Association of Polycystic Ovarian Syndrome with Endothelial Health, Cardiovascular Risk, and Cellular Aging

Objective: To study measures of endothelial health, cardiovascular risk, and cellular aging between PCOS patients and a reproductive age normative cohort.

Design: Cross-sectional study.

Subjects: Community-based PCOS patients and a normative ovarian aging cohort as controls, aged 45 or younger at the time of evaluation.

Exposure: Non-invasive measure of endothelial health measured by the EndoPAT reactive hyperemia index (RHI).

Main outcome measure(s): RHI as measure of endothelial health. Secondary outcomes included Framingham score, telomere length (TL) and mitochondria DNA (mtDNA) copy number from leukocyte cells.

Results: Our cohort included 63 PCOS participants and 130 non-PCOS participants. Mean age was significantly lower in the PCOS cohort (33.1, SD 4.7 years) compared to the non-PCOS cohort (40.8, SD 2.9 years). In multivariable-adjusted models, we found PCOS was significantly associated with endothelial dysfunction as both a categorical (OR for PCOS 0.31, 95% CI 0.10-0.97, p=0.044) and continuous (PCOS coefficient -0.37, 95% CI -0.69 to -0.05, p=0.026) outcome. For secondary outcomes, PCOS status was not significantly associated with mitochondrial DNA (PCOS coefficient -48.1, 95% CI -175.0 to 78.9, p=0.46), telomere length (PCOS coefficient 0.05, 95% CI -0.05 to 0.15, p=0.33), Framingham score (PCOS coefficient 0.002, 95% CI -0.01 to 0.02, p=0.81), or metabolic syndrome (OR for PCOS 1.29, 95% CI 0.31-5.44, p=0.73).

Conclusions: Our findings suggest that PCOS patients have impaired endothelial function compared to non-PCOS patients, though measures of cellular aging and cardiovascular risk as measured by the Framingham score did not differ between the cohorts.