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Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
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Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
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Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study

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Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study
Journal Article

Relationship between novel inflammatory markers derived from high-sensitivity C-reactive protein and heart failure: a cross-sectional study

2025
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Overview
Objective High-sensitivity C-reactive protein to HDL-C ratio (HCHR) and high-sensitivity C-reactive protein to lymphocyte count ratio (HCLR) are two novel inflammatory indicators, and heart failure (HF) is linked to chronic inflammation. This study sought to evaluate the link between HCHR, HCLR, and HF. Methods We carried out a cross-sectional investigation using the National Health and Nutrition Examination Survey (NHANES, 2015–2018). We used multivariate logistic regression to determine the association between HCHR, HCLR, and HF, followed by smoothed curve fitting and threshold effect analysis, as well as subgroup analyses of the underlying demographic variables to investigate potential impacts. The receiver operating characteristic curves were employed to examine the correlation between each index and HF. Results This study included 8751 subjects, and multivariate logistic regression after Ln conversion for HCHR and HCLR showed that subjects in the highest tertile of Ln(HCHR) had a significantly higher risk of 45% than those in the lowest tertile in the fully adjusted model 3 (OR = 1.45, 95% CI 1.02–2.07; P for trend = 0.0269), whereas subjects in the highest tertile of Ln(HCLR) had a significantly higher risk of 52% (OR = 1.52, 95% CI 1.07–2.17; P for trend = 0.0184) than those in the lowest tertile. Ln(HCHR) and HF exhibited a nonlinear relationship, with an inflection point of -2.71 and a log-likelihood ratio of 0.024. Subgroup analyses revealed no significant interactions between Ln(HCHR), Ln(HCLR), and specific subgroups (all P for interactions > 0.05). The ROC curve indicated that Ln(HCLR) had the greatest diagnostic efficacy for HF (AUC: 0.638, 95% CI 0.607–0.669), succeeded by Ln(HCHR) (AUC: 0.620, 95% CI 0.589–0.652). Conclusion Our findings indicate that Ln(HCHR) and Ln(HCLR) are positively linked with the prevalence of HF among US adults. Specifically, Ln(HCHR) levels demonstrated a nonlinear correlation with HF, featuring an inflection point at -2.71.