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The potential long-term metabolic and vascular consequences of polycystic ovarian syndrome (PCOS), the commonest reproductive endocrine disorder of women, continue to attract considerable interest. There have been numerous reports of perturbances in a range of potential vascular risk parameters in this condition. It is now well appreciated that women with PCOS as a group appear more insulin resistant for a given body mass index (BMI) and, linked to this, are at increased risk of glucose intolerance. They also display slightly raised triglyceride and lower high-density lipoprotein-cholesterol levels compared with women without PCOS and, in concert with this dyslipidemic pattern, exhibit a greater preponderance of smaller denser low-density lipoprotein particles (1). Modest elevations in inflammatory parameters such as C-reactive protein (CRP) (2, 3), indicating subclinical inflammation and independent of degree of obesity, have also been noted in PCOS. Additionally, affected women exhibit endothelial dysfunction in both micro- and macrovasculature (4), perturbation of fibrinolytic pathways (5), and subclinical atherosclerosis (6). Thus, the general thrust of evidence favors an enhanced vascular risk in women with PCOS.

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