Key result
Aspirin and warfarin fail to reduce elevated platelet activation in patients with AF.
Why the study?
Platelet function may be abnormal in patients with AF and related to abnormal thrombogenesis, prompting investigation into platelet activation and the effects of antithrombotic therapy.
Does antithrombotic therapy (aspirin or warfarin) improve platelet activation and coagulation markers in patients with atrial fibrillation compared to no therapy?
Population
238 patients with AF and 50 age- and sex-matched normal subjects
Comparison
No antithrombotic therapy vs aspirin vs dose-adjusted warfarin vs healthy controls
Design
Cross-sectional study
Authors
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No aggregation abnormalities in AF despite marker shifts; leaves open platelet activation's role in thromboembolic risk.
Cross-Sectional (n=288)
Does antithrombotic therapy (aspirin or warfarin) improve platelet activation and coagulation markers in patients with atrial fibrillation compared to no therapy?
Atrial fibrillation is associated with increased platelet activation and thrombogenesis, but standard antithrombotic therapies (aspirin, warfarin) do not significantly reduce platelet activation, suggesting it may not be the primary driver of thromboembolism in AF.
S Kamath (2002) conducted a cross-sectional in Atrial fibrillation (n=288). Antithrombotic therapy (aspirin or warfarin) vs. No antithrombotic therapy and healthy controls was evaluated on Platelet markers (plasma beta-thromboglobulin, soluble glycoprotein V), coagulation markers (fibrin D-dimer and fibrinogen), and platelet aggregation. Untreated atrial fibrillation patients had higher platelet activation markers than healthy controls, and treatment with warfarin or aspirin failed to significantly reduce platelet activation.