Serial changes in von Willehrand factor-cleaving protease (ADAMTS13) and prognosis after acute myocardial infarction

被引:67
作者
Matsukawa, Masakazu
Kaikita, Koichi [1 ]
Soejima, Kenji
Fuchigami, Shunichiro
Nakamura, Yoshinori
Honda, Tsuyoshi
Tsujita, Kenichi
Nagayoshi, Yasuhiro
Kojima, Sunao
Shimomura, Hideki
Sugiyama, Seigo
Fujimoto, Kazuteru
Yoshimura, Michihiro
Nakagaki, Tomohiro
Ogawa, Hisao
机构
[1] Kumamoto Univ, Grad Sch Med, Dept Cardiovasc Med, Kumamoto 860, Japan
[2] Fukuoka Tokushikai Med Ctr, Dept Cardiovasc Med, Fukuoka, Japan
[3] Natl Hosp Organizat, Kumamoto Med Ctr, Dept Cardiovasc Med, Kumamoto, Japan
关键词
D O I
10.1016/j.amjcard.2007.03.095
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Von Willebrand factor (VWF), a cofactor in platelet adhesion and aggregation, increases hemostasis and thrombosis. Recently, a metalloprotease that cleaves VWF multimers has been identified, namely ADAMTS13. The aim of this study was to investigate the relation between serial changes in plasma VWF and ADAMTS13 and the prognosis after acute myocardial infarction (AMI). We measured serial changes of plasma VWF and ADAMTS13 antigen levels in 92 patients with AMI and 40 control subjects. VWF levels were significantly higher in patients with AMI compared with controls (p < 0.01) on admission, peaked 3 days after admission, and remained high for 14 days. In contrast, on admission, ADAMTS13 levels were significantly lower in patients with AMI compared with controls (p < 0.0001), with minimum antigen levels reached after 3 days, and remained lower for 14 days. The ratio of VWF/ADAMTS13 antigen levels was higher in patients with AMI compared with controls throughout the time course. Cox hazards analysis revealed that the early increase of VWF and VWF/ADAMTS13 ratio levels and the early decrease of ADAMTS13 levels were significant predictors of future thrombotic events during the 1-year follow-up period. Kaplan-Meier analysis demonstrated that patients with major decreases of ADAMTS13 levels and high increases of VWF/ADAMTS13 levels had significantly greater probabilities for development of thrombotic events (p = 0.0104 and 0.0209, respectively). In conclusion, these findings suggest that monitoring the changes of VWF and ADAMTS 13 antigen levels in the early phase might be valuable for predicting and preventing thrombosis during 1-year follow-up in patients with AMI. (C) 2007 Elsevier Inc. All rights reserved.
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收藏
页码:760 / 765
页数:6
相关论文
共 31 条
[1]   Effects of inflammatory cytokines on the release and cleavage of the endothelial cell-derived ultralarge von Willebrand factor multimers under flow [J].
Bernardo, A ;
Ball, C ;
Nolasco, L ;
Moake, JF ;
Dong, JF .
BLOOD, 2004, 104 (01) :100-106
[2]   Acute release of plasminogen activator inhibitor-1 in ST-segment elevation myocardial infarction predicts mortality [J].
Collet, JP ;
Montalescot, G ;
Vicaut, E ;
Ankri, A ;
Walylo, F ;
Lesty, C ;
Choussat, R ;
Beygui, F ;
Borentain, M ;
Vignolles, N ;
Thomas, D .
CIRCULATION, 2003, 108 (04) :391-394
[3]   Proteolytic inactivation of ADAMTS13 by thrombin and plasmin [J].
Crawley, JTB ;
Lam, JK ;
Rance, JB ;
Mollica, LR ;
O'Donnell, JS ;
Lane, DA .
BLOOD, 2005, 105 (03) :1085-1093
[4]   Purification of human von Willebrand factor-cleaving protease and its identification as a new member of the metalloproteinase family [J].
Fujikawa, K ;
Suzuki, H ;
McMullen, B ;
Chung, D .
BLOOD, 2001, 98 (06) :1662-1666
[5]   Partial purification and characterization of a protease from human plasma cleaving von Willebrand factor to fragments produced by in vivo proteolysis [J].
Furlan, M ;
Robles, R ;
Lammle, B .
BLOOD, 1996, 87 (10) :4223-4234
[6]   Partial amino acid sequence of purified von Willebrand factor-cleaving protease [J].
Gerritsen, HE ;
Robles, R ;
Lämmle, B ;
Furlan, M .
BLOOD, 2001, 98 (06) :1654-1661
[7]   Reduced von Willebrand factor-cleaving protease (ADAMTS13) activity in acute myocardial infarction [J].
Kaikita, K. ;
Soejima, K. ;
Matsukawa, M. ;
Nakagaki, T. ;
Ogawa, H. .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2006, 4 (11) :2490-2493
[8]   Circulating endothelial cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute coronary syndromes [J].
Lee, KW ;
Lip, GYH ;
Tayebjee, M ;
Foster, W ;
Blann, AD .
BLOOD, 2005, 105 (02) :526-532
[9]   Mutations in a member of the ADAMTS gene family cause thrombotic thrombocytopenic purpura [J].
Levy, GG ;
Nichols, WC ;
Lian, EC ;
Foroud, T ;
McClintick, JN ;
McGee, BM ;
Yang, AY ;
Siemieniak, DR ;
Stark, KR ;
Gruppo, R ;
Sarode, R ;
Shurin, SB ;
Chandrasekaran, V ;
Stabler, SP ;
Sabio, H ;
Bouhassira, EE ;
Upshaw, JD ;
Ginsburg, D ;
Tsai, HM .
NATURE, 2001, 413 (6855) :488-494
[10]   Opposite changes of ADAMTS-13 and von Willebrand factor after cardiac surgery [J].
Mannucci, PM ;
Parolari, A ;
Canciani, MT ;
Alemanni, F ;
Camerat, M .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2005, 3 (02) :397-399