Why the study?
Does fine fibrillatory wave amplitude associate with left atrial appendage dysfunction, hypercoagulability, and cerebral embolism in patients with chronic nonrheumatic atrial fibrillation?
Does fine fibrillatory wave amplitude associate with left atrial appendage dysfunction, hypercoagulability, and cerebral embolism in patients with chronic nonrheumatic atrial fibrillation?
Fine fibrillatory waves (<1 mm) in lead V1 are a useful marker of left atrial appendage dysfunction and hypercoagulability, indicating a higher risk for cerebral embolism in patients with chronic nonrheumatic atrial fibrillation.
May flag higher embolism risk in chronic AF; hypothesis-generating for amplitude-based stratification, pending prospective validation.
Large left atrium (LA) and LA appendage (LAA) dysfunction are known to relate to cardiogenic thromboembolism, so the present study investigated the relation of the atrial fibrillatory wave (F wave) amplitude to hemostatic markers and LAA function. Transthoracic and transesophageal echocardiographic studies were performed in 82 consecutive patients with chronic, nonrheumatic atrial fibrillation (AF). Patients were divided into 2 groups according to F wave amplitude in lead V1 on the 12-lead ECG: coarse AF (the greatest amplitude of F wave > or =1 mm, n=44) and fine AF (<1 mm, n=38). Plasma levels of thrombin-antithrombin III complex, D-dimer, platelet factor 4 and beta-thromboglobulin were determined. Compared with patients with coarse AF, those with fine AF had lower LAA peak flow velocity (p<0.05) and higher prevalence of embolic cerebral infarction (50% vs 27%, p<0.05). Platelet activity did not differ between the 2 groups; however, plasma levels of thrombin-antithrombin III complex and D-dimer were significantly higher in patients with fine AF than in those with coarse AF (p<0.05). Multiple logistic regression analysis showed that fine AF was independently associated with cerebral embolism. Therefore, the presence of fine F wave in V1 would be a useful marker of LAA dysfunction and hypercoagulability, and indicate a risk for cerebral embolism in patients with chronic, nonrheumatic AF.
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Nakagawa et al. (2001) studied this question.
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