Background: In atrial fibrillation (AF), endothelial dysfunction, activation of coagulation and inflammation system have been reported to influence prothrombotic and hypercoagulable state and maintenance of AF. However, it is not known which system is most quickly changed after the onset of AF and how these factors can contribute to thrmoboembolism. Methods: The study groups were sinus rhythm (group I: n=41, M:F=24:17, 48짹15 years) without history of atrial tachyarrhythmia, paroxysmal AF(group II: n=31, M:F=25:6, 51짹13 years). Those who have risk factors for thromboembolism such as hypertension, valvular heart disease, older than 65 years were excluded from both groups. In group II, AF was terminated spontaneously during controlling ventricular reponse in 72 hours after the onset and blood samples were taken between 24 and 48 hours. Markers for endothelial function (von-Willebrand factor, vWF; factor 8 related antigen and ristocetin cofactor), inflammation [white blood cell counts, erythrocyte sedimentation rate, quantitative and high sensitivity C-reactive protein (CRP)] and coagulation system (fibrinogen, fibrinogen degradation product, fibrin d-dimer) were studied. Results: There were no significant differences in clinical characteristics between both groups. Echocardiographic parameters were not significantly different between two groups except for larger left atrial diameter in group II than group I (31.6짹5.3 mm vs. 35.6짹7.8 mm, p=0.035). vWF-factor 8 related antigen and ristocetin cofactor were not different between two groups [(group I: 131짹54%, group II: 144짹55%, p=0.297), (group I: 85짹42%, group II: 92짹24%, p=0.454)]. Quantitative CRP was not significantly different (group I: 0.31짹0.38, group II: 0.44짹0.44, p=0.170) however, high sensitivity CRP was significantly increased in group II than in group I (group I: 0.09짹0.16, group II: 0.23짹0.34, p=0.014). Fibrinogen (group I: 255짹60, group II: 284짹87, p=0.086), d-dimer (group I: 0.12짹0.10, group II: 0.11짹0.13, p=0.733) were not different significantly. Conclusion: Activation of inflammation is the quickest response after the onset of AF and may be related to thrombogenesis.