Abstract
BACKGROUND: Postmenopausal women face an increased risk of cardiovascular disease (CVD) due to estrogen withdrawal, which exacerbates traditional cardiovascular risk factors such as dyslipidemia, glucose intolerance, and hypertension. Coronary Artery Calcium Score (CACS), a well-established marker of subclinical atherosclerosis, has emerged as a key predictor of adverse cardiovascular events. Despite the recognized association between menopause and heightened CVD risk, there remains a paucity of literature exploring the specific role of menopause in influencing CACS and its implications for cardiovascular morbidity and mortality. AIM: To examine the interplay between menopause, CACS, and cardiovascular health by synthesizing existing literature. METHODS: A comprehensive literature search was conducted using PubMed and Google Scholar, focusing on studies that analyzed CACS in postmenopausal women, including the influence of factors such as hormone therapy, Triglyceride-Glucose index, bone mineral density, lipid metabolism, and type-1 diabetes. Data extraction and synthesis emphasized key patterns, metabolic influences, and potential mechanisms driving coronary calcification in menopause. RESULTS: Findings suggest that menopause contributes to increased CACS through multiple pathways, including altered lipid metabolism, insulin resistance, and arterial stiffness. Additionally, premature menopause is associated with higher CACS and elevated CVD risk. While hormone replacement therapy (HRT) appears to have a protective effect against coronary calcification, further research is needed to clarify its long-term benefits and risks. CONCLUSION: We introduce a novel framework combining CACS with metabolic and hormonal markers, and discuss estrogen-driven mechanisms and HRT considerations in postmenopausal cardiovascular risk. This review underscores the need for targeted cardiovascular risk assessment in postmenopausal women, integrating CACS with other metabolic markers to improve early detection and prevention of CVD in this high-risk population.