Suzuki T, Yamauchi K, Matsushita T, Furumichi T, Furui H, Tsuzuki J, Saito H
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Clin Cardiol. 1991 Sep;14(9):731-6. doi: 10.1002/clc.4960140907.
The present study was undertaken to determine whether the extent of Factor VII elevation correlated with the severity of coronary artery disease and whether zymogen or activated Factor VII was responsible for this elevation. A group of 69 patients with coronary artery disease with old myocardial infarction was compared with 28 control subjects. The patient groups showed elevated levels of Factor VII procoagulant activity (FVII:C) and more markedly elevated Factor VII antigen (FVII:Ag) levels than the control group; therefore they had a decreased FVII:C to FVII:Ag ratio. The increased Factor VII level in the patient groups was caused by elevated Factor VII zymogen levels, and not by activated Factor VII. Since FVII:C levels strongly correlated with the titer of thrombin-antithrombin III complexes in all patients, the hypercoagulable state accompanying severe coronary atherosclerosis seems to underlie the increase of FVII and TAT in the stable phase of myocardial infarction.
本研究旨在确定因子VII升高的程度是否与冠状动脉疾病的严重程度相关，以及是酶原还是活化的因子VII导致了这种升高。将一组69例患有陈旧性心肌梗死的冠状动脉疾病患者与28例对照受试者进行比较。患者组的因子VII促凝血活性（FVII:C）水平升高，且因子VII抗原（FVII:Ag）水平比对照组升高更明显；因此，他们的FVII:C与FVII:Ag比值降低。患者组中因子VII水平的升高是由因子VII酶原水平升高引起的，而非活化的因子VII。由于在所有患者中FVII:C水平与凝血酶 - 抗凝血酶III复合物的滴度密切相关，严重冠状动脉粥样硬化伴随的高凝状态似乎是心肌梗死稳定期FVII和TAT升高的基础。
