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26/Body surface potential mapping is no more sensitive than 12-lead ECG for measuring ventricular repolarisation in obese individuals

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Published Online: Sep 27th 2010 European Journal of Arrhythmia & Electrophysiology. 2020;6(Suppl. 1):abstr26
Authors: R Davidson (Presenting Author) - Imperial College London, London; KHK Patel - Imperial College London, London; M Brezitski - Imperial College London, London; B Statton - Imperial College London, London; A Berry - Imperial College London, London; X Li - Imperial College London, London; S Purkayastha - Imperial College London, London; J Cousins - Imperial College London, London; D O’Regan - Imperial College London, London; NS Peters - Imperial College London, London; JS Ware - Imperial College London, London; FS Ng - Imperial College London, London
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Background: Obesity is associated with pro-arrhythmic electrocardiographic (ECG) abnormalities, such as corrected QT (QTc) prolongation and increased QT dispersion (QTd), which confer a greater risk of ventricular arrhythmia and sudden cardiac death. Few studies have assessed specific measures of repolarisation (T-peak-to-T-end interval (Tpe) or the Tpe/QT, Tpe/QTc, Tpe/JT or Tpe/JTc ratios) in obesity. Owing to greater thoracic coverage, body surface potential mapping (BSPM) may provide greater sensitivity than 12-lead ECG to assess repolarisation abnormalities associated with obesity.

Aims: We aimed to assess differences in measures of ventricular repolarisation and its dispersion between obese and normal-weight individuals using 12-lead ECG. Secondly, we aimed to perform BSPM at rest and during recovery from exercise to assess whether BSPM is more sensitive than 12-lead ECG for detecting differences in ventricular repolarisation between obese and normal-weight individuals.

Methods12-lead ECGs from 22 obese (BMI-35.6±6.7) and 44 age-sex matched normal-weight (BMI-22.5±1.6) individuals were analysed. 252-lead BSPM was performed in 6 obese (BMI-39.8±9.1) and 6 age-sex matched normal-weight (BMI-23.8±0.9) individuals at rest and 2 minutes following exercise. QTd was defined as the standard deviation of QT intervals (QTstd).

Results: Obese individuals had significantly prolonged QT (380±25 vs 367±26, p<0.05), QTc (404±24 vs 379±21, p<0.0001) and JTc (304±23 vs 285±22, p<0.001) intervals at rest compared to normal-weight individuals. There were no differences in the JT or Tpe intervals or the Tpe/QT, Tpe/QTc, Tpe/JT and Tpe/JTc ratios between the groups. There were no differences in the QTstd between obese and normal-weight individuals using 12-lead ECG (19±4.3 vs 19±4.2, p>0.05) or 252-lead BSPM (20±5.7 vs 19±3.8, p>0.05). QTc prolongation was no more pronounced following exercise in obese compared to normal-weight individuals.

Conclusion: Obesity is associated with delayed ventricular repolarisation reflected by QTc and JTc interval prolongation. BSPM does not provide greater sensitivity than 12-lead ECG for measuring differences in ventricular repolarisation in obese individuals. Recovery from exercise does not unmask abnormalities of ventricular repolarisation in obese individuals which are not present at rest.

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