Abstract P435: Associations of Endogenous Sex Hormone Levels With the Prevalence and Progression of Valvular and Thoracic Aortic Calcification in the Multi-Ethnic Study of Atherosclerosis (MESA)

Abstract

Background: Sex hormone (SH) levels may contribute to sex differences in cardiovascular disease (CVD) risk among women and men. We previously found that high free testosterone (T) and low sex hormone binding globulin (SHBG) were associated with progression of coronary artery calcification in women. Extra-coronary calcification (ECC) predicts incident clinical CVD independent of traditional risk factors. We examined whether SH were also associated with ECC prevalence and progression among MESA participants free of clinical CVD at baseline. Methods: We studied 2883 postmenopausal women and 3164 men who had endogenous SH levels measured at baseline. ECC was measured by non-contrast cardiac CT at baseline and at a follow-up visit up to 5 years later. ECC included ascending and descending thoracic aortic calcification (ATAC, DTAC), mitral annular calcification (MAC) and aortic valve calcification (AVC). We used multivariable Poisson regression to evaluate associations with ECC prevalence and risk of developing ECC (Agatston scores >0) and linear mixed effects models for ECC progression, per 1 SD increment in log (SH) level in women and men separately. Results: The mean (SD) age was 64 (9) years for women and 62 (10) years for men. In women, greater free T and lower SHBG were associated with MAC incidence in a demographic-adjusted model but were no longer statistically significant after adjustment for CVD risk factors ( Table ). In men, lower free T was associated with MAC prevalence, DTAC incidence and progression while greater SHBG was associated with MAC prevalence and DTAC progression in fully adjusted models. We did not find associations of SH with AVC or ATAC in either men or women. Conclusion: In this diverse cohort free of CVD, we found certain associations of SH with measures of ECC. In particular, free T was inversely associated with prevalent MAC and DTAC progression in men independent of CVD risk factors. SH may influence vascular calcification but further work is needed to understand the clinical implications of these findings.