Changes of plasma hemostatic markers during percutaneous transluminal coronary angioplasty in patients with chronic coronary artery disease
✍ Scribed by Saito, Yasuhiro; Wada, Hideo; Yamamuro, Miho; Inoue, Akiko; Shimura, Minori; Hiyoyama, Kazuyo; Gabazza, Esteban C.; Isaka, Naoki; Shiku, Hiroshi; Takeya, Hiroyuki; Suzuki, Koji; Kumeda, Kousuke; Kato, Hisao; Nakano, Takeshi
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 111 KB
- Volume
- 61
- Category
- Article
- ISSN
- 0361-8609
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✦ Synopsis
Changes of hemostatic parameters during percutaneous transluminal coronary angioplasty (PTCA) in 75 patients with chronic coronary artery disease were evaluated. Plasma levels of D-dimer, soluble fibrin monomer, plasmin-␣2 antiplasmin inhibitor complex, and tissue factor (TF) were significantly increased in all patients with chronic coronary artery disease. The activity of antithrombin and protein C and the levels of protein C antigen were significantly decreased 1 hr after PTCA, but they returned to normal range 1 day after PTCA. There was no significant difference in the level of plasma APC-PCI complex before and 1 hr after PTCA. The plasma levels of D-dimer, soluble fibrin monomer, thrombomodulin, TF and PPIC were significantly decreased 1 hr, and the plasma levels of plasmin-␣2 antiplasmin inhibitor complex 1 day after PTCA. These findings suggest that the decrease of protein C and antithrombin resulted in activation of the coagulation system. One hour after PTCA, the plasma levels of (total-free) TF pathway inhibitor (TFPI) were significantly decreased, but the plasma levels of total and free-TFPI were significantly increased, suggesting that comsumption of (total-free) TFPI occurs during PTCA. Overall, these findings suggest that the hypercoagulable state improves during PTCA and that transient decrease of antithrombin, protein C, (total-free) TFPI or plasmin-␣2 antiplasmin inhibitor complex may cause restenosis of coronary artery.