阵发性心房颤动:VIII因子和血管性血友病因子的改变导致早期高凝。

Mariya Negrinova Negreva, Krasimira Prodanova, Katerina Vitlianova, Christiana Madjova
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引用次数: 9

摘要

阵发性心房颤动(PAF)是一种有充分证据的血栓前状态,具有显著的栓塞风险。然而,在疾病的早期阶段,精确的止血变化并没有完全研究。本研究的目的是研究血管性血友病因子(vWF)和凝血因子VIII (FVIII)在PAF临床表现的第一个小时(最多24小时)内的血浆水平和活性。材料和方法:我们连续选择51例未抗凝治疗的PAF患者(男性26例,女性25例,平均年龄59.84±1.60岁)和52例对照患者(男性26例,女性26例,平均年龄59.50±1.46岁),患者性别、伴发疾病相对应,进行治疗。使用酶联免疫测定法和光度法检测指标。结果:所有患者均于心律失常发生后第2 ~ 24 h住院(平均:8.14±0.74 h), PAF组FVIII水平(107.52±3.48%比93.85±2.93%,p < 0.05)和活动度(200.03±11.11%比109.73±4.90%,p < 0.001)高于PAF组。vWF水平(178.40±12.95%比119.53±6.12%,p < 0.001)和活度(200.92±12.45%比110.80±5.14%,p < 0.001)也较高。PAF组的这些变化与年龄、性别、体重指数或CHA2DS2-VASc评分无关(p > 0.05)。PAF持续时间是FVIII水平和活动增加的重要预测因子。随着PAF持续时间的增加,因子值也随之增加(r = 0.85, p < 0.001;R = 0.83, p < 0.001)。结论:结果显示凝血级联活化和内皮损伤,提示PAF早期仍存在高凝性。PAF的这些变化与CHA2DS2-VASc评分的危险因素无关,这表明PAF可能是一个独立的栓塞危险因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Paroxysmal atrial fibrillation: changes in factor VIII and von Willebrand factor impose early hypercoagulability.

Paroxysmal atrial fibrillation: changes in factor VIII and von Willebrand factor impose early hypercoagulability.

Paroxysmal atrial fibrillation: changes in factor VIII and von Willebrand factor impose early hypercoagulability.

Paroxysmal atrial fibrillation: changes in factor VIII and von Willebrand factor impose early hypercoagulability.

Introduction: Paroxysmal atrial fibrillation (PAF) is a well-documented prothrombotic state that carries significant embolic risk. However, precise hemostatic changes in the very early stage of the disease are not completely studied. The aim of the study was to study von Willebrand factor (vWF) and coagulation factor VIII (FVIII) plasma levels and activity in the first hours (up to 24 h) of PAF clinical manifestation.

Material and methods: We selected consecutively 51 non-anticoagulated patients (26 men, 25 women, mean age: 59.84 ±1.60) with PAF and 52 controls (26 men, 26 women, mean age: 59.50 ±1.46 years) corresponding in gender, accompanying diseases and conducted treatment. The indicators were examined using enzyme-linked immunoassays and photometric tests.

Results: All patients were hospitalized between the 2nd and 24th h after the onset of arrhythmia (mean: 8.14 ±0.74 h). Higher FVIII levels (107.52 ±3.48% vs. 93.85 ±2.93%, p < 0.05) and activity (200.03 ±11.11% vs. 109.73 ±4.90%, p < 0.001) were found in the PAF group. vWF levels (178.40 ±12.95% vs. 119.53 ±6.12%, p < 0.001) and activity (200.92 ±12.45% vs. 110.80 ±5.14%, p < 0.001) were also higher. These changes did not depend on age, sex, body mass index or CHA2DS2-VASc score in the PAF group (p > 0.05). PAF duration was a significant predictor of increased FVIII levels and activity. Increased PAF duration was followed by increased values of the factors (r = 0.85, p < 0.001; r = 0.83, p < 0.001).

Conclusions: The results presented an activated coagulation cascade and endothelial injury, suggesting hypercoagulability still in the early hours of PAF. These changes in PAF did not correlate with CHA2DS2-VASc score risk factors, outlining PAF as a possible independent embolic risk factor.

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