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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Inflammation, complement activation and endothelial function in stable and unstable coronary artery disease
Karam M Kostner1, Robert B Fahti, Colin Case
1University of Queensland, Princess Alexandra Hospital, Brisbane, Australia. kkostner@medicine.pa.uq.edu.au
Insights
Unstable angina patients show elevated inflammation and complement activation markers. These markers, including high sensitivity C-reactive protein (hs-CRP) and C3a, are linked to coronary artery disease (CAD) progression.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biochemistry
Background:
- Endothelial dysfunction is a key factor in coronary artery disease (CAD) pathogenesis.
- Complement activation and inflammation are implicated in endothelial dysfunction.
- This study investigates the link between endothelial function, inflammation (hs-CRP), and complement activation in CAD patients.
Purpose of the Study:
- To assess the association between endothelial function, hs-CRP, and complement activation markers.
- To compare these markers in patients with stable angina pectoris (SAP) versus unstable angina pectoris (UAP).
Main Methods:
- Prospective study of 78 patients (35 SAP, 43 UAP).
- Endothelial function assessed via brachial artery reactivity (BAR).
- Measured hs-CRP, C3a, C5a, and C1-Inhibitor (C1 inh.) levels.
Main Results:
- UAP patients had higher hs-CRP and C3a levels than SAP patients.
- No significant difference in BAR between UAP and SAP groups.
- In UAP patients, hs-CRP correlated with cholesterol, C3a, and C1 inh., but not BAR.
Conclusions:
- Elevated hs-CRP (inflammation) and C3a (complement activation) are observed in UAP patients.
- These markers are not elevated in SAP patients.
- hs-CRP and C1 inh. are independent predictors of UAP.
Background:
Endothelial dysfunction plays an important role in the pathogenesis of coronary artery disease (CAD). Apart from traditional risk factors complement activation and inflammation may trigger and sustain endothelial dysfunction. We sought to assess the association between endothelial function, high sensitivity C-reactive protein (hs-CRP) and markers of complement activation in patients with either stable or unstable coronary artery disease.
Methods:
We prospectively recruited 78 patients, 35 patients with stable angina pectoris (SAP) and 43 patients with unstable angina pectoris (UAP). Endothelial function was assessed as brachial artery reactivity (BAR). Hs-CRP, C3a, C5a and C1-Inhibitor (C1 inh.) were measured enzymatically.
Results:
Patients with UAP showed higher median levels of hs-CRP and C3a compared to patients with SAP, while BAR was not significantly different between patient groups. In UAP patients, hs-CRP was significantly correlated with cholesterol (r=0.27, p<0.02), C3a (r=0.32, p<0.001) and C1 INH.(r=0.41, p<0.003), but not with flow mediated dilatation (r=0.09, P=0.41). Hs-CRP and C1 INH.were found to be independent predictors of UAP in a backward stepwise logistic regression model.
Conclusions:
We conclude that both hs-CRP, a marker of inflammation and C3a, a marker of complement activation are elevated in patients with UAP, but not in patients with SAP.
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