A new analysis of long‑term data assessed whether starting menopausal hormone therapy (MHT) during the menopause transition influences later cardiovascular disease (CVD) risk. Prior research has established that women’s CVD risk rises after menopause, driven by lower estrogen levels, vascular stiffening, and adverse shifts in cholesterol and metabolism. Past studies have suggested HRT/MHT can lower heart disease risk, but much of that evidence focused on women who were already postmenopausal. This analysis used the longitudinal SWAN dataset to explore timing of initiation and associations with future cardiovascular outcomes among women who reported vasomotor symptoms.
Researchers examined 20 years of health data from more than 2,700 women enrolled in the Study of Women’s Health Across the Nation (SWAN). Participants included in this analysis self‑reported menopause‑related vasomotor symptoms such as hot flashes and night sweats, had no prior diagnosis of heart disease at baseline, and reported whether they were taking hormone therapy. The study is observational and used existing SWAN data to estimate associations between reported hormone therapy use and subsequent cardiovascular disease risk.
Overall, women who initiated hormone therapy during perimenopause or early postmenopause experienced an estimated 22% lower cardiovascular disease risk compared with women who did not take hormone therapy. The analysis therefore supports prior indications that MHT can be associated with reduced CVD risk in some populations of women when started during the menopausal transition rather than later in life.
Investigators reported a stronger association when hormone therapy was initiated within 10 years of menopause onset. In that subgroup the estimated reduction in heart disease risk was 27% compared with those who did not use hormone therapy. The authors propose these results are consistent with the hypothesis of a timing‑dependent window during the menopause transition and early postmenopause when cardiovascular effects of hormone therapy may differ.
The study found heterogeneity in estimated effects across racial and ethnic groups. The protective association was most pronounced among Black women in the cohort, with an estimated 49% lower cardiovascular disease risk associated with hormone therapy. These subgroup findings suggest the association between MHT and CVD may vary by race and underscore the importance of inclusive research and careful subgroup analysis.
Clinicians quoted in the article described plausible mechanisms by which estrogen, particularly estradiol, could influence cardiovascular risk. Proposed mechanisms include improved glucose regulation, anti‑inflammatory effects, and favorable changes in lipid subparticles such as reductions in LDL, APOB, and Lp(a) subfractions that contribute to atherogenesis. Vasomotor symptoms themselves have been associated with higher future cardiovascular risk and may coincide with an unfavorable metabolic profile including higher blood pressure, adverse cholesterol changes, and elevated fasting glucose.
Samar R. El Khoudary, PhD, MPH, BPharm, FAHA, co‑senior author of the study, emphasized the opportunity to use long‑term SWAN data to assess timing of MHT initiation among women with vasomotor symptoms. She and other clinicians noted that much previous research focused on postmenopausal initiators and that examining perimenopausal and early postmenopausal initiation addresses a key evidence gap.
Independent cardiology and OB/GYN experts who were not involved in the research described the findings as encouraging and as confirmation of earlier literature while urging individualized decision‑making. Jennifer Wong, MD, highlighted that MHT may benefit some women but is not appropriate for everyone; clinicians should consider symptom burden and individual cardiovascular risk. Prudence Hall, MD, discussed potential broad health benefits attributed to estradiol in lowering key metabolic drivers of chronic disease, while also advocating lifestyle interventions and individualized care.
The analysis is observational. Participants self‑reported vasomotor symptoms and hormone therapy use, and the article notes that residual confounding or other group differences could contribute to the observed associations. Details such as specific hormone formulations, doses, routes of administration, duration of therapy, and adjudicated cardiovascular outcomes were not reported in the source article. Authors and commentators therefore call for confirmation of these findings in randomized clinical trials before definitive conclusions about causal benefit and treatment recommendations can be made.
This analysis reinforces the concept that the timing of menopausal hormone therapy initiation may influence cardiovascular associations and that vasomotor symptoms can be a marker of elevated future cardiovascular risk. For clinicians, the findings support discussing cardiovascular risk assessment alongside symptom management when counselling perimenopausal and early postmenopausal patients. Decisions about MHT should be individualized, weighing symptom severity, cardiovascular risk profile, potential benefits and harms, and patient preferences. The study expands evidence by including perimenopausal women and examining initiation timing, but definitive practice changes await randomized trials and more detailed data on formulations and duration.