急性发作的人类心房颤动与局部心脏血小板活化和内皮功能障碍有关。

Acute onset human atrial fibrillation is associated with local cardiac platelet activation and endothelial dysfunction.

作者信息

Akar Joseph G, Jeske Walter, Wilber David J

机构信息

Cardiovascular Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.

出版信息

J Am Coll Cardiol. 2008 May 6;51(18):1790-3. doi: 10.1016/j.jacc.2007.11.083.

DOI:10.1016/j.jacc.2007.11.083

PMID:18452786

Abstract

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 micromol/l to 243.8 +/- 120.1 micromol/l, p = 0.003), decreased nitric oxide production (25.2 +/- 10.8 micromol/l to 22.3 +/- 10.0 micromol/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.

摘要

目的

本研究旨在确定急性发作的心房颤动（AF），在不依赖其他危险因素的情况下，是否易导致早期血栓前状态。

背景

多种危险因素易导致人类房颤时的高凝状态，但仅急性发作的房颤是否具有血栓形成倾向仍不清楚。

方法

阵发性房颤患者（n = 22）接受射频导管消融术。所有患者均表现为窦性心律。同时从股静脉（全身样本）和冠状窦（局部心脏样本）采集基线血样。14例患者（房颤组）通过心房猝发起搏诱发房颤。对照组（n = 8）以120次/分钟的频率进行心房起搏。15分钟后再次采集血样。使用流式细胞术检测血小板P-选择素表达（CD62）。使用酶联免疫吸附测定法检测凝血酶生成标志物（凝血酶抗凝血酶复合物、凝血酶原片段1.2）、炎症标志物（C反应蛋白、白细胞介素-6）和一氧化氮。

结果

对照组局部和全身的血小板激活均未发生变化。在房颤组中，局部心脏血小板激活（P-选择素[+]血小板百分比）显著增加（从2.2±0.6%增至2.8±1.0%，p = 0.007）；然而，全身血小板激活未发生变化。房颤组局部凝血酶生成增加（凝血酶抗凝血酶复合物：从8.5±7.6 ng/ml增至33.2±17.4 ng/ml，p = 0.003；凝血酶原片段1.2：从95.6±45.6 μmol/l增至243.8±120.1 μmol/l，p = 0.003），一氧化氮生成减少（从25.2±10.8 μmol/l降至22.3±10.0 μmol/l，p < 0.02），炎症标志物无变化。