Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients

Lucio Santangelo, Ernesto Ammendola, Vincenzo Russo, Ciro Cavallaro, Filippo Vecchione, Salvatore Garofalo, Antonio D'Onofrio, Raffaele Calabrò
Europace: European Pacing, Arrhythmias, and Cardiac Electrophysiology 2006, 8 (7): 502-5

AIMS: The aim of our study was to evaluate the effect of cardiac resyncronization therapy 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, age 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), with sinus rhythm (SR), QRS duration >120 ms (mean QRS duration=156+/-21 ms), an ejection fraction <35%, left ventricular end-diastolic diameter >55 mm, presence of atrioventricular asynchrony, intra- and inter-ventricular asynchrony, underwent permanent biventricular pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing (BiVP) and QTd, JTd, and TDR were assessed. BiVP significantly reduced QTd (73.93+/-19.4 ms during BiVP vs. 91+/-6.7 ms in SR, 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), compared with SR. Right ventricular endocardial pacing and left ventricular epicardial pacing both increased 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: BiVP causes a statistically significant reduction of ventricular heterogeneity of repolarization and has an electrophysiological anti-arrhythmic influence on the arrhythmogenic substrate of dilated cardiomyopathy.

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