Tanigawa M, Wada H, Minamikawa K, Wakita Y, Nagaya S, Mori T, Tamaki S, Nishikawa H, Kakuta Y, Nakano T
Second Department of Internal Medicine, Mie University School of Medicine, Japan.
Am J Hematol. 1995 May;49(1):1-5. doi: 10.1002/ajh.2830490102.
Plasma thrombin-antithrombin III complex (TAT), FDP-D-dimer, activated protein C (APC)-protein C inhibitor (PCI) complex, and tissue type plasminogen activator (t-PA), PA inhibitor-1 (PAI-I) were significantly increased in patients with acute myocardial infarction (AMI) at onset. These patients exhibited a hypercoagulable state and protein C activation at onset. The plasma PCI level at onset of AMI was within the normal range, but was significantly decreased after percutaneous transluminal coronary angioplasty (PTCA). After PTCA, plasma t-PA, FDP-D-dimer, and plasmin-alpha 2-plasmin inhibitor were increased but APC-PCI complex and TAT were not. The decrease in PCI after PTCA may have been caused by the activation of fibrinolysis. PCI may play an important role in the inhibition of fibrinolysis in stimulated or damaged endothelial cells. These findings suggest that the protein C pathway plays an important role in the onset of AMI and after PTCA.
急性心肌梗死（AMI）患者发病时血浆凝血酶 - 抗凝血酶III复合物（TAT）、纤维蛋白降解产物 - D - 二聚体、活化蛋白C（APC） - 蛋白C抑制剂（PCI）复合物以及组织型纤溶酶原激活剂（t - PA）、纤溶酶原激活物抑制剂 - 1（PAI - I）均显著升高。这些患者在发病时呈现高凝状态且蛋白C活化。AMI发病时血浆PCI水平在正常范围内，但经皮腔内冠状动脉血管成形术（PTCA）后显著降低。PTCA后，血浆t - PA、FDP - D - 二聚体和纤溶酶 - α2 - 纤溶酶抑制剂升高，但APC - PCI复合物和TAT未升高。PTCA后PCI降低可能是由纤溶激活所致。PCI可能在刺激或受损内皮细胞的纤溶抑制中起重要作用。这些发现提示蛋白C途径在AMI发病及PTCA后起重要作用。
