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. 2025 Jan 10:15:1501125.
doi: 10.3389/fimmu.2024.1501125. eCollection 2024.

Higher monomeric C-reactive protein levels are associated with premature coronary artery disease

Affiliations

Higher monomeric C-reactive protein levels are associated with premature coronary artery disease

Ivan Melnikov et al. Front Immunol. .

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.

Keywords: C-reactive protein; atherosclerosis; coronary artery disease; inflammation; mCRP; monomeric C-reactive protein; residual inflammatory cardiovascular risk.

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Conflict of interest statement

The authors declare that this research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Levels of (A) Monomeric C-reactive protein (mCRP) and (B) pentameric C-reactive protein (pCRP) measured using high-sensitivity assay (hsCRP) in patients with (n = 50) and without (n = 53) coronary artery disease (CAD).
Figure 2
Figure 2
A correlation of monomeric C-reactive protein (mCRP) and pentameric C-reactive protein (pCRP) measured using high-sensitivity assay (hsCRP) in the whole sample (n = 103) of study participants.
Figure 3
Figure 3
Monomeric C-reactive protein (mCRP) levels in patients without residual inflammatory cardiovascular risk (hsCRP levels below 2.0 mg/L).
Figure 4
Figure 4
ROC curves showing sensitivity and specificity of monomeric C-reactive protein (mCRP) and high-sensitivity C-reactive protein (hsCRP) levels in classification of patients to the CAD group.

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References

    1. Ridker PM. The time to initiate anti-inflammatory therapy for patients with chronic coronary atherosclerosis has arrived. Circulation. (2023) 148:1071–3. doi: 10.1161/circulationaha.123.066510 - DOI - PubMed
    1. Ridker PM. Anticytokine agents: targeting interleukin signaling pathways for the treatment of atherothrombosis. Circ Res. (2019) 124:437–50. doi: 10.1161/CIRCRESAHA.118.313129 - DOI - PMC - PubMed
    1. Rajab IM, Hart PC, Potempa LA. How C-reactive protein structural isoforms with distinctive bioactivities affect disease progression. Front Immunol. (2020) 11:2126. doi: 10.3389/fimmu.2020.02126 - DOI - PMC - PubMed
    1. Ullah N, Wu Y. Regulation of conformational changes in C-reactive protein alters its bioactivity. Cell Biochem Biophys. (2022) 80:595–608. doi: 10.1007/s12013-022-01089-x - DOI - PubMed
    1. Wu Y, Potempa LA, El Kebir D, Filep JG. C-reactive protein and inflammation: conformational changes affect function. Biol Chem. (2015) 396:1181–97. doi: 10.1515/hsz-2015-0149 - DOI - PubMed