Abstract / Summary
Background and Objectives: Obesity may adversely affect cardiovascular function and cardiac electrical activity. This study aimed to evaluate electrocardiographic indices of ventricular repolarisation in morbidly obese individuals compared with non-obese controls. Materials and Methods: This retrospective, single-centre study included 112 morbidly obese individuals with a body mass index >40 kg/m2 and 51 non-obese controls. QT and Tp-e intervals and Tp-e/QT ratios were measured from resting ECG recordings. Heart-rate-corrected QT intervals were calculated using the Bazett and Fridericia formulae. Between-group comparisons, multivariable regression analyses, sensitivity analyses, and exploratory analyses of iron metabolism parameters were performed. Multiple comparisons were adjusted using the Benjamini–Hochberg false discovery rate (FDR) procedure. Results: Morbidly obese individuals had a shorter RR interval (p = 0.020) and higher QTc-Bazett (p = 0.016) and Tp-e/QT (p = 0.030) than controls; however, these differences did not remain significant after FDR correction (all adjusted p = 0.080). QTc-Fridericia did not differ between groups (p = 0.240). After multivariable adjustment, morbid obesity was not significantly associated with Tp-e/QT (p = 0.338) or QTc-Fridericia (p = 0.177). A sensitivity analysis restricted to morbidly obese individuals without recorded comorbidities similarly showed no significant differences in ventricular repolarisation indices after FDR correction. Within the morbidly obese group, men had higher Tp-e-based indices than women after FDR correction. Exploratory analyses showed associations between iron metabolism parameters and Tp-e-based indices, with ln-ferritin remaining positively associated with Tp-e/QT after adjustment (p = 0.012). Conclusions: The present findings did not demonstrate a consistent association between morbid obesity alone and altered ventricular repolarisation, as the observed between-group differences were not robust across multiple-comparison correction, adjusted analyses, and sensitivity analyses. Sex-related differences and exploratory associations with iron metabolism suggest a multifactorial influence on ventricular repolarisation in morbid obesity. These findings warrant prospective validation using direct arrhythmic outcomes.