Heart International (May 2006)

Biventricular pacing and heterogeneity of ventricular repolarization in heart failure patients

  • Raffaele Calabrò,
  • Nicola Minnini,
  • Antonio D'Onofrio,
  • Salvatore Garofalo,
  • Filippo Vecchione,
  • Ciro Cavallaro,
  • Ernesto Ammendola,
  • Vincenzo Russo,
  • Lucio Santangelo

DOI
https://doi.org/10.4081/hi.2006.27
Journal volume & issue
Vol. 2, no. 1

Abstract

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Objective: The aim of our study was to evaluate the effect of cardiac resyncronization therapy (CRT) on QT dispersion (QTd), JT dispersion (JTd) and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. Methods and Results: Fifty patients (43 male, 7 female, aged 60.2 ± 3.1 years) suffering from congestive heart failure (N = 39 NYHA class III; N = 11 NYHA class IV) as a result of coronary artery disease (N = 19) or of dilated cardiomyopathy (N = 31), sinus rhythm, QRS duration >130 ms (mean QRS duration >156 ± 21 ms), an ejection fraction < 35%, left ventricular end-diastolic diameter >55 mm, underwent permanent biventricular DDDR pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing and QTd, JTd and TDR were assessed. Biventricular pacing significantly reduced QTd (73.93 ± 19.4 ms during BiVP vs 91 ± 6.7 ms at sinus rhythm, p = 0.004), JTd (73.18 ± 17.16 ms during BiVP vs 100.72 ± 39.04 at baseline p = 0.003), TDR (93.16 ± 15.60 vs 101.55 ± 19.08 at baseline; p<0.004), as compared to sinus rhythm. Right ventricular endocardial pacing and left ventricular epicardial pacing both enhanced QTd (RVendoP 94 ± 51 ms, p<0.03; LVepiP 116 ± 71 ms, p<0.02) and TDR (RVendoP 108.13 ± 19.94 ms; p<0.002; LVepiP 114.71 ± 26.1; p<0.05).There was no effect on JTd during right and left ventricular stimulation. Conclusions: Biventricular pacing causes a statistically significant reduction of ventricular heterogeneity of ripolarization and has an electrophysiological antiarrhythmic influence on arrhythmogenic substrate of dilatative cardiomiopathy.

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