Complement Components C1r and C8 Serve as Potential Inflammatory Biomarkers for Coronary Heart Disease Severity: The
Xia Feng1,2,3,4, Xiaoting Jiang1,2,3,4, Shaolin Gong1,2,3,4
1Department of Cardiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, People's Republic of China.
Insights
Serum C1r and C8 are elevated in coronary heart disease (CHD) and predict stenosis severity. The complement-CRP axis plays a key role in CHD risk stratification and lesion assessment.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarker Discovery
Background:
- Inflammation is integral to the development and progression of coronary heart disease (CHD).
- Identifying reliable biomarkers for CHD severity is crucial for risk stratification and patient management.
- The complement system and C-reactive protein (CRP) are implicated in inflammatory processes relevant to atherosclerosis.
Purpose of the Study:
- To investigate serum complement components (C1r, C1s, C7, C8, C9) as potential biomarkers for CHD.
- To assess the mediating role of C-reactive protein (CRP) in the relationship between complement levels and CHD severity.
- To quantify CHD severity using the Gensini score.
Main Methods:
- A prospective cross-sectional study involving 314 patients (102 controls, 212 with CHD).
- Coronary angiography was used for CHD diagnosis and Gensini score calculation to quantify stenosis severity.
- Serum complement levels were measured via ELISA; statistical analyses included Spearman correlation, multivariate logistic regression, ROC analysis, and mediation modeling.
Main Results:
- Serum C1r and C8 levels were significantly higher in patients with CHD and severe coronary stenosis.
- C1r and C8 showed positive correlations with the Gensini score and cardiac troponin T (cTnT).
- C1r was an independent predictor of moderate-to-severe stenosis (OR=2.10), and C8 also showed significance (OR=1.98). Mediation analysis revealed CRP mediated 31.6% and 46.2% of the effects of C1r and C8 on disease severity, respectively. The combined AUC for C1r and C8 was 0.769.
Conclusions:
- Serum C1r is an independent predictor of coronary heart disease severity.
- Serum C8 demonstrates a dose-dependent association with CHD severity, influenced by systemic factors.
- The complement-CRP axis is pivotal in CHD risk stratification, offering valuable insights for inflammatory biomarker assessment in coronary lesions.
Purpose:
Inflammation plays an important role in the occurrence and development of coronary heart disease (CHD). We investigated serum complement C1r, C1s, C7, C8, C9 as potential biomarkers and the mediating role of C-reactive protein (CRP) in CHD severity. The severity of coronary artery stenosis was quantified using the validated Gensini score.
Patients And Methods:
In this prospective cross-sectional study (n=314), patients were categorized into a control group (n=102) and a CHD group (n=212) via coronary angiography. CHD severity was quantified by the Gensini score (mild ≤31; moderate-to-severe >31). The study incorporated multiple known pathogenic factors such as demographic characteristics, underlying diseases, and metabolic indicators for comprehensive analysis. Serum complement levels were measured by ELISA. Spearman correlation, multivariate logistic regression, ROC analysis, and mediation modeling assessed associations and CRP's role.
Results:
Serum C1r and C8 were significantly elevated in CHD and severe stenosis groups. While C1s showed a slight increase in the severe stenosis group, it, along with C7 and C9, showed limited overall diagnostic utility for CHD. Spearman analysis revealed that C1r and C8 were positively correlated with both Gensini score and cTnT levels. In the fully adjusted model (Model 4), C1r remained a robust independent predictor of moderate-to-severe stenosis (continuous OR=2.10, 95% CI: 1.41-3.12; Q4 vs Q1 OR=5.61, 95% CI: 2.12-14.89). C8 also maintained statistical significance as a continuous variable (OR=1.98, P=0.004). Furthermore, mediation analysis indicated that CRP mediated 31.6% and 46.2% of the effects of C1r and C8 on disease severity, respectively. The combined AUC of C1r and C8 for predicting CHD was 0.769.
Conclusion:
C1r is an independent predictor of CHD severity, while C8 exhibits a dose-dependent association modulated by systemic status. Integrating anatomical and physiological markers confirms the complement-CRP axis's pivotal role in CHD risk stratification, providing evidence for inflammatory biomarkers in lesion assessment.
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