Relation of fibrillatory wave amplitude with hemostatic abnormality and left atrial appendage dysfunction in patients with chronic nonrheumatic atrial fibrillation

Citation
K. Nakagawa et al., Relation of fibrillatory wave amplitude with hemostatic abnormality and left atrial appendage dysfunction in patients with chronic nonrheumatic atrial fibrillation, JPN CIRC J, 65(5), 2001, pp. 375-380
Citations number
41
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION
ISSN journal
00471828 → ACNP
Volume
65
Issue
5
Year of publication
2001
Pages
375 - 380
Database
ISI
SICI code
0047-1828(200105)65:5<375:ROFWAW>2.0.ZU;2-T
Abstract
Large left atrium (LA) and LA appendage (LAA) dysfunction are known to rela te to cardiogenic thromboembolism, so the present study investigated the re lation of the atrial fibrillatory wave (F wave) amplitude to hemostatic mar kers and LAA function. Transthoracic and transesophageal echocardiographic studies were performed in 82 consecutive patients with chronic, nonrheumati c atrial fibrillation (AF). Patients were divided into 2 groups according t o F wave amplitude in lead V1 on the 12-lead EGG: coarse AF (the greatest a mplitude of F wave greater than or equal to1 mm, n=44) and fine AF (<1 mm, n=38). Plasma levels of thrombin-antithrombin m 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 how 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 le vels of thrombin-antithrombin ill complex and D-dimer were significantly hi gher in patients with fine AF than in those with coarse AF (p<0.05), Multip le logistic regression analysis showed that fine AF was independently assoc iated with cerebral embolism. Therefore, the presence of fine F wave in VI would be a useful marker of LAA dysfunction and hypercoagulability, and ind icate a risk for cerebral embolism in patients with chronic, nonrheumatic A F.