Key result
Bariatric surgery is linked to ~27% lower ventricular repolarization gradients in obesity.
Why the study?
Obesity increases cardiac arrhythmia risk, but the extent to which weight loss reverses subclinical proarrhythmic adaptations in arrhythmia-free individuals was unknown.
Does bariatric surgery reverse subclinical proarrhythmic structural, electrophysiological, and autonomic remodeling in arrhythmia-free obese patients?
Cohort (n=32)
No
Does bariatric surgery reverse subclinical proarrhythmic structural, electrophysiological, and autonomic remodeling in arrhythmia-free obese patients?
Absolute Event Rate: 19% vs 26%
p-value: p=0.0009
Bariatric surgery-induced weight loss partially reverses proarrhythmic structural and electrophysiological adaptations in obese individuals, particularly epicardial fat volume and ventricular repolarization gradients.
Bariatric surgery-associated weight loss may partially reverse proarrhythmic remodeling; hypothesis-generating for arrhythmia prevention, pending randomized trials.
Abstract Background Obesity confers higher risks of cardiac arrhythmias. The extent to which weight loss reverses subclinical proarrhythmic adaptations in arrhythmia-free obese individuals is unknown. Objective The purpose of this study was to study structural, electrophysiological, and autonomic remodeling in arrhythmia-free obese patients and their reversibility with bariatric surgery using electrocardiographic imaging (ECGi). Methods Sixteen arrhythmia-free obese patients (mean age 43 ± 12 years; 13 (81%) female participants; BMI 46.7 ± 5.5 kg/m²) had ECGi pre–bariatric surgery, of whom 12 (75%) had ECGi postsurgery (BMI 36.8 ± 6.5 kg/m²). Sixteen age- and sex-matched lean healthy individuals (mean age 42 ± 11 years; BMI 22.8 ± 2.6 kg/m²) acted as controls and had ECGi only once. Results Obesity was associated with structural (increased epicardial fat volumes and left ventricular mass), autonomic (blunted heart rate variability), and electrophysiological (slower atrial conduction and steeper ventricular repolarization time gradients) remodeling. After bariatric surgery, there was partial structural reverse remodeling, with a reduction in epicardial fat volumes (68.7 cm³ vs 64.5 cm³; P = .0010) and left ventricular mass (33 g/m2.7 vs 25 g/m2.7; P < .0005). There was also partial electrophysiological reverse remodeling with a reduction in mean spatial ventricular repolarization gradients (26 mm/ms vs 19 mm/ms; P = .0009), although atrial activation remained prolonged. Heart rate variability, quantified by standard deviation of successive differences in R-R intervals, was also partially improved after bariatric surgery (18.7 ms vs 25.9 ms; P = .017). Computational modeling showed that presurgical obese hearts had a larger window of vulnerability to unidirectional block and had an earlier spiral-wave breakup with more complex reentry patterns than did postsurgery counterparts. Conclusion Obesity is associated with adverse electrophysiological, structural, and autonomic remodeling that is partially reversed after bariatric surgery. These data have important implications for bariatric surgery weight thresholds and weight loss strategies.
No takes yet. Share an insight, caveat, or question.
Patel et al. (2024) conducted a cohort in Obesity (n=32). Bariatric surgery vs. Pre-surgery baseline was evaluated on Mean spatial ventricular repolarization gradients (p=0.0009). Bariatric surgery partially reversed adverse electrophysiological remodeling in obese patients, notably reducing mean spatial ventricular repolarization gradients from 26 mm/ms to 19 mm/ms (p=0.0009).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: