Abstract 9934: Levels of Plasma Pentraxin 3 Predict Presence of Thin-cap Fibroatheroma in Patients with Stable Angina Pectoris: Assessment by Optical Coherence Tomography

Abstract

Background: Thin-cap fibroatheroma (TCFA) is the primary type of rupture prone plaque, but biomarkers predicting it are not established. Recently, pentraxin 3 (PTX3) has been shown to be a novel biomarker specific to vascular inflammation. The aim of this study was to clarify the association between plasma PTX3 level and TCFA as determined by optical coherence tomography (OCT) in patients with stable angina pectoris (SAP). Methods: Thirty-four patients with SAP who underwent OCT at de novo culprit lesions before percutaneous coronary intervention were evaluated. TCFA was defined as a plaque with lipid contents in >90°and with thinnest part of the fibrous cap measuring <70μ m. Plasma PTX3 and serum high sensitive C-reactive protein (hsCRP) were measured among these patients. Plasma PTX3 level was categorized into low (< 25th percentile), intermediate (25th to 75th percentiles), and high (> 75th percentile) groups. Results: Fourteen patients with TCFA and 20 patients without TCFA were identified. Levels of PTX3 (median [interquartile range]) were significantly greater in patients with TCFA than without TCFA (4.66 [2.44 - 6.80]) vs. 2.60 [1.79 - 3.18] ng/mL; p = 0.009). Levels of hsCRP were comparable between the two groups. PTX3 level significantly inversely correlated with fibrous cap thickness (r = -0.53, p = 0.009), but hsCRP did not. The frequency of TCFA was 22, 29, and 88% in low, intermediate, and high PTX3 group, respectively (p = 0.009). Univariate analysis revealed that hypercholesterolemia, statin use, and level of PTX3 were related to the presence of TCFA. Multivariate logistic regression analysis in these factors showed that plasma PTX3 level was the significant independent factor associated with TCFA existence (OR, 1.99; 95%CI, 1.10 - 3.58; p = 0.023). The area under the receiver-operating characteristics curve for PTX3 level for prediction of TCFA was 0.766 (p = 0.009). The optimal cut-off value of PTX3 for predicting TCFA was 2.88 ng/mL (sensitivity 71%, specificity 70%). Conclusions: Plasma PTX3 level was associated with the presence of TCFA and thinner fibrous cap thickness at coronary culprit lesions in patients with SAP. These findings suggest that plasma PTX3 might be a useful marker reflecting the plaque vulnerability.