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Overweight Women with Polycystic Ovary Syndrome Have Evidence of Subclinical Cardiovascular Disease

Monash University Department of Medicine, Dandenong Hospital, Melbourne, Victoria 3175, Australia

Address all correspondence and requests for reprints to: Dr. Helena Teede, Department of Vascular Science and Medicine, Dandenong Hospital, David Street, Dandenong Victoria 3175, Australia. E-mail: helena.teede{at}med.monash.edu.au.

Context: Polycystic ovary syndrome (PCOS) is associated with insulin resistance (IR) and the metabolic syndrome. There are no adequate data demonstrating significantly increased cardiovascular disease (CVD) mortality. In the absence of clinical outcome studies, surrogate markers of early CVD can provide insight into early CVD.

Objective: The aim of this study was to clarify whether overweight women with PCOS have an increased prevalence of cardiovascular risk factors and early CVD, compared with age- and body mass index-matched controls, to determine the contribution of PCOS per se to CVD status.

Design and Patients: This was a case control study of 100 overweight women with PCOS and 20 subjects of similar body mass index and age.

Main Outcome Measures: Noninvasive markers of early CVD [carotid intimal media thickness, pulse wave velocity (PWV), and brachial arterial flow-mediated vasodilation] were measured. Metabolic parameters studied included insulin, glucose, C-reactive protein, lipids, and androgens.

Results: Subjects with PCOS had elevated testosterone (2.5 ± 0.2 vs. 1.3 ± 0.1 nmol/liter), dehydroepiandrosterone sulfate (4.9 ± 0.3 vs. 3.6 ± 0.4 mmol/liter), fasting insulin (19.6 ± 1.4 vs. 6.8 ± 0.8 µU/ml), and homeostasis model assessment of IR (4.1 ± 0.3 vs. 1.3 ± 0.2), compared with controls. In addition, those with PCOS had elevated cholesterol (5.1 ± 0.1 vs. 4.6 ± 0.2 mmol/liter) and triglycerides (1.4 ± 0.1 vs. 0.9 ± 0.1 mmol/liter), whereas there were no differences in either C-reactive protein or 24-h ambulatory blood pressure parameters. Subjects with PCOS also had increased arterial stiffness (PWV, 7.4 ± 0.1 vs. 6.6 ± 0.2 m/sec) and endothelial dysfunction (flow-mediated vasodilation, 9.8 ± 0.4 vs. 13.3 ± 0.9), compared with controls. There was no difference in mean intimal media thickness between the groups. Stepwise regression in PCOS subjects showed that IR and lipids were independent predictors of PWV.

Conclusion: Overweight women with PCOS have increased cardiovascular risk factors and evidence of early CVD, compared with weight-matched controls, potentially related to IR.

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