title: Haemostatic and haemodynamic abnormalities associated with left atrial thrombosis in non-rheumatic atrial fibrillation.
abstract: OBJECTIVE
  To evaluate the role of haemostatic and haemodynamic variables in left atrial thrombosis in non-rheumatic atrial fibrillation.
  
  
  METHODS
  Case-control study.
  
  
  METHODS
  One hundred and nine patients with non-rheumatic atrial fibrillation.
  
  
  METHODS
  Peak blood velocity measured at three sites in the left atrium. Venous blood sampled for coagulant proteins and markers of haemostatic activation.
  
  
  METHODS
  Presence of left atrial thrombus and spontaneous echo contrast at transoesophageal echocardiography.
  
  
  RESULTS
  Left atrial thrombus was identified in 19 patients (18%), 16 of whom had spontaneous echo contrast. Patients with thrombus had reduced peak left atrial appendage velocity compared with those without (0.17 v 0.26 m/s; P < 0.001), but no significant reductions in peak mid-left atrial or mitral valve outflow velocity. Patients with thrombus had increased plasma markers of platelet activation-beta thromboglobulin (56.8 v 30.4 IU/ml; P < 0.001) and platelet factor 4 (6.1 v 3.5 IU/ml; P < 0.01)-and of thrombogenesis: thrombin-antithrombin complexes (5.59 v 3.06 micrograms/ml; P < 0.001) and D-dimers (479 v 298 ng/ml; P < 0.01). von Willebrand factor was also increased (1.81 v 1.52 IU/ml; P < 0.05). A multiple logistic regression model identified left atrial appendage velocity (P = 0.001), beta thromboglobulin (P = 0.002), and von Willebrand factor (P = 0.04) as the independent associates of left atrial thrombosis, ahead of the presence of spontaneous echo contrast.
  
  
  CONCLUSIONS
  Haemostatic and haemodynamic abnormalities are associated with left atrial thrombus in non-rheumatic atrial fibrillation, and may help stratify thromboembolic risk.
authors.affiliation: Division of Medicine, University of Leeds, United Kingdom.
authors.forename: R M
authors.initials: RM
authors.lastname: Heppell
authors.forename: K E
authors.initials: KE
authors.lastname: Berkin
authors.forename: J M
authors.initials: JM
authors.lastname: McLenachan
authors.forename: J A
authors.initials: JA
authors.lastname: Davies
mesh_terms: D000368:Aged; D000990:Antithrombin III / Q000032:analysis; D001281:Atrial Fibrillation / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D017548:Echocardiography, Transesophageal; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006325:Heart Atria / Q000000981:diagnostic imaging; D006331:Heart Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D008297:Male; D010447:Peptide Hydrolases / Q000032:analysis; D010978:Platelet Factor 4 / Q000032:analysis; D013927:Thrombosis / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D001620:beta-Thromboglobulin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; C036309:fibrin fragment D; D014841:von Willebrand Factor; D010978:Platelet Factor 4; D000990:Antithrombin III; D010447:Peptide Hydrolases