Table of Contents
ISRN Vascular Medicine
Volume 2011 (2011), Article ID 358426, 6 pages
http://dx.doi.org/10.5402/2011/358426
Research Article

Pentraxin 3 Released from Neutrophils Increases Plasma Levels in Patients with Acute Coronary Syndrome

1Department of Cardiology, Juntendo University Nerima Hospital, 3-1-10 Takanodai, Nerima-ku, Tokyo 177-8521, Japan
2Department of Cardiology, Juntendo University Shizuoka Hospital, Izunokuni, Shizuoka 410-2295, Japan
3Department of Cardiology, Juntendo University School of Medicine, Tokyo 113-8431, Japan
4Division of Cellular and Molecular Pathology, Department of Cellular Function, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan
5Laboratory for Systems Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo 153-0041, Japan

Received 10 August 2011; Accepted 26 September 2011

Academic Editor: A. Habib

Copyright © 2011 Kenji Inoue et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Our recently developed ELISA system for the detection of human pentraxin 3 (PTX3) in plasma has demonstrated that plasma PTX3 levels are increased in patients with unstable angina pectoris. However, the origin of the PTX3 from the ruptured plaque or a systemic process and which cells release PTX3 remain unclear. Methods. Blood samples were taken using an aspiration catheter from the site of the ruptured plaque and from the aorta during acute coronary interventions in 118 patients with acute coronary syndrome. These samples were analyzed for PTX3, and brain natriuretic peptide (BNP) was used as a control. Aspirated thrombi from patients with acute myocardial infarction (AMI) (n = 32) were examined by histological staining. Results. Plasma PTX3 levels were higher in blood samples taken from the site of plaque rupture compared to samples taken from the aorta ( 5 . 6 1 ± 1 . 9 1  ng/mL versus 4.72 ± 5.61 ng/mL, 𝑃 < 0 . 0 5 ). On the other hand, BNP levels, as reference, were not different between the samples (P = 0.45). PTX3-positive neutrophils accounted for 70.4% of cells in harvested thrombi, with the remaining cells consisting of mononuclear cells. Conclusions. Infiltrating neutrophils in thrombi at the plaque rupture site are a diagnostically important source of PTX3 in patients with acute coronary syndrome.