Serum PTX3 Levels Correlate with Fibrous Cap Discontinuity and Focal Inflammation in Carotid Vulnerable Plaque: A High-Resolution Magnetic Resonance Vessel Wall Imaging Study.

Background

Pentraxin 3 (PTX3) is a well-established inflammatory biomarker with significant implications in the pathogenesis and prognostic assessment of cardiovascular diseases. This study aimed to investigate the potential value of serum PTX3 as a circulating biomarker when combined with the high-resolution magnetic resonance vessel wall imaging (HR-VWI) for identifying carotid vulnerable plaque (CVP) and its specific vulnerable features.

Methods

This prospective cross-sectional study enrolled 86 patients with carotid atherosclerosis who underwent HR-VWI. Patients were classified into CVP and non-carotid vulnerable plaque (NCVP) groups, and CVP was divided into unilateral carotid vulnerable plaque (UCVP) and bilateral carotid vulnerable plaque (BCVP). CVP was defined as meeting ≥ 1 major criteria: lipid-rich necrotic core (LRNC) maximum area percentage > 40% combined with thin fibrous cap (FC), intraplaque hemorrhage (IPH), FC discontinuity, and focal inflammation. Multivariate logistic regression analysis identified factors influencing CVP and the formation of specific vulnerable features.

Results

Serum PTX3 levels progressively increased across the NCVP, UCVP, and BCVP groups (median 638.23, 858.52, 1113.62 pg/mL; p < 0.001). PTX3 independently predicted the presence of CVP (OR = 2.88; 95% CI: 1.16-8.91; p = 0.039) and specific vulnerable features, including FC discontinuity (OR = 2.47; 95% CI: 1.32-4.63; p = 0.005) and focal inflammation (OR = 2.25; 95% CI: 1.18-4.32; p = 0.014) with high diagnostic performance for these conditions. PTX3 levels exhibited a moderate positive correlation with the number of vulnerable features (r = 0.610, p < 0.01).

Conclusions

Elevated serum PTX3 levels were significantly associated with HR-VWI-defined carotid plaque vulnerability and its severity, serving as a reliable circulating biomarker for identifying FC discontinuity and focal inflammation.