Presentation Number: |
1020-37 |
Abstract Title: |
The Release of Long Pentraxin 3 in Vulnerable Plaques In Vivo |
Presentation Start/End Time: |
Monday, Mar 26, 2007, 3:30 PM - 4:30 PM |
Topic: |
08. Vascular Biology/Atherosclerosis/Thrombosis/Endothelium |
Author Block: |
Satoru Suwa, Kenji Inoue, Seigo Ito, Iwao Okai, Katsumi Miyauchi, Shinya Okazaki, Yasumasa Fujiwara, Masataka Sumiyoshi, Hiroyuki Daida, Juntendo Shizuoka Hospital, Shizuoka, Japan, Juntendo Nerima Hospital, Tokyo, Japan |
Keywords: |
Atherosclerosis,Vascular biology,Myocardial infarction, pathophysiology,Unstable angina |
Learning Objective 1: |
Demonstrate that PTX3 was increased in acute coronary syndrome. |
Learning Objective 2: |
Demonstrate that PTX3 was released from ruptured plaque. |
Background: Elevated plasma levels of the pentraxin protein family member C-reactive protein (CRP) is associated with increased risk of cardiovascular disease in high-risk subjects. The long pentraxin member, PTX3, unlike CRP, is expressed in vascular cells including, endothelial cell (EC), smooth muscle cells, and neutrophils, but not in liver. Interestingly, PTX3 was suppressed by statin mostly in EC, as revealed by gene chip analysis. Therefore we believe that PTX 3 represents a ‘vascular CRP’. The present study was designed to investigate the plasma levels of PTX3 in various vascular diseases including abdominal aortic aneurysm (AA), arteriosclerosis obliterance (ASO), and acute coronary syndrome (ACS). Method: Plasma samples were obtained from 252 consecutive subjects admitted to a university hospital for coronary artery assessment by coronary angiography. From these subjects, we analyzed the plasma levels of PTX3 in 8 patients with AA, 14 patients with ASO, and 40 patients with ACS. Additionally, we collected plasma samples from 17 patients with ACS who underwent primary PCI with the use of a embolization protection device and aspiration catheter (PercuSurge GuardWire). The Guardwire balloon was placed just distal to the site of the lesion prior to the major branch, where the thrombus could embolize. Using the aspiration catheter, without inflating the balloon of the Guardwire, 9 aspirations were done across the lesion. PTX3 were measured in blood obtained from the distal site of coronary occlusion and from the aorta. RESULTS: Compared to the AA (2.77 ng/mL (95% CI: 2.17-3.36) ) or ASO (3.01 ng/mL (95% CI: 2.02-4.01) ) group, PTX3 levels were significantly higher in the ACS group (5.20 ng/mL (95% CI: 4.16-6.24) ). The plasma levels of PTX3 were significantly higher in the aspirated blood at the distal site of coronary culprit lesion than in the peripheral arterial blood or aorta (P<0.05). CONCLUSIONS: These findings indicate that plasma levels of PTX3 are increased in ‘active’ vascular disease, but not in 'chronic' vascular disease, and originate mainly from the site of ruptured plaques relative to the systemic circulation. |
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