Complement C3 and C-reactive protein in male survivors of myocardial infarction
Angela M Carter1, Usha K Prasad, Peter J Grant
1University of Leeds, UK. a.carter@leeds.ac.uk
Insights
Elevated complement C3 levels are independently associated with myocardial infarction (MI), suggesting it may be a more specific inflammatory marker than C-reactive protein (CRP) for cardiovascular disease risk.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarkers
Background:
- Inflammatory processes are integral to cardiovascular disease (CVD) pathogenesis.
- Understanding specific inflammatory markers is crucial for risk assessment.
Purpose of the Study:
- To compare the association of complement C3 and C-reactive protein (CRP) with myocardial infarction (MI).
- To evaluate their relationship with cardiovascular risk factors.
Main Methods:
- Study included 342 Caucasian male patients with MI and 193 age-matched healthy controls.
- Complement C3 and CRP levels were quantified using ELISA.
- Logistic regression and ROC analyses were employed.
Main Results:
- Both C3 and CRP were significantly elevated in MI patients versus controls.
- C3 showed independent association with MI, persisting after adjustment for CRP and fibrinogen.
- CRP's independent association with MI was lost when C3 was included.
Conclusions:
- Elevated C3 is independently associated with MI.
- C3 may serve as a more specific inflammatory marker for MI than CRP.
- Combined C3 and fibrinogen best predicted MI in ROC analysis.
Background:
Inflammatory processes play a fundamental role in the development of cardiovascular disease.
Objectives:
To compare the associations of complement C3 and C-reactive protein (CRP) with myocardial infarction (MI) and cardiovascular risk factors.
Methods:
342 Caucasian male subjects aged < or =65 years with MI and 193 Caucasian age matched healthy male control subjects were recruited. C3 and CRP were measured by ELISA.
Results:
C3 and CRP were significantly higher (p<0.001) in patients compared with healthy subjects (patients vs. healthy subjects, C3: 1.22gL(-1) vs. 1.00gL(-1); CRP: 1.41mgL(-1) vs. 0.72mgL(-1)). In a logistic regression model, including conventional cardiovascular risk factors, C3 was independently associated with MI (odds ratio for a 1 S.D. increase in C3: 2.29 [1.58, 2.92]); and this association remained after including CRP and/or fibrinogen in the model. CRP was independently associated with MI after accounting for conventional risk factors (odds ratio for a 1 S.D. increase in CRP: 1.47 [1.16, 1.87]), however, this association was lost when C3and/or fibrinogen were included in the model. Receiver operating characteristic (ROC) analysis indicated that the model which best predicted MI was the model including C3 and fibrinogen.
Conclusions:
These data suggest that elevated C3 is independently associated with MI and that elevated C3 may be a more specific marker of the inflammatory processes underpinning MI than CRP.
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