Abstract 1492: High IP-10 Levels Identify Plaques with a Vulnerable Phenotype
Introduction: Atherosclerosis is considered a Th1 cell driven disease, directed by the key cytokine interferon-gamma. Th1 cells are in part recruited by the chemokine interferon-gamma inducible protein-10 (IP-10). Our previous studies in an animal model of vulnerable plaque identified IP-10 as a possible biomarker for rupture. The aim of this study was to validate these findings in endartherectomy tissue and corresponding plasma.
Methods: IP-10 content of 109 human end-atherectomies and corresponding plasmas from the Athero-express database was analyzed.
Results: In high IP-10 quartiles, 69% of plaques were atheromatous, whereas the lowest quartile consisted of 68% fibrous plaques (p<0.001). CRP and ApoB failed to show such characteristics. Furthermore, higher IP-10 concentrations were associated with a gradual reduction in smooth muscle cell and collagen content, while macrophage numbers remained fairly constant. Consequently, IP-10 is dose dependently associated with a more vulnerable phenotype. Following, we selected high and low quartile serum levels of IP-10 (n=10, n=9 respectively) to predict tissue IP-10 levels. Despite this small sample size a clear trend was noted in plasma (126±69 vs. 214±208pg/ml, for low and high quartiles, respectively).
Conclusion: In animal studies we identified IP-10 as possible biomarker. This study confirmed these findings, by showing that IP-10 levels in human carotid plaques identifies plaques with a more vulnerable phenotype. Further studies may prove a similar role for plasma IP-10, which might be an interesting biomarker for vulnerable plaque diagnosis.