Left Ventricular Conduction Delays Induced by Right Ventricular Apical Pacing: Effect of Left Ventricular Dysfunction and Bundle Branch Block

NIRAJ VARMA M.D., F.R.C.P.,

NIRAJ VARMA M.D., F.R.C.P.

Cardiac Electrophysiology Laboratory, University Hospitals/Case Western Reserve University, Cleveland, Ohio, USA

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NIRAJ VARMA M.D., F.R.C.P.,

NIRAJ VARMA M.D., F.R.C.P.

Cardiac Electrophysiology Laboratory, University Hospitals/Case Western Reserve University, Cleveland, Ohio, USA

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First published: 25 October 2007

https://doi.org/10.1111/j.1540-8167.2007.00995.x

Citations: 62

Address for correspondence: Niraj Varma, M.D., F.R.C.P., Cardiac Electrophysiology Laboratory, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA. Fax: 708-216-6829; E-mail: [email protected]

Manuscript received 18 May 2007; Revised manuscript received 20 August 2007; Accepted for publication 23 August 2007.

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Abstract

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 ≤ 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 ≥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.

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Volume19, Issue2

February 2008

Pages 114-122

Left Ventricular Conduction Delays Induced by Right Ventricular Apical Pacing: Effect of Left Ventricular Dysfunction and Bundle Branch Block

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Left Ventricular Conduction Delays Induced by Right Ventricular Apical Pacing: Effect of Left Ventricular Dysfunction and Bundle Branch Block

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