Key result
Smoking–low HDL-C phenotype is linked to ~140% higher odds of high carotid plaque burden.
Why the study?
Community-dwelling individuals at high cardiovascular risk are clinically heterogeneous, but whether distinct clinical-metabolic phenotypes differ in carotid plaque burden remains unclear.
Do distinct clinical-metabolic risk phenotypes associate with different levels of carotid plaque burden in community-dwelling individuals at high cardiovascular risk?
Cross-Sectional (n=1,015)
Yes
Do distinct clinical-metabolic risk phenotypes associate with different levels of carotid plaque burden in community-dwelling individuals at high cardiovascular risk?
Distinct clinical-metabolic phenotypes, particularly blood pressure-loaded and smoking-low HDL-C patterns, are associated with significantly higher carotid plaque burden in high-risk community-dwelling individuals, highlighting substantial vascular heterogeneity within this population.
May stratify plaque risk via metabolic phenotypes in high-risk cohorts; leaves open causal links and need for prospective validation.
Background: Community-dwelling individuals at high cardiovascular risk are clinically heterogeneous, but whether distinct clinical-metabolic phenotypes differ in carotid plaque burden remains unclear. Methods: From 4191 participants in a community-based screening project conducted in two communities in Guangzhou, 1015 individuals in the high-cardiovascular-risk stage with nonmissing high-plaque-burden status were included. All 1015 participants underwent exploratory clustering using 17 clinical, metabolic, lifestyle-related, and disease-history variables. High plaque burden was defined as bilateral carotid plaques, multiple plaques, or maximum plaque thickness at or above the 75th percentile among plaque-positive participants. Logistic regression examined associations between phenotypes and high plaque burden. Results: Among the 1015 participants included in the clustering analysis, 329 (32.4%) met the definition of high plaque burden. Four phenotypes were identified: relatively low metabolic burden, older age–ASCVD burden, smoking–low HDL-C, and blood pressure-loaded phenotypes. The corresponding prevalences of high plaque burden were 15.9%, 44.4%, 49.7%, and 33.2%. After adjustment for age and sex, all three non-reference phenotypes showed higher odds of high plaque burden. In sensitivity analysis excluding age and prior ASCVD from clustering, the blood pressure-loaded phenotype remained associated with high plaque burden. Conclusions: Four exploratory clinical-metabolic phenotypes showed different levels of carotid plaque burden among community-dwelling individuals at high cardiovascular risk. The blood pressure-loaded and smoking–low HDL-C phenotypes were associated with greater plaque burden and may provide an exploratory framework for describing heterogeneity within high-risk populations.
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Lv et al. (2026) conducted a cross-sectional in High cardiovascular risk (n=1,015). Smoking-low HDL-C phenotype vs. Relatively low metabolic burden phenotype was evaluated on High carotid plaque burden (OR 2.40, 95% CI 1.42-4.08, p=0.001). The smoking-low HDL-C phenotype was associated with significantly higher odds of high carotid plaque burden compared to the relatively low metabolic burden phenotype (OR 2.40).
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