Testosterone and cardiovascular disease in women

By contrast to the neutral or even beneficial associations between endogenous testosterone levels and cardiovascular disease for men, the few retrospective or cross-sectional case-control studies in women revealed pro-atherogenic associations of androgens with CAD (Wu and von Eckardstein 2003). Only scanty prospective data is available on the importance of testosterone as a cardiovascular risk factor in women. Barrett-Connor and Goodman-Gruen(1995) reported a 19-year follow-up of 651 postmenopausal women. Serum levels of testosterone, bioavailable testosterone, and androstendione did not differ between those women with and those without a coronary artery disease history at baseline. Cardiovascular mortality during follow-up was not associated with any androgen serum level (Barrett-Connor and Goodman-Gruen 1995).

Indirect evidence for the atherogenicity of androgens in women was derived from the findings of clinical studies that women with coronary artery disease were affected more frequently than control women by clinical symptoms of androgen excess such as hirsutism and polycystic ovaries (Amowitz and Sobel 1999; Dunaif 1997; Lobo and Carmina 2000; Rajkhova etal. 2000). Cross-sectional data consistently showed a strong obesity-independent association with a cluster of cardiovascular risk factors including insulin resistance, dyslipidaemia and impaired fibrinolysis. It was therefore suggested that the chronically abnormal hormonal and metabolic milieu in the polycystic ovary syndrome (PCOS), starting from adolescence, may predispose these women to premature atherosclerosis. Based on calculated risk profiles, women with polycystic ovary syndrome were predicted to have a 7-fold increased relative risk for myocardial infarction. In agreement with this concept, a combined angiography and pelvic ultrasound study of 143 women aged <60 years observed significant associations between the presence of polycystic ovaries with the presence and severity of coronary artery disease and a family history of myocardial infarction as well as with elevated levels of insulin and triglycerides and lower levels of HDL-C (Birdsall etal. 1997). In an electronbeam computer tomography study, non-diabetic women with the polycystic ovary syndrome showed more coronary artery calcification, a marker of coronary atherosclerosis, than healthy controls matched by age and body mass index (Christian et al. 2003). Two case-control studies found significantly increased carotid artery intima-media thickness in women with PCOS compared to age-matched controls independently of BMI, fat distribution and other risk factors (Guzick et al. 1996; Talbott et al. 2000). By contrast to these data, the one and only long-term longitudinal study did not find any association between PCOS and coronary artery disease incidence. The authors compared the mortality and morbidity rates of 786 out of 1028 women diagnosed to have PCOS between 1930-1979 with 1060 age-matched control women over a mean period of 30 years. Despite significantly increased prevalences of diabetes, hypertension, and hypercholesterolemia among women with PCOS, the standardised odds ratios of coronary artery disease mortality and coronary artery disease morbidity were only little and insignificantly increased in women with PCOS (Pierpoint etal. 1998; Wild et al. 2000). Hence coronary artery disease risk in women with PCOS may have been overestimated previously. It may, however, also be that treatment of women with PCOS with estrogens have counteracted the effects of increased risk factors and pre-symptomatic disease.

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