Meus Rafal, Son Maksim, Sobczyk Dorota, Undas Anetta
From the Institute of Cardiology, Jagiellonian University Medical College, Cracow, Poland (R.M., M.S., A.U.); and John Paul II Hospital, Cracow, Poland (D.S., A.U.).
Stroke. 2016 Jul;47(7):1872-8. doi: 10.1161/STROKEAHA.116.012856. Epub 2016 Jun 14.
We hypothesized that formation of left atrial appendage (LAA) thrombi of unknown origin is associated with altered fibrin clot properties and blood hypercoagulability.
In a case-control study, we investigated 32 patients with a history of LAA thrombus after successful anticoagulant treatment versus 32 control subjects matched for age, sex, and diabetes mellitus. All subjects had previous ischemic stroke, transient ischemic attack, or migraine associated with patent foramen ovale. Patients with documented atrial fibrillation were excluded. We determined plasma fibrin clot permeability, fibrinolytic efficiency, thrombin generation, platelet and endothelial markers. Stroke or transient ischemic attack were assessed during a median follow-up of 74 (range 19-98) months.
Compared with controls, patients with LAA thrombus more frequently were smokers (43.8% versus 18.8%) and had 20% prolonged clot lysis time, lower plasminogen (-14%), and higher plasminogen activator inhibitor-1 (+17%), thrombin-antithrombin complexes (+17%), CD40 ligand (+30%), P-selectin (+29%), and von Willebrand factor (+30%, all P<0.05). Occurrence of LAA thrombus was predicted by von Willebrand factor (β=0.038, P=0.004), plasminogen (β=-0.048, P=0.01), plasminogen activator inhibitor-1 (β=-0.161, P=0.03), and clot permeability (β=-1.076, P=0.03). During follow-up, cerebrovascular events occurred in 10 (33.33%) of the 30 available patients in the LAA thrombus group, including 7 (23.3%) with recurrent LAA thrombus and 4 (13.33%) with documented atrial fibrillation. Recurrent LAA thrombus was associated with lower baseline Ks and higher thrombin generation, fibrinogen, plasminogen activator inhibitor-1, and soluble CD40 ligand (all P<0.05).
Prothrombotic blood alterations could be involved in the LAA thrombus formation in patients without documented atrial fibrillation and are associated with increased risk of stroke or transient ischemic attack during follow-up.
我们推测不明原因的左心耳（LAA）血栓形成与纤维蛋白凝块特性改变和血液高凝性有关。
在一项病例对照研究中，我们调查了32例成功抗凝治疗后有LAA血栓病史的患者，并与32例年龄、性别和糖尿病相匹配的对照者进行比较。所有受试者既往均有缺血性卒中、短暂性脑缺血发作或与卵圆孔未闭相关的偏头痛。排除有记录的房颤患者。我们测定了血浆纤维蛋白凝块通透性、纤溶效率、凝血酶生成、血小板和内皮标志物。在中位随访74（19 - 98）个月期间评估卒中或短暂性脑缺血发作情况。
与对照组相比，LAA血栓患者吸烟者更常见（43.8%对18.8%），凝块溶解时间延长20%，纤溶酶原降低（-14%），纤溶酶原激活物抑制剂-1升高（+17%），凝血酶 - 抗凝血酶复合物升高（+17%），CD40配体升高（+30%），P - 选择素升高（+29%），血管性血友病因子升高（+30%，所有P<0.05）。血管性血友病因子（β = 0.038，P = 0.004）、纤溶酶原（β = -0.048，P = 0.01）、纤溶酶原激活物抑制剂-1（β = -0.161，P = 0.03）和凝块通透性（β = -1.076，P = 0.03）可预测LAA血栓的发生。在随访期间，LAA血栓组30例可评估患者中有10例（33.33%）发生脑血管事件，包括7例（23.3%）复发性LAA血栓和4例（13.33%）有记录的房颤。复发性LAA血栓与较低的基线Ks以及较高 的凝血酶生成、纤维蛋白原、纤溶酶原激活物抑制剂-1和可溶性CD40配体有关（所有P<0.05）。
血栓前血液改变可能参与无记录房颤患者的LAA血栓形成，并与随访期间卒中或短暂性脑缺血发作风险增加有关。
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