Sex and menopause influence ventricular repolarization and arrhythmia risk through hormonal effects that may be detectable on the electrocardiogram (ECG). Women have longer QT intervals and narrower QRS-T angles than men, with ECG-based sex misclassification associated with worse outcomes in females. While female hormones are cardioprotective, their decline after menopause may alter ECG patterns. This study aims to identify sex and menopause-related ECG markers of ventricular repolarization and explore their underlying factors. We analyzed ECG markers of ventricular repolarization (the corrected QT, QTc, and T-peak-end, Tpec, intervals and the mean spatial QRS−T angle) in 55,730 healthy individuals from the UK Biobank stratified by sex, and females further subdivided into premenopausal (F-NoMP) and postmenopausal (F-MP) groups. ECG indices were computed per lead and summarized using principal component analysis. Group comparisons used one-tailed Mann–Whitney tests. Significant differences were examined with multiple linear regression to identify key demographic, clinical and cardiac structural and functional contributors. Comparison between sex-specific groups, males showed lower QTc and higher Tpec and QRS−Ta values than females, as well as higher R and T-wave amplitudes in ECG waveforms. Height, body mass index (BMI) and alcohol consumption contributed most in males, whereas menopause, diastolic blood pressure and pulse rate in females. Between F-NoMP and F-MP groups, only Tpec and QRS−Ta differed with F-MP women showing higher values and ECG waveform amplitudes. These differences were driven by left ventricle (LV) wall thickness and LV ejection fraction in both groups and specifically in F-MP, by age, BMI and LV mass. Our results suggest that both sex and menopause are reflected in ECG markers of ventricular repolarization, with F-MP showing subtle changes in morphology toward a pattern analogous to men respect to F-NoMP. These findings suggest the need for further research on hormonal influences in ECG characteristics and arrhythmogenic risk stratification.