Elmas Elif, Kaelsch Thorsten, Wolpert Christian, Sueselbeck Tim, Bertsch Thomas, Dempfle Carl Erik, Borggrefe Martin
Department of Cardiology, First Department of Medicine, University of Heidelberg, Mannheim, Germany.
Clin Cardiol. 2006 Apr;29(4):165-9. doi: 10.1002/clc.4960290408.
In most cases, sudden cardiac death is triggered by ischemia-related ventricular tachyarrhythmias and accounts for 50% of deaths from cardiovascular disease in developed countries. Chronic elevation of indicators of coagulation activation has been found in patients with coronary heart disease, but a role of coagulation activation as a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (MI) has not been investigated.
We enrolled 50 patients with a history of MI, of whom 26 presented with VF in the acute phase of myocardial ischemia; 24 patients had an acute MI without ventricular tachyarrhythmias. Levels of thrombin-antithrombin complexes (TAT), prothrombin fragment F1 + 2 (F1 + 2), fibrinopeptide A (FPA), plasmin-antiplasmin complexes (PAP), protein C, antithrombin, activated partial thromboplastin time (aPTT), thromboplastin time, D-Dimer, fibrinogen, and high-sensitivity C-reactive protein (hs-CRP) were measured in plasma samples of all patients. Blood collection was obtained sequentially in two separate settings. Patients were studied at a median of 351 days after the acute coronary event.
Higher levels of TAT complexes (13.4 +/- 22.2 vs. 3.03 +/- 4.3 microg/l; p = 0.02), FPA (79.7 +/- 132.3 vs. 24.04 +/- 41.3 ng/ml; p = 0.04), and F1+2 (1.89 +/- 1.3 vs. 1.16 +/- 0.5 nmol/l; p = 0.01) were observed in patients with VF compared with patients without ventricular tachyarrhythmias during the acute phase of MI. D-Dimer levels displayed a trend without reaching statistical significance (0.69 +/- 0.48 vs. 0.48 +/- 0.24 mg/l; p = 0.06). No differences were found in hs-CRP (3.25 +/- 4.5 vs. 4.4 +/- 8.8 mg/l; p = 0.5) and fibrinogen (2.8 +/- 0.9 vs. 2.7 +/- 0.9 g/l; p = 0.6) measurements. Repeat assessment of markers of coagulation activation at a median of 847 days revealed a highly significant decrease in patients with VF.
Markers of thrombin generation are transiently increased in patients with VF during the acute phase of MI. These findings have implications for risk assessment and genetic screening of patients prone to VF during acute myocardial ischemia.
在大多数情况下，心脏性猝死由缺血相关的室性快速心律失常引发，在发达国家占心血管疾病死亡人数的50%。已在冠心病患者中发现凝血激活指标长期升高，但凝血激活作为急性心肌梗死（MI）期间心室颤动（VF）潜在危险因素的作用尚未得到研究。
我们纳入了50例有MI病史的患者，其中26例在心肌缺血急性期出现VF；24例急性MI患者无室性快速心律失常。在所有患者的血浆样本中检测凝血酶 - 抗凝血酶复合物（TAT）、凝血酶原片段F1 + 2（F1 + 2）、纤维蛋白肽A（FPA）、纤溶酶 - 抗纤溶酶复合物（PAP）、蛋白C、抗凝血酶、活化部分凝血活酶时间（aPTT）、凝血酶原时间、D - 二聚体、纤维蛋白原和高敏C反应蛋白（hs - CRP）水平。在两个不同时间点依次采集血液样本。患者在急性冠脉事件发生后中位351天接受研究。
与急性MI期无室性快速心律失常的患者相比，VF患者的TAT复合物水平更高（13.4±22.2对3.03±4.3微克/升；p = 0.02）、FPA水平更高（79.7±132.3对24.04±41.3纳克/毫升；p = 0.04）、F1 + 2水平更高（1.89±1.3对1.16±0.5纳摩尔/升；p = 0.01）。D - 二聚体水平呈趋势性变化但未达到统计学显著性（0.69±0.48对0.48±0.24毫克/升；p = 0.06）。hs - CRP（3.25±4.5对4.4±8.8毫克/升；p = 0.5）和纤维蛋白原（2.8±0.9对2.7±0.9克/升；p = 0.6）测量值无差异。在中位847天重复评估凝血激活标志物时发现，VF患者的这些标志物显著降低。
MI急性期VF患者的凝血酶生成标志物短暂升高。这些发现对急性心肌缺血期间易发生VF患者的风险评估和基因筛查具有重要意义。
