Bariatric surgery reduces ventricular repolarisation gradients in obese patients - results from an electrocardiographic imaging study
Authors: Patel K , Bajaj N , Li X , Statton B , Stoks J , Nyamakope K , Davidson R , Savvidou S , Purkayastha S , Ware JS , O’regan D , Lambiase P , Cluitmans M , Peters NS , Ng FS 
Published: May 2022

Abstract

Funding Acknowledgements
Type of funding sources: Public Institution(s). Main funding source(s): National Institute for Health Research (NIHR) British Heart Foundation

Background
Obesity confers higher risks of atrial arrhythmias and is associated with abnormal ventricular repolarisation. Despite this, the proarrhythmic substrate in obesity and its reversibility with weight loss has not been studied in-depth.

Purpose
To characterise the proarrhythmic substrate in obese patients, and its reversibility with bariatric surgery, using electrocardiographic imaging (ECGi).

Methods
ECGi was performed in 8 obese patients before (PreOb) and after (PostOb) bariatric surgery (mean age 39+/-11years, 7 female), and in 8 age- and sex-matched non-obese controls (NOb) (40+/-11 years). ECGi recordings were made at rest, on exercise, and during recovery from exercise. For ECGi analysis, &gt;2000 atrial and ventricular epicardial electrograms were calculated from body surface potential recordings from 256 sites and information from cardiac magnetic resonance imaging, by solving the inverse problem. Local atrial and ventricular epicardial activation times (AT) were calculated as the steepest downslope of their respective activation complexes, and local ventricular repolarisation times (RT) as the steepest upslope of the T-wave. Atrial activation gradients (ATG) and ventricular repolarisation gradients (RTG) were calculated as the maximum difference within 10mm radius divided by the corresponding Euclidean distance.

Results
BMI was greater in PreOb vs NOb (46.6+/-4.8 vs 23.8+/-2.6kg/m2, p&lt;0.0001) and decreased with surgery (PostOb 35.3+/-4.2kg/m2, p&lt;0.0001). Total atrial AT was prolonged in PreOb vs NOb (68+/-12 vs 45+/-10ms, p=0.016) and did not change post-surgery (PreOb vs PostOb: 68+/-12 vs 67+/-16ms, p=0.81). Atrial ATG were also greater in PreOb vs NOb: max 254+/-111 vs 106+/-58ms, p=0.035; mean 24+/-6 vs 12+/-6ms, p=0.0087) and did not change with weight loss (PreOb vs PostOb: max 254+/-111 vs 222+/-69ms/mm, p=0.61; mean 24+/-6 vs 21+/-7ms/mm, p=0.52). Ventricular RTG were greater in PreOb vs NOb (max: 287+/-73 vs 131+/-89ms/mm, p=0.012; mean: 33+/-10 vs 17+/-9ms/mm, p=0.0052). Ventricular RTG decreased with weight loss (PreOb vs PostOb: max 287+/-73 vs 151+/-54ms/mm, p=0.0070; mean: 33+/-10 vs 21+/-8ms/mm, p=0.018), and were similar between PostOb and NOb (max, p=0.81; mean p=0.58). Ventricular AT and RT were non-different in NOb, PreOb and PostOb.

Conclusion
Obesity is associated with pro-arrhythmic electrophysiological remodelling, including steeper ventricular repolarisation gradients and slower atrial activation. At 6 months post-bariatric surgery, there was a reduction in ventricular repolarisation gradients though atrial conduction abnormalities persisted. These findings provide a mechanistic insight into obesity-related arrhythmic risks and its potential reversibility with weight loss surgery.