Elevated Levels of Systemic Pentraxin 3 Are Associated With Thin-Cap Fibroatheroma in Coronary Culprit Lesions: Assessment by Optical Coherence Tomography and Intravascular Ultrasound
What is the association between the presence of thin-cap fibroatheroma (TCFA) and systemic levels of pentraxin 3 (PTX3), a novel inflammatory marker?
The authors performed optical coherence tomography and intravascular ultrasound on 75 patients, of whom 47 had stable angina pectoris and 28 had an acute coronary syndrome (ACS). TCFA was defined as lipid-rich plaque with a fibrous cap <65 mm thick. Systemic levels of PTX3 were compared between patients with and without TCFA.
TCFA was identified in 38 patients. Levels of PTX3 were significantly higher in patients with TCFA (p < 0.001), and correlated inversely with fibrous cap thickness and positively with the remodeling index. When patients were stratified by presence or absence of ACS, higher levels of PTX3 were seen in patients with TCFA in both those with ACS (6.22 ng/ml vs. 2.50 ng/ml) and stable angina (3.58 ng/ml vs. 1.94 ng/ml). In multivariate analysis, a higher PTX3 level was the most powerful predictor of TCFA (odds ratio, 3.26; 95% confidence interval, 1.75-6.05; p < 0.001).
The authors concluded that systemic PTX3 levels are associated with TCFA, and may help identify coronary plaque vulnerability.
This study adds to the growing body of literature identifying an association between PTX3 levels and coronary plaque instability. Elevated levels have been associated with unstable coronary plaques in prior studies, although deficiency of PTX3 has been associated with increased vascular inflammation and atherosclerosis in animal models (Norata, Circulation 2009;120: 699-708). PTX3 is probably a marker rather than a mediator of plaque inflammation. This small study is interesting, but larger studies are needed to define the clinical role of PTX3 for risk stratification and guiding therapy.
Keywords: Inflammation, Coronary Artery Disease, Acute Coronary Syndrome, C-Reactive Protein, Serum Amyloid P-Component, Atherosclerosis, Plaque, Atherosclerotic, Biological Markers, Troponin I, Fibrosis
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