Sex Hormones and Coronary Artery Calcium Progression in Postmenopausal Women: MESA
Vinita Subramanya, Di Zhao, Pamela Ouyang · Prospective cohort study
BlueRipple Assessment
This MESA substudy examined associations between endogenous sex hormone levels and coronary artery calcium (CAC) progression and incident coronary heart disease events in 2,759 postmenopausal women followed over several years with serial CAC scoring.
Higher testosterone levels were associated with greater CAC progression and incident CHD in postmenopausal women. Higher estradiol levels showed a weaker and inconsistent association. Sex hormone binding globulin (SHBG) was inversely associated with CHD events. The associations with testosterone persisted after adjusting for traditional cardiovascular risk factors.
This prospective data adds to an emerging picture of hormonal influence on coronary atherosclerosis in women. The mechanism by which endogenous testosterone promotes CAC progression is not clearly established — proposed pathways include effects on lipid metabolism, insulin sensitivity, and direct vascular effects on smooth muscle proliferation. The finding is observational and cannot establish causality.
For clinical practice, this study primarily adds context for understanding cardiovascular risk in postmenopausal women and reinforces the importance of individualized risk assessment that accounts for hormonal milieu. It does not yet suggest specific interventional targets.
We rate the evidence moderate. A prospective MESA substudy in 2,759 postmenopausal women demonstrating that higher endogenous testosterone is associated with CAC progression and incident CHD — providing observational evidence for hormonal contributions to coronary atherosclerosis in postmenopausal women.
The original source
Subramanya V, Zhao D, Ouyang P, et al. Association of endogenous sex hormones with coronary artery calcium progression and incident coronary heart disease events in post-menopausal women: the Multi-Ethnic Study of Atherosclerosis (MESA). J Cardiovasc Comput Tomogr. 2019 Jan–Feb;13(1):35–42.
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