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Research progress regarding the " Vascular Injury marker Pentraxin 3(PTX3)" will be presented at The American college of cardiology held on March 24-27th, 2007 in New Orleans.


1)Presentation Number: 1020-2
Monday, Mar 26, 2007, 3:30 PM - 4:30 PM
08. Vascular Biology/Atherosclerosis/Thrombosis/Endothelium

"Long Pentraxin 3 Is More Specific Than C-Reactive Protein as a Marker for Vascular Inflammation"
Taro Shiga, Koji Maemura, Yasushi Imai, Daiji Kawanami, Norihiko Takeda, Jiro Ando, Toshihiro Morita, Ichiro Manabe, Dobun Hayashi, Hiroshi Ohtsu, Akira Sugiyama, Kyoko Miyamoto, Mina Sagara, Yukio Ito, Tsutomu Yamazaki, Yasunobu Hirata, Tatsuhiko Kodama, Ryozo Nagai,
Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Background: C-reactive protein (CRP) is an established marker to predict cardiovascular events. The long pentraxin 3 (PTX3) shares structural homology with CRP and is produced abundantly by vascular endothelial cells and macrophages while CRP is mainly produced in the liver. Thus PTX3 is expected to be a more specific marker for cardiovascular inflammation.
Methods and Results: We established a high sensitivity assay method for PTX3, and examined plasma PTX3 and serum CRP levels in 269 consecutive patients who underwent coronary angiography (20 to 89 years old age, 74 % male). The correlation between the concentrations of PTX3 and CRP was not significant (Spearman's p=0.158), suggesting that PTX3 is independent of CRP as a marker for cardiovascular events. Notably, PTX3 levels in patients taking statins or aspirin were lower than those in control patients. Among all enrolled patients, PTX3 but not CRP levels were significantly higher in the acute coronary syndrome (ACS) group than other groups. Only after exclusion of patients with intercurrent diseases that may affect CRP levels, both PTX3 and CRP levels were higher in unstable angina group than stable angina group. However, the analysis by ROC showed PTX3 was superior to CRP for the detection of UAP (Figure). Finally neither PTX3 nor CRP showed any apparent correlation with the number of diseased vessels.
Conclusions: Plasma PTX3 levels were elevated in UAP patients. PTX3 may reflect active inflammation that leads to plaque rupture more specifically than CRP.

2)Presentation Number: 1020-37
Monday, Mar 26, 2007, 3:30 PM - 4:30 PM
08. Vascular Biology/Atherosclerosis/Thrombosis/Endothelium

"The Release of Long Pentraxin 3 in Vulnerable Plaques In Vivo"
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

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 �evascular CRP�f. 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).

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