Gender differences in J point height exist. Previous studies suggest male sex hormones mediate effects on cardiovascular disease through myocardial repolarization. Our objective was to assess whether male and female sex hormones are associated with J point amplitude in healthy subjects. We conducted a cross-sectional study of 475 healthy, mixed racial population of men, and premenopausal women (age 33 ± 9 years, 56% male). Baseline J point amplitude (JPA) was obtained from continuous surface electrocardiograms. Plasma testosterone (T), dihydrotestosterone, estrone, 17-estradiol (E2), and sex hormone–binding globulin were measured. A free testosterone index (FTI) was calculated. Multivariate regression analysis stratified by gender and electrocardiographic lead location was used to determine independent predictors of maximum JPA. Regression analysis demonstrated FTI levels were positively associated with JPA in lateral leads (β = +0.01, p <0.05) in men but not in women. Total testosterone was positively associated with anterior electrocardiographic lead JPA in women (β = +0.5, p <0.02), but not in men. E2 was positively associated with inferior lead JPA (β = +1.2, p <0.03) in men but not in women. Total testosterone levels were positively associated with JPA in anterior leads (β = +0.054, p <0.05) in women. Male volunteers in the highest tertile of FTI demonstrated greater lateral JPA compared with the lowest tertile (p <0.05). Women in the highest tertile of FTI demonstrated greater anterior lead JPA compared with the lowest tertile (p <0.05). In conclusion, in a young, healthy population, the female sex hormone E2 and an FTI are independent determinants of JPA in men, whereas T is associated with JPA in women.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine