Acute onset human atrial fibrillation is associated with local cardiac platelet activation and endothelial dysfunction
Acute onset human atrial fibrillation is associated with local cardiac platelet activation and endothelial dysfunction
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DOI：
10.1016/j.jacc.2007.11.083
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发表时间：
2008-05-06
影响因子：
24
通讯作者：
Wilber, David J.
中科院分区：
文献类型：
--
作者：
Akar, Joseph G.;Jeske, Walter;Wilber, David J.
目的本研究的目的是确定是否急性发作的心房颤动（AF），独立于其他危险因素，易患早期血栓前state.Background几个危险因素易患高凝状态在人类AF，但是否急性发作的AF单独是prothrombotic仍然uncleared.Methods阵发性AF患者（n = 22）进行射频导管消融。所有患者均为窦性心律。从股静脉（全身样本）和冠状窦（局部心脏样本）同时采集基线血样。房颤组14例，采用心房短阵起搏诱发房颤。对照组（n = 8）行心房起搏，起搏频率为120次/min，15 min后采血，流式细胞术检测血小板P-选择素（CD 62）表达。凝血酶生成的标志物（凝血酶抗凝血酶复合物，凝血酶原片段1.2），炎症（C-反应蛋白，白细胞介素-6），和一氧化氮测定使用酶联免疫吸附试验。在AF组中，局部心脏血小板活化（P-选择素[+]血小板百分比）显著增加（2.2 +/- 0.6%至2.8 +/-1.0%，p = 0.007）;然而，全身血小板活化没有变化。AF组局部凝血酶生成增加（凝血酶抗凝血酶复合物：8.5 +/- 7.6 ng/ml至33.2 +/- 17.4 ng/ml，p = 0.003;凝血酶原片段1.2：95.6 +/- 45.6 μ mol/l至243.8 +/- 120.1 μ mol/l，p = 0.003），一氧化氮生成减少（25.2 +/- 10.8 μ mol/l至22.3 +/- 10.0 μ mol/l，p < 0.02），炎症标志物无变化。结果表明，房颤如何单独，独立于其他危险因素，可能有助于高凝状态。
Objectives The purpose of this study was to determine whether acute onset atrial fibrillation (AF), independent of other risk factors, predisposes to an early prothrombotic state.Background Several risk factors predispose to the hypercoagulable state in human AF, but whether acute onset AF alone is prothrombotic remains unclear.Methods Patients with paroxysmal AF (n = 22) underwent radiofrequency catheter ablation. All patients presented in sinus rhythm. Baseline blood samples were obtained simultaneously from the femoral vein (systemic sample) and the coronary sinus (local cardiac sample). The AF was induced by burst atrial pacing in 14 patients (AF group). A control group (n = 8) underwent atrial pacing at 120 beats/min. Blood samples were recollected after 15 min. Platelet P-selectin expression (CD62) was measured using flow cytometry. Markers of thrombin generation (thrombin antithrombin complex, prothrombin fragment 1.2), inflammation (C-reactive protein, interleukin-6), and nitric oxide were measured using enzyme-linked immunosorbent assays.Results Neither local nor systemic platelet activation changed in the control group. In the AF group, local cardiac platelet activation (percent P-selectin [+] platelets) increased significantly (2.2 +/- 0.6% to 2.8 +/- 1.0%, p = 0.007); however, systemic platelet activation did not change. The AF group had increased local thrombin generation (thrombin antithrombin complex: 8.5 +/- 7.6 ng/ml to 33.2 +/- 17.4 ng/ml, p = 0.003; prothrombin fragment 1.2: 95.6 +/- 45.6 mu mol/l to 243.8 +/- 120.1 mu mol/l, p = 0.003), decreased nitric oxide production (25.2 +/- 10.8 mu mol/l to 22.3 +/- 10.0 mu mol/l, p < 0.02), and no change in inflammatory markers.Conclusions Human AF causes local cardiac platelet activation within minutes of onset. The results demonstrate how AF alone, independent of other risk factors, may contribute to the hypercoagulable state.