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JOURNAL ARTICLE

Biventricular pacing has an advantage over left ventricular epicardial pacing alone to minimize proarrhythmic perturbation of repolarization

Masahide Harada, Toshiyuki Osaka, Eriko Yokoyama, Yoshio Takemoto, Atsushi Ito, Itsuo Kodama
Journal of Cardiovascular Electrophysiology 2006, 17 (2): 151-6
16533252

INTRODUCTION: Cardiac resynchronization therapy (CRT) by simultaneous biventricular pacing is now widely accepted as a new therapeutic option for patients with severe congestive heart failure (CHF). Recent studies have shown comparable hemodynamic benefits of left ventricular (LV) pacing alone. The clinical usefulness of CRT, however, might be compromised by potential exaggeration of arrhythmogenic substrates through a modification of ventricular repolarization.

METHODS AND RESULTS: We compared ECG parameters during sinus rhythm (SR), atrioventricular synchronous pacing at the right ventricular apex (RV(end)P), at LV epicardium (LV(epi)P), and at both sites (BiVP) in acute homodynamic studies of 14 CHF patients scheduled for CRT (QRS duration = 144 +/- 23 msec, LVEF = 27 +/- 10%). The maximum rate of increase in LV pressure (LVdp/dt(max)) was decreased significantly during RV(end)P, whereas it was increased similarly during LV(epi)P and BiVP compared with SR. QTc was increased during RV(end)P (by 10.2%) and LV(epi)P (by 26.1%). QTc dispersion (QTc(max)-QTc(min) in the six precordial leads) was also increased during LV(epi)P (by 66.5%). These parameters were unaffected during BiVP. JTc was unchanged, and the interval from the peak to the end of the T wave (Tc(peak-end)) was increased slightly (by 19.3%) during RV(end)P. Both JTc and Tc(peak-end) were increased dramatically during LV(epi)P (by 18.2% and 55.4%, respectively), but increased only modestly during BiVP (by 6.6% and 15.8%, respectively).

CONCLUSIONS: LV(epi)P causes much greater increase in spatial dispersion of ventricular repolarization than BiVP in CHF patients. BiVP may have a substantial advantage over LV(epi)P to minimize the proarrhythmic perturbation of ventricular repolarization in association with CRT.

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