Abstract

Weight-stable obese subjects have an increased risk of arrhythmias and sudden death, even in the absence of cardiac dysfunction, and the risk of sudden cardiac death (SCD) with increasing weight is seen in both genders. The mechanism of unexplained deaths in obese patients is still unclear and may be related to ventricular repolarization abnormalities. The aim of this study is to determine the effect of severe obesity on spatial and transmural ventricular repolarization and to clarify the influence of bariatric surgery with a consequent substantial weight loss on arrhythmogenic substrate in the morbidly obese population. For the study, we enrolled 100 severely obese patients; 50 age-matched non-obese healthy subjects were also recruited as controls. All subjects underwent conventional 12-lead electrocardiography for analysis of spatial and transmural ventricular repolarization assessed by corrected QT dispersion (QTc-d), corrected JT dispersion (JTc-d) and transmural dispersion of repolarization, (TDR). All subjects underwent bariatric surgery and were resubmitted to electrocardiographic, biochemical and anthropometric examination 12 months postoperatively. Severely obese patients had greater values in QTc-d, JTc-d and TDR than the normal-weight controls. Bariatric surgery reduced significantly the QTc-d value, JTc-d value and TDR value. There was a significant correlation between decrease of heterogeneity of repolarization indexes (QTd, JTd and TDR) and bariatric surgery-induced weight loss. In severely obese patients, surgically-induced weight loss is associated with significant decrease in the heterogeneity of ventricular repolarization. The reduction of spatial (QTc-d, JTc-d) and transmural dispersion of repolarization (TDR) may be of clinical significance, by reducing the risk of potentially fatal arrhythmias in morbidly obese subjects.

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