Vascular function in the diagnostic categories of polycystic ovary syndrome

• Published in: Human reproduction (Oxford) 2011-08, Vol.26 (8), p.2192-2199
• Main Authors: Moran, Lisa J., Cameron, James D., Strauss, Boyd J., Teede, Helena J.
• Format: Article
• Language: English
• Subjects: Adult; Arginine - analogs & derivatives; Arginine - blood; Biological and medical sciences; C-Reactive Protein - metabolism; Cardiovascular Diseases - etiology; Cardiovascular Diseases - physiopathology; Cross-Sectional Studies; Endothelium, Vascular - physiopathology; Female; Gynecology. Andrology. Obstetrics; Humans; Insulin Resistance; Medical sciences; Overweight - complications; Phenotype; Plasminogen Activator Inhibitor 1 - blood; Polycystic Ovary Syndrome - diagnosis; Polycystic Ovary Syndrome - physiopathology; Vascular Resistance
• ISSN: 0268-1161; 1460-2350
• DOI: 10.1093/humrep/der159

BACKGROUND Polycystic ovary syndrome (PCOS) is associated with increased risk of cardiovascular disease (CVD). However, it is unknown whether CVD risk is equivalent across the different diagnostic categories or phenotypes of PCOS, particularly in the new phenotypes that affect up to 50% of women with PCOS. Surrogate markers of CVD include endothelial function and arterial stiffness that are independent risk factors for CVD. The primary aim of this study was to assess whether milder phenotypes of PCOS have elevated CVD risk compared with controls. METHODS This was a cross-sectional study, conducted in an academic medical centre, of overweight premenopausal women with either National Institute of Health (NIH) PCOS (n = 29) or milder non-NIH PCOS (n = 25) and controls without PCOS (n = 27). Primary outcomes were markers of vascular health, including endothelial function [peripheral arterial tonometry (PAT), asymmetric dimethylarginine (ADMA) and plasminogen activator inhibitor-1 (PAI-1)] and arterial stiffness [central pulse wave velocity (PWVc)]. Secondary outcomes were insulin resistance, glucose tolerance and inflammation (C-reactive protein). RESULTS ADMA was significantly different across the three groups (P = 0.003). ADMA was similar for NIH and non-NIH PCOS (0.56 ± 0.01 versus 0.53 ± 0.02 µmol/l, P = 1.0) and higher for both NIH PCOS compared with controls (0.56 ± 0.01 versus 0.46 ± 0.02 µmol/l, P = 0.003) and non-NIH PCOS compared with controls (0.53 ± 0.02 versus 0.46 ± 0.02 µmol/l, P = 0.046). PAI-1 (P = 0.20), PAT (P = 0.95) and PWVc (P = 0.67) were similar for the three groups. All results were maintained after adjustment for age and body mass index where significant differences in these potentially confounding factors occurred between groups. CONCLUSIONS Women with NIH and non-NIH PCOS have elevated ADMA compared with controls independent of age and adiposity. This suggests that CVD risk, reflected by endothelial dysfunction, is increased in both traditional NIH and new milder non-NIH PCOS phenotypes. However, no differences in other markers of endothelial function or arterial stiffness were apparent between phenotypes in this PCOS cohort.