ArticleFrontiers in immunology2024
Higher monomeric C-reactive protein levels are associated with premature coronary artery disease.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- CRP Is a Key Indicator of Rheumatoid Arthritis-Associated Vascular Injury and Neurodegeneration.International journal of molecular sciences · 2026Review
- Review
- The Role of the Gut Microbiota in Vascular Physiology and Health.International journal of molecular sciences · 2025Review
- Inflammatory markers guide early risk stratification and prognosis in elderly patients with acute myocardial infarction.Scientific reports · 2025Article
- The Pathogenic Role of C-Reactive Protein in Diabetes-Linked Unstable Atherosclerosis.International journal of molecular sciences · 2025Review
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12 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: Chronic inflammation is a major risk factor for coronary artery disease (CAD). Currently, the inflammatory cardiovascular risk is assessed via C-reactive protein (CRP) levels measured using a high-sensitivity assay (hsCRP). Monomeric CRP (mCRP) is a locally produced form of CRP that has emerged as a potential biomarker of inflammation. Aim: This study investigated whether mCRP levels are associated with premature CAD. Materials and methods: This study comprised 103 participants of both sexes, including 50 patients 56 ± 7 years old with premature CAD and 53 patients 51 ± 10 years old without CAD. CAD was verified using coronary angiography, hsCRP levels were measured using a standard assay, and mCRP levels were measured using fluorescent cytometric beads conjugated with an anti-mCRP antibody. Results: The levels of hsCRP were 0.99 (0.59; 3.10) mg/L vs. 0.63 (0.35; 1.85) mg/L (p = 0.067), and mCRP 6.84 (4.20; 13.78) µg/L vs. 2.57 (0.32; 5.66) µg/L (p <0.001) in patients with CAD vs. patients without CAD, respectively. There was a weak positive correlation between the mCRP and hsCRP levels (ρ = 0.214; p = 0.030). hsCRP levels were below 2.0 mg/L (i.e., residual inflammatory cardiovascular risk should have been excluded) in 70% of patients with CAD and 79% of patients without CAD (p = 0.365). mCRP levels differed between the groups of patients with hsCRP levels below 2.0 mg/L: 5.14 (4.07; 10.68) µg/L vs. 2.77 (0.53; 5.00) µg/L in patients with or without CAD, respectively (p <0.001). Logistic regression analysis demonstrated that mCRP levels were independently associated with premature CAD. The adjusted odds ratio was 1.18 (95% CI 1.06-1.33, p = 0.004) per each µg/L increase in mCRP levels. Conclusion: Higher mCRP levels were associated with premature CAD, independent of hsCRP levels and traditional risk factors.
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