Abstract
Left atrial (LA) thrombus formation is the presumed origin of thromboembolic complications in patients with atrial fibrillation (AF). Beyond clinical risk factors, the factors causing formation of LA thrombi are not well known. In this case-control study, we analyzed clinical characteristics and genetic thrombophilia markers (factor V Leiden (FVL), prothrombin G20210A (FIIV), Tyr2561 variant of von Willebrand factor (VWF-V)) in 42 patients with AF and LA thrombus (LAT) and in 68 control patients with AF without LAT (CTR). Patients with LAT had more clinical conditions predisposing to stroke (mean CHA2DS2-VASc-score 3.4 ± 1.5 vs. 1.9 ± 1.4; P < 0.001), a higher LA volume (96 ± 32 vs. 76 ± 21 ml, P = 0.002) and lower LA appendage emptying velocity (0.21 ± 0.11vs. 0.43 ± 0.19 m/s, P < 0.001). Prevalence of FVL, FIIV and VWF-V mutations was not different, but in the subgroup of patients <65 years (y) there was a tendency for a higher incidence of VWF-V with a prevalence of 27% (LAT <65 y) vs. 7% (CTR <65 y, P = 0.066). These findings warrant further investigation of the VWF-V as a risk factor for LA thrombogenesis in younger patients.
Highlights
Atrial fibrillation (AF) is the most common sustained arrhythmia in the general population and associated with a highly elevated risk of stroke and systemic embolism.[1]
Since predisposition for left atrium (LA) thombus through prothrombotic genetic variants is not established yet for atrial fibrillation, we studied gene variants known for their influence on venous thromboembolism and coronay artery disease
We found that left atrial size and function, estimated by echocardiography, is disturbed in patients with left atrial thrombus developing on anticoagulation
Summary
Atrial fibrillation (AF) is the most common sustained arrhythmia in the general population and associated with a highly elevated risk of stroke and systemic embolism.[1] Oral anticoagulation therapy (OAC) prevents the majority of ischemic strokes in patients with AF, but there is a residual stroke rate of ca 1%/ year.[2] Many thrombo-embolic events are believed to start with thrombus formation in the left atrium (LA), often in its appendage. LA thrombus formation is driven by slow blood flow, thrombogenic factors in the atrial endothelium and in the blood (Virchows triad).[3] The detection of LA thrombi in patients requires transoesophageal echocardiography. Based on observational data from transesophageal echocardiograms, the prevalence of LA thrombus in anticoagulated patients with AF ranges from 0%4 to 6.4%,5 with most studies finding LA thrombus with an incidence between 0.7% and 1.9%5-7 (Table 1)
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Schedule a callMore From: Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
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