The Silent Vascular Shift: Endothelial Dysfunction and Cardiovascular Risk in Menopausal Women

Cardiovascular disease (CVD) is the leading cause of death among women worldwide, with the risk significantly increasing after menopause. Hormonal changes during menopause influence the pathophysiology of endothelial dysfunction and atherosclerosis. Lowering levels of estrogen causes vascular hardening, decreased nitric oxide bioavailability, and a sharpened inflammatory response, which may contribute to increased cardiovascular risk during middle life in women. To review the role of endothelial health in cardiovascular risk among postmenopausal women, discuss the underlying mechanisms, and explore current management strategies aimed at reducing the incidence and impact of coronary artery disease.

A comprehensive literature search via PubMed, Scopus, and Web of Science (2015-- 2025) via search strings (menopause OR perimenopause OR postmenopause) AND (endothelial dysfunction OR endothelial function OR nitric oxide OR vascular inflammation) AND (cardiovascular disease OR atherosclerosis OR cardiovascular risk) was conducted, with a focus on large epidemiological cohorts, randomized controlled trials, and mechanistic studies.

Postmenopausal women have a higher risk of developing CVD, and they have comparatively deteriorated endothelial dysfunction.

Compared with men, women experience unique changes in lipid profiles, metabolic syndrome, and fat distribution during and after menopause, which increase their cardiovascular risk. Traditional risk factors, such as hypertension, diabetes, smoking, physical inactivity, and obesity, also affect women differently. Hormonal changes during menopause further influence the pathophysiology of endothelial dysfunction and atherosclerosis. Lifestyle interventions, such as structured exercise, show promise for reducing risk, but evidence supporting the use of phytoestrogens and nutraceuticals is limited and heterogeneous.

Menopause is a high-risk critical phase of increased cardiovascular risk through endothelial dysfunction. Multifaceted prevention measures, such as primary early intervention and individualized responses, are necessary to minimize long-term morbidity and mortality.