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Cardiovascular disease (CVD) continues to be the primary cause of mortality and morbidity globally with middle-aged women presenting with additional and possibly, overlooked risk factors.1 Despite several awareness programmes, there remain several gaps in the political education and representation needs of this group, which includes those from low socioeconomic status (SES) and culturally diverse backgrounds. These […]

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

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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Published Online: Sep 27th 2010 European Journal of Arrhythmia & Electrophysiology. 2020;6(Suppl. 1):abstr26
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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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