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Published on: May 6, 2014
Role of Interleukin-18 and the Thrombus Precursor Protein in Coronary Artery Disease
Carlos Scherr1,2,3, Denilson Campos de Albuquerque2, Roberto Pozzan4
1Ministério da Saúde, Brasília, DF, Brasil.
Insights
Interleukin 18 (IL-18) and thrombus precursor protein (TpP) levels were elevated in patients with acute coronary syndrome (ACS). These biomarkers may indicate plaque instability in acute coronary artery disease (CAD), but not in the chronic phase.
Area of Science:
- Cardiology
- Biomarker Research
- Atherosclerosis Studies
Background:
- Coronary artery disease (CAD) is a leading global cause of mortality.
- Early identification of high-risk individuals for CAD remains a significant clinical challenge.
- Atherogenesis involves complex biological processes that can be elucidated through biomarker analysis.
Purpose of the Study:
- To evaluate the diagnostic potential of interleukin 18 (IL-18) and thrombus precursor protein (TpP) as biomarkers for coronary artery disease (CAD).
- To assess the association of IL-18 and TpP levels with acute coronary syndrome (ACS) and chronic CAD.
- To investigate the role of these biomarkers in the context of atherogenesis and plaque instability.
Main Methods:
- A cross-sectional cohort study involving 119 patients categorized into three groups: acute coronary syndrome (ACS), chronic CAD, and a control group.
- Serum levels of IL-18 and TpP were measured in all participants.
- Statistical analyses included Chi-square test, Analysis of Variance (ANOVA), and Tukey's test to compare biomarker levels across groups.
Main Results:
- Mean IL-18 and TpP levels were significantly higher in the acute coronary syndrome group compared to both the chronic CAD and control groups (p < 0.002 for IL-18, p < 0.001 for TpP).
- Elevated IL-18 and TpP concentrations were observed in acute CAD patients, suggesting a link to plaque instability.
- No significant difference in IL-18 and TpP levels was found between the chronic CAD group and the control group.
Conclusions:
- Increased levels of IL-18 and TpP are associated with acute coronary syndrome, indicating their potential role in atherosclerotic plaque instability.
- These biomarkers may not be significantly elevated in the chronic phase of coronary artery disease.
- Further research is warranted to explore the clinical utility of IL-18 and TpP in the early assessment and management of CAD.
Abstract:
Background Coronary failure is the leading cause of death worldwide and identifying patients at higher risk for coronary artery disease (CAD) is a challenge. Objectives To test the biomarkers interleukin 18 (IL-18) and thrombus precursor protein (TpP), involved in atherogenesis, to aid in the early assessment of CAD. Methods This was a cross-sectional cohort of 119 patients, stratified into three groups: Group I - acute coronary syndrome (39); Group II - chronic CAD (40) and Group III - control, without coronary lesion, but who might have risk factors for CAD (40). Statistical analysis was performed using the statistical program SPSS (Statistical Package for the Social Sciences) for Windows ,version 17.0 of 2008. The significance level was set at 0.05 or 5% (p <0.05), with a 95% confidence interval. Chi-square test (χ2), Analysis of variance (ANOVA), and Tukey's test were used. Results The mean age was 60.36 ± 9.64 years; there was a prevalence of females in Group III (65.0% p = 0.002), but without statistical significance for the means of IL-18 and TpP. The means of IL-18 and TpP were increased in Group I when compared to the other groups; IL-18 = 1325.44 ± 1860.13 ng/dL, p = 0.002; TpP = 35.86 ± 28.36 µg / mL, p <0.001). When compared two-by-two, it was observed that Group I had higher mean IL-18 and TpP values than Group II (IL-18 = 353.81 ± 273.65 ng / dL; TpP = 25.66 ± 12, 17 µg / mL) and Group III (IL-18 = 633.25 ± 993.93 ng / dL; TpP = 18.00 ± 8.45 µg / mL). Conclusion There was an increase in these biomarkers in acute CAD, suggesting a relationship with the atherosclerotic plaque instability process, but not with the chronic phase. (Arq Bras Cardiol. 2020; 114(4):692-698).
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