title: Left atrial appendage function and abnormal hypercoagulability in patients with atrial flutter.
abstract: OBJECTIVE
  The prevalence of thromboembolism might be higher than previously recognized in patients with atrial flutter (AFL) based on findings of transesophageal echocardiography (TEE). To evaluate the potential prothrombotic state in patients with AFL, TEE findings and hemostatic markers were compared among patient groups with AFL, normal sinus rhythm (NSR) and chronic nonvalvular atrial fibrillation (AF).
  
  
  METHODS
  Cross-sectional study at a university hospital.
  
  
  METHODS
  In 28 patients (mean age, 63 years) with AFL, 58 patients (mean age, 66 years) with AF, and 27 patients (mean age, 61 years) with NSR who underwent TEE, plasma levels of markers for platelet activity (platelet factor 4 and beta-thromboglobulin [beta-TG]), thrombotic status (thrombin-antithrombin III complex and prothrombin fragments 1 and 2) and fibrinolytic status (d-dimer and plasmin-alpha(2)-plasmin inhibitor complex) were determined.
  
  
  RESULTS
  Left atrial appendage (LAA) blood flow velocity in patients with AFL was higher (p < 0.05) than that in patients with AF, but was lower (p < 0.05) than that in patients with NSR (AF, 25 +/- 2; AFL, 44 +/- 4; NSR, 60 +/- 4 cm/s). Dense left atrial spontaneous echo contrast (SEC) was found in 4 patients (14%) with AFL and 16 patients (28%) with AF. There was no significant difference in plasma levels of hemostatic markers between the AFL group and the NSR group. AFL patients with impaired LAA function (LAA flow < 30cm/s, dense SEC, or both), however, showed higher level of d-dimer and beta-TG than those without impaired LAA function (d-dimer, 1.9 +/- 0.6 microg/mL vs 0.4 +/- 0.1 microg/mL; beta-TG, 73 +/- 17 ng/mL vs 33 +/- 5 ng/mL, p < 0.05).
  
  
  CONCLUSIONS
  Patients with AFL as a whole are not in the prothrombotic state as compared with those with AF. However, patients with AFL and impaired LAA function are at potentially high risk for thromboembolism and might require anticoagulation.
authors: Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Toyama, Japan.
authors: Kenji
authors: K
authors: Sakurai
authors: Tadakazu
authors: T
authors: Hirai
authors: Keiko
authors: K
authors: Nakagawa
authors: Tomoki
authors: T
authors: Kameyama
authors: Takashi
authors: T
authors: Nozawa
authors: Hidetsugu
authors: H
authors: Asanoi
authors: Hiroshi
authors: H
authors: Inoue
mesh_terms: D000368:Aged; D020517:Atrial Appendage / Q000503:physiopathology*; D001281:Atrial Fibrillation / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D001282:Atrial Flutter / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004452:Echocardiography; D017548:Echocardiography, Transesophageal; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006487:Hemostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010978:Platelet Factor 4 / Q000032:analysis; D012307:Risk Factors; D013923:Thromboembolism / Q000097:blood / Q000209:etiology; D019851:Thrombophilia / Q000150:complications* / Q000175:diagnosis; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D001620:beta-Thromboglobulin; C036309:fibrin fragment D; D010978:Platelet Factor 4