Key result
Each 1-SD increase in the CRP-LAP-pulse pressure (CLP) composite was associated with a 22% higher hazard of incident CVD (HR 1.22; 95% CI 1.16-1.28; P<0.001) across adapted CKM stages.
Why the study?
Cardiovascular-kidney-metabolic (CKM) stages summarize disease progression but may conceal variation in biological burden and cardiovascular risk. Whether a composite of C-reactive protein, lipid accumulation product, and pulse pressure is associated with incident CVD and absolute-risk gradients within adapted CKM stages required investigation.
Is a higher composite score of C-reactive protein, lipid accumulation product, and pulse pressure (CLP) associated with an increased risk of incident cardiovascular disease and absolute-risk gradients across adapted CKM stages in middle-aged and older Chinese adults without baseline CVD?
Cohort (n=7,779)
Yes
Is a higher composite score of C-reactive protein, lipid accumulation product, and pulse pressure (CLP) associated with an increased risk of incident cardiovascular disease and absolute-risk gradients across adapted CKM stages in middle-aged and older Chinese adults without baseline CVD?
A composite index combining C-reactive protein, lipid accumulation product, and pulse pressure independently predicts 9-year incident cardiovascular disease and uncovers substantial absolute-risk heterogeneity within categorical CKM stages, particularly stage 2.
Answers are grounded in this paper and cite their sources.
May refine absolute CVD risk within CKM stages; extends heterogeneity observations but remains hypothesis-generating pending validation.
Cardiovascular-kidney-metabolic (CKM) stages summarize disease progression but may conceal variation in biological burden and cardiovascular risk. We investigated whether a composite of C-reactive protein (CRP), lipid accumulation product (LAP), and pulse pressure (PP) was associated with incident cardiovascular disease (CVD) and absolute-risk gradients within adapted CKM stages. This prospective analysis included 7779 CHARLS participants aged 45 years or older without baseline CVD. CLP was calculated as the equal-weight sum of standardized ln(CRP + 1), ln(LAP), and PP. During a median follow-up of 9.0 years, 1911 CVD events occurred. Each 1-SD higher CLP was associated with higher CVD hazard after multivariable adjustment (hazard ratio, 1.22; 95% confidence interval, 1.16–1.28); the hazard ratio for quartile 4 versus quartile 1 was 1.85 (1.60–2.13). Nine-year cumulative incidence increased from 13.9% to 27.8% across CLP quartiles and from 16.2% to 29.8% within adapted stage 2. Relative associations did not differ significantly across stages (P for interaction = 0.147). Results were robust in competing-risk, selection-weighted, and alternative event-time analyses. CLP captured continuous multidomain burden and identified substantial absolute-risk heterogeneity within adapted CKM stages. These findings support epidemiologic characterization and require external validation before clinical use.
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Ren¹ et al. (2026) conducted a cohort in Cardiovascular-kidney-metabolic (CKM) stages 0-3 without baseline cardiovascular disease (n=7,779). C-reactive protein-lipid accumulation product-pulse pressure (CLP) composite (per 1-SD increment and Quartile 4 vs Quartile 1) vs. Lower CLP levels (per 1-SD decrement or Quartile 1 reference) was evaluated on Incident cardiovascular disease (composite of physician-diagnosed heart disease and/or stroke) (HR 1.22 per 1-SD (HR 1.85 for Q4 vs Q1), 95% CI 1.16-1.28, p=<0.001). Each 1-SD increase in the CRP-LAP-pulse pressure (CLP) composite was associated with a 22% higher hazard of incident CVD (HR 1.22; 95% CI 1.16-1.28; P<0.001) across adapted CKM stages.
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