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Arterial stiffness is increased in asymptomatic nondiabetic postmenopausal women with a polycystic ovary syndrome phenotype

Armeni, Elenia; Stamatelopoulos, Kimonb; Rizos, Demetriosc; Georgiopoulos, Georgeb; Kazani, Mariab; Kazani, Aikaterinia; Kolyviras, Athanasiosb; Stellos, Konstantinosb; Panoulis, Konstantinosa; Alexandrou, Andreasa; Creatsa, Mariaa; Papamichael, Christosb; Lambrinoudaki, Irenea

doi: 10.1097/HJH.0b013e3283630362
ORIGINAL PAPERS: Metabolic syndrome

Objective: The metabolic dysfunction accompanying the polycystic ovary syndrome (PCOS) may increase the risk of hypertension and cardiovascular disease (CVD). Although menopause per se may be an additional risk factor of CVD, the association between PCOS in postmenopausal women and cardiovascular risk has not been adequately investigated. We aimed to evaluate the effect of PCOS on markers of subclinical atherosclerosis in nondiabetic postmenopausal women.

Methods: This cross-sectional study included 286 postmenopausal women with intact ovaries. PCOS phenotype was defined if three of the following were present: insulin resistance, current hyperandrogenism or history of clinical androgen excess, history of infertility, central obesity and history of irregular menses. Traditional CVD risk factors, as well as indices of arterial structure (intima–media thickness, atheromatous plaques presence) and function [flow-mediated dilation, pulse wave velocity (PWV), augmentation index] were compared between women with a PCOS phenotype and the rest of the sample, who served as controls.

Results: Women with the PCOS phenotype (N = 43) had higher SBP and triglycerides and lower high-density lipoprotein (HDL)-cholesterol than controls. Mean values of PWV differed significantly between PCOS cases and controls (9.46 ± 1.74 vs. 8.60 ± 1.51 m/s, P = 0.001, univariate). Multivariate regression analysis showed that the PCOS phenotype, age and SBP were the only independent predictors of PWV.

Conclusion: Arterial stiffness is increased in asymptomatic, nondiabetic women with a putative PCOS phenotype, independently of age, BMI or blood pressure. This might present one mechanism through which PCOS increases the risk of CVD and hypertension later in life.

a2nd Department of Obstetrics and Gynecology, University of Athens, Aretaieio Hospital

bDepartment of Therapeutics, University of Athens, Alexandra Hospital

cHormonal Laboratory, University of Athens, Aretaieio Hospital, Athens, Greece

Correspondence to Irene Lambrinoudaki, 2nd Department of Obstetrics and Gynecology, University of Athens, Aretaieio Hospital, 27, Themistokleous Street, Dionysos, GR-14578 Athens, Greece. Tel: +30 210 6410944; fax: +30 210 6410325; e-mail:

Abbreviations: CCA, common carotid artery; CVD, cardiovascular disease; E2, estradiol; FAI, free androgen index; FEI, free oestrogen index; FMD, flow-mediated dilation; FSH, follicle-stimulating hormone; HDL-cholesterol, high-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment of insulin resistance; ICA, internal carotid artery; IMT, intima–media thickness; LDL-cholesterol, low-density lipoprotein cholesterol; PCOS, polycystic ovary syndrome; PWV, pulse wave velocity; SHBG, sex hormone binding globulin; WHR, waist-to-hip ratio

Received 27 September, 2012

Revised 22 April, 2013

Accepted 6 May, 2013

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins