Key result
Non-obese women with PCOS had a significantly reduced number of circulating CD34+133+ vascular progenitor cells (317.5 vs 558.3) and increased central arterial stiffness compared to healthy controls.
Why the study?
Does non-obese PCOS associate with reduced vascular progenitor cell number/function and increased central arterial stiffness compared to healthy controls?
Cross-Sectional (n=26)
No
Does non-obese PCOS associate with reduced vascular progenitor cell number/function and increased central arterial stiffness compared to healthy controls?
Non-obese women with PCOS exhibit reduced circulating vascular progenitor cells and increased central arterial stiffness, suggesting early vascular aging that may contribute to their increased cardiovascular risk.
Answers are grounded in this paper and cite their sources.
Non-obese PCOS associated with early vascular changes; hypothesis-generating and should not yet change practice.
OBJECTIVE: Subjects with Polycystic ovarian syndrome (PCOS) are at increased risk of Type 2 diabetes mellitus (T2DM). The mechanism of this enhanced risk is unclear. Circulating vascular progenitor cells (VPC) are immature bone marrow derived cells capable of differentiating into mature endothelial cells. VPC number/function and central arterial stiffness predict cardio-metabolic disease in at-risk populations. DESIGN: We studied VPC and arterial stiffness measures in non-obese PCOS subjects as compared to age and body mass index (BMI) matched healthy controls in a cross-sectional study. METHODS: Fourteen subjects with PCOS and 12 controls of similar age, BMI (all <30 kg/m(2)) and metabolic profile were studied. VPC number and in vitro function were studied by flow cytometry and tube formation assays respectively. Augmentation index (AIx), a measure of central arterial stiffness, and central (aortic) blood pressures (BP) were measured by applanation tonometry. RESULTS: Subjects with PCOS had a reduced number, mean±SEM, of circulating CD34(+)133(+) VPCs (317.5±51.0 vs. 558.3±101.2, p = 0.03) and impaired in vitro tube formation (completed tube area 1.0±0.06 vs. 1.2±0.05×10(6) µm(2) p = 0.02). PCOS subjects had significantly higher AIx (18.4±1.9% vs. 4.9±2.0%) and this difference remained significant even after adjustments for age, BMI and smoking (p = 0.003) in multivariate analyses. Central systolic and pulse pressure were higher in PCOS subjects but these differences were not statistically significant after adjustment for age. Brachial systolic and pulse pressures were similar. VPC number/function and arterial stiffness or BP measures were not correlated. CONCLUSIONS: Non-obese PCOS is characterized by a reduced VPC number, impaired VPC function and increased central arterial stiffness. These changes in novel vascular risk markers may explain the enhanced risk of T2DM and CVD in PCOS.
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Dessapt-Baradez et al. (2011) conducted a cross-sectional in Polycystic Ovary Syndrome (n=26). Polycystic Ovary Syndrome vs. Healthy controls matched for age and BMI was evaluated on Circulating CD34+133+ vascular progenitor cell (VPC) number per 10^6 lymphomonocyte events (p=0.03). Non-obese women with PCOS had a significantly reduced number of circulating CD34+133+ vascular progenitor cells (317.5 vs 558.3) and increased central arterial stiffness compared to healthy controls.
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