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急性冠状动脉综合征患者凝血酶生成增加,但活化因子VII的血浆水平正常。

Heightened thrombin formation but normal plasma levels of activated factor VII in patients with acute coronary syndromes.

作者信息

Merlini P A, Ardissino D, Oltrona L, Broccolino M, Coppola R, Mannucci P M

机构信息

2nd Division of Cardiology, Ca' Granda Niguarda Hospital, Milan, Italy.

出版信息

Arterioscler Thromb Vasc Biol. 1995 Oct;15(10):1675-9. doi: 10.1161/01.atv.15.10.1675.

DOI:10.1161/01.atv.15.10.1675
PMID:7583543
Abstract

Plaque rupture with the exposure of a tissue factor-rich procoagulant surface is considered the common pathogenetic mechanism of unstable angina and myocardial infarction. Activated factor VII, the key enzyme for initiating blood coagulation under resting conditions, is increased in pathological situations associated with tissue factor exposure. We measured the plasma levels of activated factor VII and studied their relation with signs of coagulation enzyme activity in patients with acute coronary syndromes. The plasma levels of activated factor VII, prothrombin fragment 1 + 2, and fibrinopeptide A were measured on admission in consecutive patients presenting with acute myocardial infarction (n = 28), unstable angina (n = 32), and stable angina (n = 17) and in age- and sex-matched healthy individuals (n = 33). Plasma determinations of the same markers were also repeated at 15 days and 3 and 6 months. On admission, the patients with unstable angina or myocardial infarction had significantly higher plasma levels of prothrombin fragment 1 + 2 (P < .0001) and fibrinopeptide A (P < .0001) than those with stable angina or healthy individuals, whereas no differences were detected in the plasma levels of activated factor VII. During follow-up there was a significant decrease in the plasma levels of fibrinopeptide A both in patients with unstable angina (P < .001) and in those with myocardial infarction (P < .001), whereas no changes in plasma prothrombin fragment 1 + 2 or activated factor VII levels were observed. Hence, in the acute and chronic phases of myocardial infarction and unstable angina, heightened coagulation enzyme activity is not accompanied by an increase in activated factor VII.

摘要

斑块破裂并暴露出富含组织因子的促凝血表面被认为是不稳定型心绞痛和心肌梗死常见的发病机制。活化因子VII是静息状态下启动血液凝固的关键酶,在与组织因子暴露相关的病理情况下会升高。我们测定了急性冠状动脉综合征患者血浆中活化因子VII的水平,并研究了其与凝血酶活性指标的关系。对连续收治的急性心肌梗死患者(n = 28)、不稳定型心绞痛患者(n = 32)、稳定型心绞痛患者(n = 17)以及年龄和性别匹配的健康个体(n = 33)入院时测定血浆活化因子VII、凝血酶原片段1 + 2和纤维蛋白肽A的水平。在15天、3个月和6个月时也重复测定相同标志物的血浆水平。入院时,不稳定型心绞痛或心肌梗死患者血浆中凝血酶原片段1 + 2(P <.0001)和纤维蛋白肽A(P <.0001)的水平显著高于稳定型心绞痛患者或健康个体,而活化因子VII的血浆水平未检测到差异。随访期间,不稳定型心绞痛患者(P <.001)和心肌梗死患者(P <.001)血浆中纤维蛋白肽A的水平均显著下降,而血浆凝血酶原片段1 + 2或活化因子VII水平未观察到变化。因此,在心肌梗死和不稳定型心绞痛的急性和慢性阶段,凝血酶活性增强并未伴随活化因子VII的增加。

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