title: C-reactive protein and left atrial appendage velocity are independent determinants of the risk of thrombogenesis in patients with atrial fibrillation.
abstract: BACKGROUND
  The association between inflammatory status and thrombosis in patients with atrial fibrillation (AF) is unclear. We studied the correlation between inflammation and the risk of thrombogenesis in patients with AF and the relationship of inflammation with other factors associated with thrombotic risk.
  
  
  METHODS
  We studied 150 consecutive patients (69 men, age 65+/-12 years) with persistent non-valvular AF who had transesophageal echocardiography prior to cardioversion. Patients underwent also measurements of high-sensitivity C-reactive protein, fibrinogen, D-dimer, and hematocrit levels.
  
  
  RESULTS
  Patients were divided into two groups according to the presence (n=52) or absence (n=98) of dense spontaneous echo contrast (SEC) in left atrium or left atrial appendage. The two groups were similar for age, sex, and major clinical risk factors. Patients with dense SEC had significantly larger left atrium diameter (p=0.007), lower left atrial appendage mean velocity (p<0.0001), and higher levels of C-reactive protein (p=0.003), D-dimer (p=0.008), and fibrinogen (p=0.006). At multivariate analysis, only left atrial appendage velocity (odds ratio: 19.11; 95% confidence interval 4.2-80.9) and C-reactive protein (odds ratio: 3.41; 95% confidence interval 1.2-9.8) were significantly associated with thrombus and/or dense SEC. However, there was no relationship between C-reactive protein levels and left atrial appendage velocity (p=0.24, r=-0.09).
  
  
  CONCLUSIONS
  Our results show that left atrial appendage velocity and C-reactive protein are independently associated with the risk of thromboembolism in AF. Thus, blood stasis and inflammation appear to constitute two major distinct components of thrombogenesis.
authors.affiliation: Department of Cardiology, San Filippo Neri Hospital, Rome, Italy. c.cianfrocca@mclink.it
authors.forename: Cinzia
authors.initials: C
authors.lastname: Cianfrocca
authors.forename: Maria Luisa
authors.initials: ML
authors.lastname: Loricchio
authors.forename: Francesco
authors.initials: F
authors.lastname: Pelliccia
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Pasceri
authors.forename: Antonio
authors.initials: A
authors.lastname: Auriti
authors.forename: Leopoldo
authors.initials: L
authors.lastname: Bianconi
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Guido
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Rosano
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mercuro
authors.forename: Massimo
authors.initials: M
authors.lastname: Santini
mesh_terms: D000368:Aged; D020517:Atrial Appendage / Q000502:physiology*; D001281:Atrial Fibrillation / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D016279:Atrial Function, Left / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D002097:C-Reactive Protein / Q000502:physiology*; D003430:Cross-Sectional Studies; D017548:Echocardiography, Transesophageal; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology
chemical_list: D002097:C-Reactive Protein