title: Thoracic aortic plaque enhances hypercoagulability in patients with nonrheumatic atrial fibrillation.
abstract: BACKGROUND
  Patients with atrial fibrillation (AF) are at risk for thromboembolism, and coexistent cardiovascular diseases could affect their prothrombotic profiles. The relationship between plasma hemostatic markers and aortic atherosclerosis was determined in patients with AF or in sinus rhythm (SR).
  
  
  RESULTS
  Sixty patients with nonrheumatic AF and 46 patients in SR who underwent transesophageal echocardiography and did not receive anticoagulant therapy constituted the study group. Markers for platelet activity (platelet factor 4 and beta-thromboglobulin), thrombotic status (thrombin-antithrombin III complex and prothrombin fragment 1+2 (F1+2)) and fibrinolytic status (plasmin-alpha2-plasmin inhibitor complex (PIC) and D-dimer) were determined. Levels of F1+2, PIC and D-dimer were higher in AF patients with severe atheroma than in those without severe atheroma (p<0.05). In patients in SR, hemostatic markers were not significantly increased even if they had severe aortic atherosclerosis. AF (Odds ratio (OR) 4.06, p=0.04) and age>or=75 years (OR 3.98, p=0.02) were independently predictive of elevated D-dimer levels and severe atheroma was predictive of elevated F1+2 levels (OR 5.52, p=0.04).
  
  
  CONCLUSIONS
  Elderly patients with AF and severe aortic atherosclerosis might be in a prothrombotic state, and could benefit from intensive antithrombotic therapy.
authors.affiliation: Second Department of Internal Medicine, University of Toyama, Japan.
authors.forename: Keiko
authors.initials: K
authors.lastname: Nakagawa
authors.forename: Tadakazu
authors.initials: T
authors.lastname: Hirai
authors.forename: Kenji
authors.initials: K
authors.lastname: Sakurai
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Ohara
authors.forename: Takashi
authors.initials: T
authors.lastname: Nozawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Inoue
mesh_terms: D000368:Aged; D000990:Antithrombin III; D001018:Aortic Diseases / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D001146:Arrhythmia, Sinus / Q000097:blood / Q000150:complications / Q000503:physiopathology; D050197:Atherosclerosis / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D001281:Atrial Fibrillation / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D017548:Echocardiography, Transesophageal; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D010978:Platelet Factor 4 / Q000378:metabolism; D011516:Prothrombin; D012307:Risk Factors; D013923:Thromboembolism / Q000209:etiology / Q000503:physiopathology; D019851:Thrombophilia / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D000979:alpha-2-Antiplasmin / Q000378:metabolism; D001620:beta-Thromboglobulin / Q000378:metabolism
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; C045879:prothrombin fragment 1.2; D010978:Platelet Factor 4; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases; D005341:Fibrinolysin