Increased tissue factor pathway inhibitor in patients with acute myocardial infarction

✍ Scribed by Kamikura, Yuko; Wada, Hideo; Yamada, Atsushi; Shimura, Minori; Hiyoyama, Katsuyo; Shiku, Hiroshi; Tanigawa, Motoaki; Nishikawa, Hideo; Yamada, Norikazu; Isaka, Naoki; Nakano, Takeshi; Kumeda, Kousuke; Kato, Hisao

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 73 KB
• Volume: 55
• Category: Article
• ISSN: 0361-8609
• DOI: 10.1002/(sici)1096-8652(199707)55:4<183::aid-ajh3>3.0.co;2-o

✦ Synopsis

We examined hemostatic abnormalities in 23 patients with acute myocardial infarction (AMI), 10 with pulmonary embolism (PE), and 10 with deep vein thrombosis (DVT). At the onset of AMI, plasma levels of tissue-type plasminogen activator (t-PA), PA inhibitor-I (PAI-I), fibrin-D-dimer, thrombin-antithrombin complex (TAT), and plasmin-plasmin inhibitor complex (PPIC) were significantly increased. Both the plasma total TFPI and free-TFPI levels in the AMI patients were significantly higher than those in the healthy volunteers, PE patients, and DVT patients. There was no significant difference in total TFPI or free-TFPI among patients with PE, those with DVT, and healthy volunteers. One hour after percutaneous transluminal coronary angioplasty (PTCA) in the AMI group, the total TFPI level was further increased, and it was significantly reduced 24 hr after PTCA, to a level similar to that in healthy volunteers. Free-TFPI showed a pattern similar to that of total TFPI. The ratio of free-TFPI/total TFPI was highest 1 hr after PTCA. Increased TFPI in AMI patients might be released from ischemic tissues.