Left ventricular conduction delays induced by right ventricular apical pacing: effect of left ventricular dysfunction and bundle branch block.

BACKGROUND

RV apical pacing (RVP) may be deleterious, possibly by simulating LBBB, i.e., prolonging QRS duration (QRSd) and LV activation (LVAT). However, determinants of electrical delays are unknown.

HYPOTHESIS

LV dysfunction (LVEF <or= 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.

METHODS

RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.

RESULTS

During LBBB and RVP, LVAT/QRSd was >or=85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 +/- 18 ms) was delayed by RVP (129 +/- 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 +/- 27, LVAT 186 +/- 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 +/- 27, LVAT 191 +/- 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 +/- 24, LVAT 169 +/- 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 +/- 29, LVAT 137 +/- 33 ms, n = 41) were enhanced by RVP (QRSd 218 +/- 28, LVAT 191 +/- 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).

CONCLUSION

RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.