title: Pathophysiologic correlates of thromboembolism in nonvalvular atrial fibrillation: II. Dense spontaneous echocardiographic contrast (The Stroke Prevention in Atrial Fibrillation [SPAF-III] study).
abstract: We analyzed transesophageal echocardiograms from 772 participants in the Stroke Prevention in Atrial Fibrillation (SPAF-III) study, characterizing spontaneous echocardiographic contrast (SEC) in the left atrium or appendage as faint or dense. The association of dense SEC with stroke risk factors and anatomic, hemodynamic, and hemostatic parameters related to specific thromboembolic mechanisms was evaluated by multivariate analysis. Spontaneous echocardiographic contrast was present in 55% of patients and was dense in 13%. Age (odds ratio [OR] 2.4/decade, P <.001), constant atrial fibrillation (OR 6.9, P <.001), history of hypertension (OR 3. 2, P <.001), and current tobacco smoking (OR 2.6, P =.04) were independent clinical predictors of dense SEC. Multivariate analysis of clinical, echocardiographic, and hemostatic parameters yielded age as the sole independent clinical predictor of dense SEC (OR 2. 4/decade, P <.001). Other independent predictors were measures of left atrial/appendage flow dynamics, left atrial size (OR 2.4/cm diameter, M-mode, P <.001), atherosclerotic aortic plaque (OR 2.8, P =.002), and plasma fibrinogen >350 mg/dL (P <.001). Results were similar when SEC of any density was analyzed. In conclusion, SEC occurred in more than half of these patients with prospectively defined nonvalvular atrial fibrillation but was usually faint. Dense SEC was strongly associated with previously reported clinical predictors of stroke, linking them to thromboembolism through atrial stasis. Diverse pathophysiologic factors including atrial stasis, fibrinogen level, and aortic plaque influence SEC.
authors.affiliation: Division of Cardiology, Hennepin County Medical Center, Minneapolis, MN 55415, USA. asing001@maroon.tc.mn.edu
authors.forename: R W
authors.initials: RW
authors.lastname: Asinger
authors.forename: J
authors.initials: J
authors.lastname: Koehler
authors.forename: L A
authors.initials: LA
authors.lastname: Pearce
authors.forename: M
authors.initials: M
authors.lastname: Zabalgoitia
authors.forename: J L
authors.initials: JL
authors.lastname: Blackshear
authors.forename: P E
authors.initials: PE
authors.lastname: Fenster
authors.forename: R
authors.initials: R
authors.lastname: Strauss
authors.forename: D
authors.initials: D
authors.lastname: Hess
authors.forename: G D
authors.initials: GD
authors.lastname: Pennock
authors.forename: R M
authors.initials: RM
authors.lastname: Rothbart
authors.forename: J L
authors.initials: JL
authors.lastname: Halperin
mesh_terms: D000368:Aged; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology; D001783:Blood Flow Velocity; D003287:Contrast Media / Q000008:administration & dosage; D004359:Drug Therapy, Combination; D015150:Echocardiography, Doppler; D017548:Echocardiography, Transesophageal / Q000379:methods*; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D002542:Intracranial Embolism and Thrombosis / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D008297:Male; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012307:Risk Factors; D020521:Stroke / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D003287:Contrast Media; D010975:Platelet Aggregation Inhibitors; D014859:Warfarin; D001241:Aspirin