Hypercoagulability and haemodynamic abnormalities in atrial fibrillation.

Non-valvar atrial fibrillation confers a substantial risk for stroke and thromboembolism which is estimated to be between 4-5% and 12% per year depending on associated risk factors.'2 Recent studies have established the value of warfarin as thromboprophylaxis in atrial fibrillation; however, this treatment carries with it the inconvenience of regular monitoring of anticoagulation intensity and the risk of bleeding.' 2 Attention has therefore focused on the development of alternative, safe, and convenient antithrombotic regimens, and appropriate thromboembolic risk stratification. For example, a low intensity fixed dose warfarin-aspirin regimen has certain attractions for convenience, but the recent third Stroke Prevention in Atrial Fibrillation study demonstrated the lower efficacy of this regimen compared with conventional, adjusted dose, warfarin therapy.3 Careful risk stratification has also been advocated to ensure that patients with atrial fibrillation at high risk of stroke and thromboembolism receive warfarin, while low risk patients are at least treated with aspirin. A strategy of prescribing warfarin to every patient with atrial fibrillation, irrespective of risk stratification, may increase risk of bleeding, particularly intracranial haemorrhage, and cause unnecessary inconvenience to patients.4 Most risk stratification can be performed on clinical criteria alone, with some refinement of risk stratification using echocardiography.2 However, other developments to assist thromboembolic risk stratification are needed; one area may be the study of various haemostatic and clotting indices that suggest a hypercoagulable state. As long as 150 years ago, Virchow5 postulated three components for thrombogenicity: abnormalities in the blood vessel wall, blood flow, and blood constituents. These three basic postulates appear to be fulfilled in patients with atrial fibrillation. Clinical and echocardiographic criteria may help identify the first two of Virchow's basic postulates for thrombogenesis-abnormalities of vessels and blood flow, such as heart valve disease and cardiac impairment. It is also well recognised that atrial fibrillation confers a hypercoagulable state, satisfying the third ofVirchow's postulates.6 The hypercoagulable state in chronic atrial fibrillation appears to be independent of the underlying aetiology or any structural heart disease, including left atrial size or left ventricular function.79 Patients with paroxysmal atrial fibrillation have also been shown to demonstrate abnormalities of haemostasis'"II related to the duration of a paroxysm of atrial fibrillation and whether the patient was in atrial fibrillation at the time of sampling." l Patients who are started