV in patients with normal atrioventricular conduction.