Mechanisms of thrombogenesis in atrial fibrillation: Virchow's triad revisited

Summary

Atrial fibrillation is the most common sustained cardiac arrhythmia, which is associated with a high risk of stroke and thromboembolism. Increasing evidence suggests that the thrombogenic tendency in atrial fibrillation is related to several underlying pathophysiological mechanisms. Abnormal changes in flow are evident by stasis in the left atrium, and seen as spontaneous echocontrast. Abnormal changes in vessel walls—essentially, anatomical and structural defects—include progressive atrial dilatation, endocardial denudation, and oedematous or fibroelastic infiltration of the extracellular matrix. Additionally, abnormal changes in blood constituents are well described, and include haemostatic and platelet activation, as well as inflammation and growth factor changes. These changes result in the fulfilment of Virchow's triad for thrombogenesis, and accord with a prothrombotic or hypercoagulable state in this arrhythmia. In this Review, we present an overview of the established and purported mechanisms for thrombogenesis in atrial fibrillation.