Merlini P A, Bauer K A, Oltrona L, Ardissino D, Cattaneo M, Belli C, Mannucci P M, Rosenberg R D
2nd Division of Cardiology, Ca'Granda Niguarda Hospital, Milan, Italy.
Circulation. 1994 Jul;90(1):61-8. doi: 10.1161/01.cir.90.1.61.
The blood coagulation system is activated in the acute phase of unstable angina and acute myocardial infarction. However, it remains unclear whether augmented function of the hemostatic mechanism serves only as a marker of the acute thrombotic episode or whether a hypercoagulable state persists for a prolonged period after clinical stabilization.
We prospectively measured the plasma concentrations of prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA) in consecutive patients presenting with unstable angina (n = 81) or acute myocardial infarction (n = 32), respectively. At 6 months, plasma determinations were repeated in patients experiencing an uneventful clinical course (unstable angina, n = 57; myocardial infarction, n = 23). We quantitated the plasma levels of F1 + 2 and FPA in control patients with stable angina (n = 37) or healthy individuals (n = 32) who were matched for age and sex. The median plasma concentrations of F1 + 2 and FPA are significantly higher in patients presenting with unstable angina (F1 + 2, 1.08 nmol/L; FPA, 2.4 nmol/L) or acute myocardial infarction (F1 + 2, 1.27 nmol/L; FPA, 3.55 nmol/L) compared with patients with stable angina (F1 + 2, 0.74 nmol/L; FPA, 1.3 nmol/L; P < .0001) or healthy individuals (F1 + 2, 0.71 nmol/L; FPA, 0.80 nmol/L; P < .0001). At 6 months, the median plasma levels of F1 + 2 in patients exhibiting an uneventful clinical course did not differ from values obtained at admission (unstable angina, 1.26 versus 1.07 nmol/L, P = NS; myocardial infarction, 1.22 versus 1.29 nmol/L, P = NS), whereas the median plasma levels of FPA in the same two subpopulations were significantly reduced (unstable angina, 1.1 versus 2.9 nmol/L, P = .0003; myocardial infarction, 1.1 versus 3.0 nmol/L; P = .0028).
During the acute phase of unstable angina and myocardial infarction, patients exhibit increased coagulation system activity. Over the next 6 months, patients with unstable angina or myocardial infarction experiencing an uneventful clinical course manifest a persistent hypercoagulable state with minimal generation of fibrin.
在不稳定型心绞痛和急性心肌梗死的急性期，血液凝固系统被激活。然而，目前尚不清楚止血机制功能增强仅仅是急性血栓形成事件的一个标志物，还是在临床病情稳定后高凝状态会持续很长一段时间。
我们前瞻性地分别测定了连续就诊的不稳定型心绞痛患者（n = 81）或急性心肌梗死患者（n = 32）血浆中凝血酶原片段1 + 2（F1 + 2）和纤维蛋白肽A（FPA）的浓度。在6个月时，对临床过程平稳的患者（不稳定型心绞痛，n = 57；心肌梗死，n = 23）再次进行血浆测定。我们对年龄和性别匹配的稳定型心绞痛对照患者（n = 37）或健康个体（n = 32）的血浆F1 + 2和FPA水平进行了定量分析。与稳定型心绞痛患者（F1 + 2，0.74 nmol/L；FPA，1.3 nmol/L；P <.0001）或健康个体（F1 + 2，0.71 nmol/L；FPA，0.80 nmol/L；P <.0001）相比，不稳定型心绞痛患者（F1 + 2，1.08 nmol/L；FPA，2.4 nmol/L）或急性心肌梗死患者（F1 + 2，1.27 nmol/L；FPA，3.55 nmol/L）的血浆F1 + 2和FPA中位数浓度显著更高。在6个月时，临床过程平稳的患者中，F1 + 2的血浆中位数水平与入院时的值无差异（不稳定型心绞痛，1.26对1.07 nmol/L，P =无显著性差异；心肌梗死，1.22对1.29 nmol/L，P =无显著性差异），而在这两个亚组中FPA的血浆中位数水平均显著降低（不稳定型心绞痛，1.1对2.9 nmol/L，P =.0003；心肌梗死，1.1对3.0 nmol/L；P =.0028）。
在不稳定型心绞痛和心肌梗死的急性期，患者表现出凝血系统活性增加。在接下来的6个月里，临床过程平稳的不稳定型心绞痛或心肌梗死患者表现出持续的高凝状态，纤维蛋白生成极少。
