**3. Conclusion**

The mechanisms underlying thrombogenesis in atrial fibrillation are clearly complex and re‐ main only partly understood. Abnormal changes in flow, vessel wall, and blood constituents in atrial fibrillation fulfil Virchow's triad for thrombogenesis, and accord with a prothrombotic or hypercoagulable state in this arrhythmia. That this process is related purely to blood stasis is no longer accepted. Various abnormal changes related both to atrial fibrillation and its comorbidi‐ ties impart a synergistic effect in maintaining a hypercoagulable state in this condition.
