Key result
AE-PCOS is linked to ~1 mmHg greater diastolic blood pressure variability versus controls.
Why the study?
AE-PCOS is linked to hypertension and cardiovascular risk, but little is known about beat-to-beat BPV in this population despite prior evidence of blunted baroreflex sensitivity.
Is androgen excess polycystic ovary syndrome associated with greater beat-to-beat blood pressure variability in adult women compared to overweight/obese and lean controls?
Cross-Sectional (n=46)
Is androgen excess polycystic ovary syndrome associated with greater beat-to-beat blood pressure variability in adult women compared to overweight/obese and lean controls?
Women with androgen excess polycystic ovary syndrome exhibit greater beat-to-beat blood pressure variability, a marker of cardiovascular risk, which is not solely explained by obesity.
Alerts clinicians to possible CV risk via BP variability in AE-PCOS; leaves open prognostic value and needs larger trials.
Androgen excess polycystic ovary syndrome (AE-PCOS) is associated with elevated risk for hypertension and cardiovascular disease. Greater beat-to-beat blood pressure variability (BPV) has emerged as a novel marker of cardiovascular risk. Little is known about beat-to-beat BPV in AE-PCOS, but prior studies suggest blunted baroreflex sensitivity (BRS), a major contributor to beat-to-beat BP regulation. Both obesity and androgen excess are implicated as driving factors of cardiovascular risk in AE-PCOS. We hypothesized that 1) beat-to-beat BPV would be greater in AE-PCOS compared to both women with overweight/obesity (OW/OB) and lean controls; 2) beat-to-beat BPV would be augmented in OW/OB compared to lean controls. We measured beat-to-beat BP (finger photoplethysmography) during ~5-10 minutes of supine rest in 18 lean controls, 14 OW/OB controls, and 14 women with AE-PCOS. Serum testosterone was measured and spontaneous cardiovagal BRS was assessed via sequence technique. In AE-PCOS, resting BP was greater than lean controls (P<0.05) and serum testosterone greater than both control groups (P<0.001). Diastolic BP standard deviation was greater in AE-PCOS (3.9 ± 1.0 mmHg) compared to both control groups (lean: 3.0 ± 1.5; OW/OB: 2.9 ± 1.2 mmHg; P=0.007). Cardiovagal BRS was not different between groups (P=0.196). Neither cardiovagal BRS nor serum testosterone were related to beat-to-beat BPV in AE-PCOS. Collectively, these data suggest greater beat-to-beat BPV in AE-PCOS which cannot be accounted for by obesity alone and is not associated with cardiovagal BRS or circulating androgens.
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Young et al. (2026) conducted a cross-sectional in Androgen excess polycystic ovary syndrome (n=46). Androgen excess polycystic ovary syndrome vs. Lean and overweight/obese controls was evaluated on Diastolic blood pressure standard deviation (p=0.007). Women with AE-PCOS had greater diastolic blood pressure variability (3.9 ± 1.0 mmHg) than lean (3.0 ± 1.5 mmHg) and overweight/obese controls (2.9 ± 1.2 mmHg; P=0.007).
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