女性在停經後心血管疾病的發生率較停經前增加，其冠心病臨床表徵亦與男性不同，性別間賀爾蒙的差異可能為原因之一。女性賀爾蒙雌激素主要負責女性的生殖功能，透過雌激素受器的基因作用，影響細胞核內訊息RNA以及蛋白質的合成與表現，亦可藉由非基因作用，產生不同的訊息傳遞路徑而影響細胞反應。雌激素可以增加血管內皮的一氧化氮合成與釋放，使血管擴張；在血管平滑肌細胞，雌激素則可調節細胞膜上的離子通道，使血管放鬆，產生擴張的效果；雌激素還具有抗氧化的作用，可減少內皮與平滑肌細胞凋亡的作用，與冠狀動脈疾病息息相關。此外，雌激素可增加心肌細胞中的心房利鈉肽與腦利鈉肽，使血管擴張；抑制p38α引發的心肌細胞凋亡訊息路徑，且可抑制調鈣素活性，而維持細胞中鈣離子濃度的恆定性，以減少左心室肥大。然而，對於停經後女性心血管疾病的預防與治療效果，臨床研究結果發現使用雌激素賀爾蒙療法有增加血管栓塞的副作用。雌激素在心血管系統的作用仍有待更多研究探討可能的細胞生理反應與臨床效應。

The increasing incidence of coronary artery disease (CAD) after menopause and the different clinical manifestations of CAD between males and females might be due to sex hormonal differences. By regulating the activities and expression levels of signal molecules, female hormone estrogens regulate cell function through estrogen receptors, which includes genomic and nongenomic activities. Estrogens upregulate nitric oxide synthase and release nitric oxide in endothelial cells, thus inducing vasodilatation. Estrogens are also able to activate signal pathways that regulate ion channels, which can cause smooth muscle to relax. There are anti-apoptosis and anti-oxidation effects of estrogens on endothelium and vascular smooth muscle that are also beneficial to vasodilatation. Furthermore, estrogens can act on cardiomyocytes through increased atrial natriuretic peptide and brain natriuretic peptide levels; inhibition of the p38α apoptosis signal pathway, and antagonization by calcineurin, which maintains cytosolic calcium hemostasis. These effects of estrogens might help to prevent progression of ventricular hypertrophy. Postmenopausal estrogens insufficiency may account for the increased incidence of cardiovascular disease among older women; however the clinical use of hormone replacement therapy is still controversial due to adverse embolic effects. More research is necessary to determine the appropriate therapeutic intervention in terms of estrogens and the choice needs to be based on both clinical impacts and biomolecular activity.