Laboratory for Clinical Thrombosis and Hemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands.
J Thromb Haemost. 2011 Mar;9(3):450-6. doi: 10.1111/j.1538-7836.2010.04162.x.
Despite improved treatment options, myocardial infarction is still an important cause of morbidity and mortality. One of the contributing mechanisms in the acute myocardial infarction (AMI) is plasma hypercoagulability.
We investigated hypercoagulability in 135 (first) patients with AMI using thrombin generation (TG) testing. TG testing was performed in plasmas, drawn upon admission and before medication administration, and subsequently after 4 days, 3 and 6 months. Further, we evaluated determinants of thrombin generation using multiple regression analysis of major coagulation proteins and inhibitors. Admission TG results were also related to 1-year outcome: cardiovascular death, recurrent myocardial infarction, a second coronary intervention [percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)] and ischemic stroke.
At day 0, the TG parameters peak height, endogenous thrombin potential (ETP) and lag time were increased compared with a reference population. Peak height and lag time stayed persistently increased in patients. The lowest half of the ETP values was statistically not significantly associated with an occurrence of endpoints. The lowest half of the ETP values combined with the upper half of the D-dimer values were associated with endpoints; odds ratio 5.8 (1.1-30.7). Tissue factor pathway inhibitor (TFPI) seems to be an important determinant of TG in AMI and healthy persons.
TG reflects acute hypercoagulability during AMI and partly also in the 6-month period after the acute event. TG shows a trend of an inverse association with risk of recurrent ischemic cardiovascular complications. Unraveling mechanisms in TG might improve our understanding of the pathophysiology of AMI and direct future improvements in medical care.
尽管治疗方法有所改善，但心肌梗死仍然是发病率和死亡率的重要原因。在急性心肌梗死（AMI）中，其中一个促成机制是血浆高凝状态。
我们使用凝血酶生成（TG）检测来研究 135 名（首次）AMI 患者的高凝状态。TG 检测在入院时和药物治疗前抽取的血浆中进行，并在第 4 天、3 个月和 6 个月后进行。此外，我们使用主要凝血蛋白和抑制剂的多元回归分析来评估血栓生成的决定因素。入院时的 TG 结果也与 1 年的预后相关：心血管死亡、复发性心肌梗死、第二次冠状动脉介入治疗[经皮冠状动脉介入治疗（PCI）或冠状动脉旁路移植术（CABG）]和缺血性中风。
在第 0 天，与参考人群相比，TG 参数峰值高度、内源性凝血酶潜能（ETP）和滞后时间增加。峰值高度和滞后时间在患者中持续升高。ETP 值最低的一半与终点事件的发生没有统计学意义上的关联。ETP 值最低的一半与 D-二聚体值最高的一半相结合与终点事件相关；比值比为 5.8（1.1-30.7）。组织因子途径抑制剂（TFPI）似乎是 AMI 患者和健康人 TG 的重要决定因素。
TG 反映了 AMI 期间的急性高凝状态，在急性事件后 6 个月内也部分反映了这种状态。TG 显示与复发性缺血性心血管并发症风险呈负相关趋势。阐明 TG 的机制可能有助于我们更好地理解 AMI 的病理生理学，并为未来的医疗护理改进提供指导。
