Detailed definition
Premenopausal women have lower cardiovascular event rates than age-matched men, partly because of estrogen's favorable effects on lipid profiles, vascular endothelial function, and metabolic markers. After menopause, this advantage erodes: LDL rises, HDL may fall, visceral adiposity increases, and insulin sensitivity often worsens. Cardiovascular event rates in postmenopausal women approach those of men of the same age within 10–15 years. Within the timing hypothesis framework, HRT started within 10 years of menopause has neutral or favorable cardiovascular signals (KEEPS, ELITE, observational data); HRT started after age 60 has neutral or unfavorable signals (WHI in older subgroup). Mechanistically, healthy early-postmenopausal endothelium responds favorably to estrogen, while atherosclerotic later-postmenopausal vasculature may not. Foundational cardiovascular risk reduction in midlife women includes blood pressure control, lipid management, weight and waist management, smoking cessation, and physical activity.
Why it matters in menopause
For a 52-year-old woman with vasomotor symptoms and average cardiovascular risk, initiating transdermal estradiol within the timing window has a generally favorable cardiovascular signal alongside symptom benefit. For a 65-year-old woman with established coronary disease who has never been on HRT, the calculus is different and HRT is not first-line for cardioprotection.
Related terms
Sources
External references: Wikipedia.