Serial changes in von Willebrand factor-cleaving protease (ADAMTS13) and prognosis after acute myocardial infarction.
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 ADAMTS13 antigen levels in the early phase might be valuable for predicting and preventing thrombosis during 1-year follow-up in patients with AMI.
Matsukawa
Masakazu
M
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Kaikita
Koichi
K
Soejima
Kenji
K
Fuchigami
Shunichiro
S
Nakamura
Yoshinori
Y
Honda
Tsuyoshi
T
Tsujita
Kenichi
K
Nagayoshi
Yasuhiro
Y
Kojima
Sunao
S
Shimomura
Hideki
H
Sugiyama
Seigo
S
Fujimoto
Kazuteru
K
Yoshimura
Michihiro
M
Nakagaki
Tomohiro
T
Ogawa
Hisao
H
D051722:ADAM Proteins / Q000097:blood*; D000071120:ADAMTS13 Protein; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000789:Angina, Unstable / Q000209:etiology; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D002303:Cardiac Output, Low / Q000209:etiology; D016022:Case-Control Studies; D005260:Female; D005500:Follow-Up Studies; D005544:Forecasting; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D010343:Patient Admission; D010359:Patient Readmission; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D013927:Thrombosis / Q000209:etiology; D014841:von Willebrand Factor / Q000032:analysis*
D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D014841:von Willebrand Factor; D006493:Heparin; D051722:ADAM Proteins; D000071120:ADAMTS13 Protein; C099604:ADAMTS13 protein, human; D001241:Aspirin