Elevated levels of systemic pentraxin 3 are associated with thin-cap fibroatheroma in coronary culprit lesions: assessment by optical coherence tomography and intravascular ultrasound.

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.