PTX3 as a novel inflammatory biomarker in patients with myocarditis

Abstract

Abstract Background Pentraxin-3 (PTX3) is an acute phase protein, which plays pivotal roles in innate immunity and inflammation. Among cardiovascular diseases, PTX3 was found to be elevated in acute myocardial infarction, chronic heart failure, and cardiac arrest. So far, however, PTX3 has never been investigated in the context of myocarditis. Purpose To evaluate PTX3 as a circulating marker of inflammation in patients with suspected myocarditis. Methods We enrolled 30 consecutive inpatients with new diagnosis of myocarditis, proven both by the updated Lake Louise criteria on cardiac magnetic resonance (CMR), and by the Dallas criteria on endomyocardial biopsy (EMB) (100%). Circulating serum PTX3 was assessed at the time of EMB, by ELISA technique using a commercial kit. Normal values for PTX3 were considered as <2 ng/mL, as in previous studies. A normal control group (n=10) was used for results validation of PTX3. Results In our cohort (77% males, age 50±18 y; median left ventricle ejection fraction [LVEF] 50%, IQR 30–59%), PTX3 levels were assessed in 30 patients. PTX3 levels were elevated in 26/30 (87%) patients with myocarditis (median 4,36 ng/mL, IQR 2,44–6,72, range 1,20–40,0), and in none (0/10) among healthy controls (median 1,28 ng/mL, IQR 1,04–1,36, range 0,77–1,94) (p=0,001). In the study group, the yield of other cardiac biomarkers was lower: 12/30 (40%) for C-reactive protein, 23/30 (77%) for T-troponin, and 20/30 (67%) for NTproBNP. PTX3 was constantly elevated in patients presenting with heart failure (HF) (16/16, 100%), compared with those presenting with acute coronary syndrome-like (8/10, 80%), or arrhythmias (2/4, 50%) (p=0,024). In particular, elevated PTX3 was associated with systolic dysfunction (LVEF <50%) at discharge (16/16 vs. 10/14, p=0,022). Conclusion Our preliminary data suggest PTX3 as a novel biomarker with potential diagnostic and prognostic value for myocarditis and inflammatory cardiomyopathy. Funding Acknowledgement Type of funding sources: None.