P283 - ATHEROSCLEROTIC CARDIOVASCULAR DISEASE, CARDIAC FUNCTION AND ATHEROGENIC DYSLIPIDEMIA IN YOUNG WOMEN WITH AND WITHOUT POLYCYSTIC OVARY SYNDROME: A STUDY ON THE NATURAL HISTORY OF CARDIOVASCULAR RISK

Background: Polycystic ovary syndrome (PCOS) is associated with increased cardiometabolic risk and cardiovascular disease (CVD). We have shown high-risk young adolescents and women with and without PCOS exhibit atherogenic dyslipidemia and atherosclerotic CVD (ACVD), and impaired cardiac function compared to healthy-weight controls. The aim of this study was to determine the natural history of cardiometabolic risk factors, carotid intimal medial thickness (cIMT) and cardiac function in young adolescents and women with and without PCOS.

METHODS AND RESULTS: Datasets from the PCOS-Together (n=80, Canadian) and Androgens and Insulin Resistance Study (n=88, AIRS Children's Hospital Colorado, USA) were combined and harmonized for age-BMI matched (BMI >25 kg/m2) females aged 12-45 years with (PCOS) and without PCOS (non-PCOS control), and non-PCOS healthy-weight controls (BMI < 25 kg/m2). Data included biochemical assessments (blood lipids, apoB, remnant-cholesterol, hormones, insulin, glucose). 2D/3D-echocardiography was performed and carotid intimal medial thickness (cIMT) and cardiac function indices collected. Data from PCOS and non-PCOS controls were compared to non-PCOS healthy-weight controls in age groups: 12-19, 20-29 and 30-45

Free Testosterone, fasting triglycerides, remnant-cholesterol, apoB, non-HDL-C, LDL-C, insulin and HOMA-IR were increased in PCOS and non-PCOS controls, compared to healthy-weight controls at all age groups. cIMT, cardiac left ventricular (LV) mass and LV posterior wall thickness tended to be higher in PCOS and non-PCOS controls across all age groups, and increased by 10-20% at 30-45 yrs compared to healthy-weight controls. Cardiac E/A ratio was lower in PCOS and non-PCOS controls across all age groups, and declined in those with PCOS at 30-45 yrs. LV ejection fraction was lower in those with PCOS at 20-29 and 30-45 yrs, and LV global longitudinal strain was impaired in PCOS and non-PCOS controls at 30-45 yrs compared to healthy-weight controls.

Conclusion: Our data shows the natural history of ACVD and impaired cardiac morphology and function in young women with and without PCOS, and these outcomes tend to be exacerbated in those with PCOS. Recommendations to develop early screening and detection protocols, and studies to develop targeted interventions to mitigate CVD development in high-risk young women with and without PCOS are warranted.