Abstract 3591: Pentraxin 3, a New Inflammatory Maker for Endothelial Cells, Predicts Cardiac Events in Patients with Heart Failure
Background: Pentraxin 3 (PTX3) is a member of the pentraxin superfamily. The classical short pentraxin C-reactive protein (CRP) is produced in the liver in response to inflammatory signals. PTX3 is rapidly produced and released from endothelial cells in response to primary inflammatory signals. The purpose of the present study was to examine clinical significance of plasma PTX3 levels in patients with heart failure.
Methods: Plasma PTX3 levels were measured in 148 patients who were hospitalized for congestive heart failure (CHF) and 25 control subjects without CHF. They were followed-up for 548 ± 321 days with the end points of cardiac death and re-hospitalization due to progressive heart failure.
Results: Plasma PTX3 levels increased with advancing New York Heart Association (NYHA) functional class (NYHA I: 3.3 ± 2.2, II: 4.4 ± 2.9, III: 11.1 ± 22.9, IV: 26.3 ± 33.7 ng/ml, P < 0.0001). Normal upper limit of PTX3 was determined as mean ± 2SD value from 25 control subjects (4.4 ng/ml). Abnormally high PTX3 levels (> 4.4 ng/ml) were observed in 22.2%, 35.3%, 64.8%, and 93.8% of patients through NYHA I to IV (P < 0.001). The PTX3 level was higher in cardiac event group than event free group (15.8 ±30.3 vs. 5.5 ± 5.7 ng/ml, P=0.0014). Kaplan-Meier survival curves demonstrated that cardiac event rate was higher in high PTX3 group than in normal PTX3 group (51.3% vs. 21.3%, P=0.0008). The relative risk of cardiac events in high PTX3 group was 2.7-fold compared to normal PTX3 group (P=0.0013).
Conclusion: Elevation of plasma PTX3 level, a new inflammatory marker of endothelial cells, predicts adverse clinical outcomes in patients with CHF.