Li-Saw-Hee F L, Blann A D, Edmunds E, Gibbs C R, Lip G Y
University Department of Medicine, City Hospital, Birmingham, United Kingdom.
Clin Cardiol. 2001 May;24(5):409-14. doi: 10.1002/clc.4960240512.
There is increasing evidence that chronic atrial fibrillation (AF) is associated with a prothrombotic or hypercoagulable state.
This study was undertaken to determine whether short-term exercise in patients with chronic AF would shift the overall hemostatic balance toward a more prothrombotic state with a reduction in fibrinolytic potential.
We recruited 20 patients (13 men; mean age 65 years +/- 11 standard deviation [SD]) with chronic AF who were not treated with antithrombotic therapy and exercised them to exhaustion using a multistage treadmill exercise (standard Bruce) protocol. Blood samples were taken pre exercise, immediately after cessation of exercise, and at 20 min post exercise. The prothrombotic state was quantified by fibrinogen (an index of hemorheology and a coagulation factor), soluble P-selectin (sP-sel, marking platelet activation), von Willebrand factor (vWF, an index of endothelial dysfunction), and plasminogen activator inhibitor-1 (PAI-1, a regulator of fibrinolytic activity) levels. There were two groups of age- and gender-matched controls in sinus rhythm: (1) healthy controls, and (2) "hospital controls" who were patients with vascular disease.
Baseline levels of vWf (p = 0.034) and fibrinogen (p < 0.0001), but not sP-sel (p = 0.075) were significantly elevated in patients with AF compared with both control groups in sinus rhythm. The PAI-1 levels were highest in the hospital control patients, but not in chronic AF (p = 0.041). Following treadmill exercise, achieving a mean metabolic equivalent of 4.9 METS (+/- 1.75 SD) and total exercise duration of 4.9 min (+/- 2 SD), there was a significant rise in plasma fibrinogen (repeated measures analysis of variance [ANOVA] p = 0.047) and a reduction in PAI-1 levels (p = 0.025) in patients with AF. There were no significant changes seen in vWf (p = 0.308) or sP-sel (p = 0.071) levels. No significant changes in these indices were seen in hospital controls (all p = not significant), despite a much longer duration of exercise with greater workload.
Patients with chronic AF have increased vWf and fibrinogen levels compared with sinus rhythm. Exercise to exhaustion influences the hypercoagulable state in chronic AF, with a rise in plasma fibrinogen and possible increase in fibrinolytic activity. Nevertheless, acute exercise does not appear to have a significant influence on endothelial dysfunction or platelet activation in patients with AF.
越来越多的证据表明,慢性心房颤动(房颤)与血栓前状态或高凝状态有关。
本研究旨在确定慢性房颤患者的短期运动会否使整体止血平衡向血栓前状态转变,同时纤溶潜力降低。
我们招募了20例未接受抗血栓治疗的慢性房颤患者(13例男性;平均年龄65岁±11标准差[SD]),采用多级跑步机运动(标准布鲁斯)方案让他们运动至力竭。在运动前、运动停止后即刻以及运动后20分钟采集血样。通过纤维蛋白原(血液流变学指标和凝血因子)、可溶性P-选择素(sP-sel,标记血小板活化)、血管性血友病因子(vWF,内皮功能障碍指标)和纤溶酶原激活物抑制剂-1(PAI-1,纤溶活性调节剂)水平对血栓前状态进行量化。有两组年龄和性别匹配的窦性心律对照组:(1)健康对照组,(2)患有血管疾病的“医院对照组”。
与窦性心律的两组对照组相比,房颤患者的vWf(p = 0.034)和纤维蛋白原(p < 0.0001)基线水平显著升高,但sP-sel(p = 0.075)未显著升高。PAI-1水平在医院对照患者中最高,但在慢性房颤患者中并非如此(p = 0.041)。在跑步机运动后,房颤患者达到平均代谢当量4.9梅脱(±1.75 SD),总运动持续时间4.9分钟(±2 SD),血浆纤维蛋白原显著升高(重复测量方差分析[ANOVA] p = 0.047),PAI-1水平降低(p = 0.025)。vWf(p = 0.308)或sP-sel(p = 0.071)水平未见显著变化。医院对照组这些指标未见显著变化(所有p = 无显著性差异),尽管运动持续时间长得多且工作量更大。
与窦性心律相比,慢性房颤患者的vWf和纤维蛋白原水平升高。运动至力竭会影响慢性房颤的高凝状态,导致血浆纤维蛋白原升高,纤溶活性可能增加。然而,急性运动似乎对房颤患者的内皮功能障碍或血小板活化没有显著影响。