ArticleFrontiers in endocrinology2026
Differences in clinical characteristics and cardiovascular disease risk prediction among Chinese women with polycystic ovary syndrome phenotypes: a cross-sectional study.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Genistein in polycystic ovary syndrome: mechanisms, preclinical evidence, and translational potential.Frontiers in global women's health · 2026Review
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9 authors.
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Abstract
Background: Polycystic ovary syndrome (PCOS) is associated with increased cardiovascular disease (CVD) risk, but differences across phenotypes in Chinese women remain unclear. This study aimed to characterize clinical profiles of PCOS phenotypes, predict CVD risks, and evaluate associations between phenotypes and CVD risk. Methods: A total of 206 women with PCOS were included from an initial cohort of 211 and classified into four phenotypes according to Rotterdam criteria. Clinical data, laboratory results, and imaging measurements were collected. CVD risks were estimated using the China-PAR model. One-way ANOVA and the Kruskal-Wallis test were used for continuous variables, and Pearson's chi-square or Fisher's exact test for categorical variables. Firth logistic regression was employed to assess the association between PCOS phenotypes and CVD risk, and mediation analysis detected the indirect effects. Results: Among 206 patients with PCOS, 104 (50.5%), 36 (17.5%), 19 (9.2%) and 47 (22.8%) were classified as phenotype A, B, C and D. BMI, WC, SBP, and DBP were significantly higher in phenotypes A, B, and C than in D (P<0.05). UA, LDL-C, TG, and HOMA-IR were significantly higher in phenotypes A and B than in D, while HDL-C and ISI-Matsuda were significantly lower (P<0.05). Lifetime CVD risk scores were significantly higher in phenotypes A, B, and C compared with D (P< 0.05), with values of 15.55%, 17.65%, 17.30%, and 9.90%. After adjusting for diet, physical activity, and medication use, phenotypes A (OR 3.18, 95% CI: 1.30-8.84, P = 0.010), B (OR 4.90, 95% CI: 1.58-16.44, P = 0.006), and C (OR 4.67, 95% CI: 1.39-16.64, P = 0.013) were significantly associated with higher odds of high lifetime CVD risk compared with D. The mediating effects of BMI, HOMA-IR, and UA were significant (P< 0.05), with BMI exhibiting the largest mediating effect, accounting for 94.7%, 70.9%, and 42.9% of the total effect in phenotypes A, B, and C compared with D. Conclusions: Our results demonstrated that more adverse clinical abnormalities and significantly higher CVD risk in women with phenotypes A, B, and C compared with D. BMI, HOMA-IR, and UA play a significantly mediating role between phenotypes and CVD risk. This study suggests that it may be necessary to conduct regular CVD risk assessments for patients with different phenotypes of PCOS, in order to guide early individualized treatment strategies, with a focus on weight and metabolic management.
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