IJCS | Volume 32, Nº1, January/ February 2019

4 Burlá et al. Vascular changes in polycystic ovarian syndrome Int J Cardiovasc Sci. 2019;32(1)3-9 Original Article Despite the association of PCOS with cardiovascular (CV) risk factors, recent studies showed controversial results regarding the incidence of CV events in women with PCOS. 5,6 A retrospective cohort study in United Kingdom showed a high incidence of DM, myocardial infarction (MI) and angina in women with PCOS, with over a quarter of the elderly individuals having had MI or angina. 5 However, a retrospective cohort study in the United States observed no increase in CV events in PCOS women, 6 which may be explained by different PCOS profiles, androgen levels, insulin resistance and body composition of the populations. 7 Thus, markers of atherosclerosis could be of help in improving CV risk stratification in PCOS women. Endothelial function and vascular stiffness are surrogate markers of early atherosclerosis and can be easily measured by noninvasive methods, such as flow-mediated vasodilation (FMD) and carotid-femoral pulse wave velocity (PWV), respectively. 8,9 Moreover, both FMD and PWV have shown to be independent predictors of CV events in the general population. 10,11 A recent meta-analysis reported that PCOS women have approximately 4% lower FMD, irrespective of bodymass index (BMI) and age. 12 However, there was significant heterogeneity across studies included in this meta- analysis. 12 Previous studies have shown an association between PCOS and PWV, 13,14 but these results could be influenced by age, BMI and comorbidity, in special the presence of hypertension. Other studies that controlled for these confounders did not find a correlation between PCOS and PWV. 15–18 The aimof the present studywas to compare endothelial function and pulse wave reflection between young, overweight women with PCOS and healthy controls. Methods Study population This study recruited 52 consecutive women from the outpatient internal medicine and general gynecology clinics of our institution. We included patients with Rotterdam criteria for PCOS and age between 18-40 years. Exclusion criteria were evidence of secondary hypertension, BMI (calculated as weight divided by height squared) ≥ 35 kg/m², smoking, coronary artery disease, kidney or thyroid disease, hormone replacement therapy, DM or impaired tolerance glucose, severe dyslipidemia (LDL-cholesterol ≥ 4.14 mmol/L and/or triglycerides ≥ 3.39 mmol/L), use of lipid-lowering drugs, prolactin (PRL) > 25 ng/ml or pregnancy. Control group was composed by healthy female patients without PCOS criteria from the same institution. The protocol was approved by the local Ethics Committee Research (2795-CEP/HUPE), and all patients gave written informed consent. PCOS was diagnosed according to the 2003 Rotterdam Criteria with at least two of the following features: oligomenorrhea (or amenorrhea) or hirsutism, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound. Patients with oligomenorrhea or hyperandrogenism caused by any other clinical conditions were excluded, such as nonclassical 21-hydroxylase deficiency, congenital adrenal hyperplasia, hypothyroidism, Cushing’s syndrome, or significant elevation in serum PRL. Laboratory evaluation Venous blood samples were collected after 12 hours of fasting. Serum lipids (total cholesterol, high-density lipoprotein [HDL]-cholesterol, triglycerides), and blood glucose were measured using an auto analyzer technique (Technicon DAX 96; Miles Inc). Low-density lipoprotein (LDL)-cholesterol was calculated with the Friedewald formula when triglyceride values were < 400 mg/dL. Insulin was measured by radioimmunoassay, and serum C-reactive protein levels were measured by nephelometry using an immunochemistry system. Serum levels of testosterone and PRL were measured during the early follicular phase (days 2 to 5 of the menstrual cycle) and dehydroepiandrosterone sulphate (DHEAS) were measured using enzyme-linked immunosorbent assay (ELISAs). Assessment of endothelial function FMD was assessed as a measure of endothelial function. 19 The participant was positioned supine with the arm in a comfortable position, and the brachial artery was imaged above the antecubital fossa. After 10 minutes of rest, the right brachial artery was scanned in longitudinal section, 5 cm above the antecubital fossa, using a linear array transducer to acquire the baseline diameter of the brachial artery. A cuff was then inflated to at least 50 mmHg above systolic blood pressure and deflated after 5 minutes to induce reactive hyperemia. A pulse wave Doppler recording in the artery lumen documented the flow increase, and themaximal diameter 30, 60, and 90 seconds after cuff release was registered.