Risk factors and possible mechanisms of saphenous vein graft failure after coronary artery bypass surgery

Song, Yanqiu; Guo, Zhigang

doi:10.1097/cm9.0000000000000872

Cited by 4 publications

(2 citation statements)

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“…Estrogen reduces vascular in ammation by reducing monocyte adhesion to vascular endothelial cells through an endoplasmic reticulum-dependent mechanism [20,21]. It improves atherosclerosis by reducing apoptosis of vascular endothelial cells [22] and inhibiting the proliferation and migration of vascular smooth muscle cells [23]. High estrogen levels can also in uence immune function and contribute to the shift of Th1/Th2 and Th17/Treg immune balance toward Th2 and Treg, exerting anti-in ammatory effects [24].…”

Section: Introductionmentioning

confidence: 99%

“…As a metabolic disease, CAD is mainly manifested by disturbance of lipid metabolism causing lipid accumulation in the vascular wall. And it is closely related to the SDOH [22], which are often ignored in the studies focusing on the impact of female hormone levels and CAD [23,24]. The low socioeconomic status, limited formal education, stress levels, poor healthy diet, and limited access to quality health care are often associated with the female gender, resulting in fewer health resources for women [26], which are major confounding factors when comparing sub-groups of CAD patients.…”

Section: Introductionmentioning

confidence: 99%

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Association between the female hormone intake and coronary artery disease in the women: A study based on NHANES 1999-2020

Qu,

Zhang,

et al. 2023

Preprint

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Although many studies have reported the relationship between female hormone intake and the coronary artery disease(CAD) development their association has not been elucidated and defined. Based on data from the Third National Health and Nutrition Examination Survey, this study assessed the relation between female hormone intake and the CAD development in 38745 eligible female participants. Many sociocultural determinants of health (SDOH) factors are significantly related to CAD occurrence and female hormone intake. Stratified analysis of SDOH factors showed that female hormone intake reduces the risk of CAD in women aged ≥ 60 years old. For women who received higher levels of education, female hormone intake is a risk factor for CAD. For women in poverty or wealth, female hormone intake is a risk factor for congestive heart failure and stroke, but it is a protective factor for the four clinical features of CAD for women in middle-income levels. Moreover, for women with menarche at 13–15 years old, menopause at 30–49 years old, and pregnancies 7–9 times, as well as with a low-sugar, low-fat, low-cholesterol diet and proper folic acid intake, female hormone intake have a protective effect on the development of CAD. We conclude that the appropriate female hormone intake plays a protective role in the occurrence of CAD, but it also exerts an adverse effect on CAD under a different SDOH background. It suggested that the patients must be rigorously screened for SODH background in clinical applications of female hormones to exert a protective effect on CAD.

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