Objectives: This study sought to determine whether systemic levels of pentraxin 3 (PTX3), a novel inflammatory marker, are associated with thin-cap fibroatheroma (TCFA).
Background: Biomarkers predicting the presence of TCFA in vivo have not been established.
Methods: We evaluated 75 patients (stable angina pectoris, n = 47; acute coronary syndrome, n = 28) with de novo culprit lesions who were examined by optical coherence tomography and intravascular ultrasound. We defined TCFA as lipid-rich plaque with a fibrous cap <65 μm thick. Systemic levels of PTX3 were compared between patients with and without TCFA.
Results: Thirty-eight and 37 patients with and without TCFA, respectively, were identified. Levels of PTX3 were significantly higher in patients with than in those without TCFA (p < 0.001) and correlated inversely with fibrous cap thickness (r = -0.71, p = 0.001) and positively with the remodeling index (r = 0.25, p = 0.037). Multivariate logistic regression analysis showed that a higher PTX3 level was the most powerful predictor of TCFA (odds ratio: 3.26, 95% confidence interval: 1.75 to 6.05, p < 0.001). Receiver-operating characteristic curve analysis showed that >3.24 ng/ml of PTX3 could predict TCFA with 84% sensitivity and 86% specificity.
Conclusions: Higher levels of systemic PTX3 are associated with TCFA. Systemic PTX3 levels comprise a useful inflammatory marker that reflects coronary plaque vulnerability.
Keywords: ACS; AMI; C-reactive protein; CRP; CSA; EEM; IVUS; OCT; P+M; PTX3; SAP; TCFA; UAP; acute coronary syndromes; acute myocardial infarction; cross-sectional area; external elastic membrane; high-sensitivity C-reaction protein; hs-CRP; intravascular ultrasound; optical coherence tomography; pentraxin 3; plaque plus media; stable angina pectoris; thin-cap fibroatheroma; unstable angina pectoris; vulnerable plaque.
Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.