Platelets and atrial fibrillation.

Atrial fibrillation is the commonest sustained cardiac rhythm abnormality, leading to substantial mortality and morbidity from stroke, thromboembolism and heart failure. Whilst the benefits of antithrombotic therapy in preventing stroke in atrial fibrillation are increasingly recognised, further developments in thromboprophylaxis are needed, especially since warfarin confers the inconvenience of regular anticoagulation monitoring and the benefits of aspirin are inconsistent. An understanding of the role of platelets in atrial fibrillation may contribute to the development of new or combination antiplatelet agents that may provide a viable alternative to warfarin for thromboprophylaxis in atrial fibrillation. Important insights into the pathophysiology of thrombus formation (thrombogenesis) in atrial fibrillation can be made by reference to the different components of Virchow’s triad for thrombogenesis, that is, abnormal blood flow, abnormal blood constituents and vessel wall abnormalities. Various studies have confirmed that atrial fibrillation confers a hypercoagulable state, with abnormalities of haemostasis and endothelial function in this condition, that can be altered by introducing antithrombotic therapy and cardioversion from atrial fibrillation to sinus rhythm. The hypercoagulable state in atrial fibrillation is also additive to the presence of structural and flow abnormalities in these patients, such as heart failure or valvular heart disease, thus fulfilling Virchow’s triad and substantially increasing the risk of stroke and thromboembolism. There have been many studies which have focused on clinical risk factors and structural heart disease as risk factors for thrombogenesis in atrial fibrillation. However, the studies exploring the presence of a hypercoagulable state in atrial fibrillation have concen-