Prognostic impact of fibrinogen in carotid atherosclerosis: nonspecific indicator of inflammation or independent predictor of disease progression?
BACKGROUND
Fibrinogen is a key factor in the coagulation cascade, it exhibits proinflammatory properties, and it is suggested to play a pivotal role in atherogenesis. We investigated whether fibrinogen predicts future progression of carotid atherosclerosis, analyzing whether fibrinogen levels add to the prognostic information of other inflammatory parameters.


METHODS
We prospectively studied 1268 consecutive patients without recent (12 months) symptoms from cerebrovascular disease. Patients underwent serial ultrasound investigations in 6- to 9-month intervals, categorizing carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed, or occluded. Fibrinogen levels were determined at baseline and follow-up. The risk for progressive carotid atherosclerosis according to fibrinogen levels was calculated, adjusting for traditional risk factors and other inflammatory parameters (C-reactive protein and serum amyloid A).


RESULTS
Progression of carotid atherosclerosis was found in 117 of 1268 patients (9.2%) after a median of 8 months (range 6 to 18). Adjusted hazard ratios for atherosclerosis progression with increasing quartiles of baseline fibrinogen were 1.83 (P=0.037), 2.09 (P=0.008), and 2.45 (P=0.002), respectively, compared with the lowest quartile. Fibrinogen at follow-up also was associated with progressive disease (P=0.004). However, additionally adjusting for other inflammatory parameters diminished these associations to a nonsignificant level.


CONCLUSIONS
Elevated fibrinogen, reflecting the level of inflammatory activity, is associated with progression of carotid atherosclerosis, as it was demonstrated previously for other inflammatory parameters. However, this association seems to be nonspecifically related to the extent of the inflammatory process in atherosclerotic disease rather than to specific properties of fibrinogen.
Sabeti
Schila
S
Department of Angiology, Medical University of Vienna, Austria.
Exner
Markus
M
Mlekusch
Wolfgang
W
Amighi
Jasmin
J
Quehenberger
Peter
P
Rumpold
Helmut
H
Maurer
Gerald
G
Minar
Erich
E
Wagner
Oswald
O
Schillinger
Martin
M
D000368:Aged; D050197:Atherosclerosis / Q000473:pathology; D015415:Biomarkers; D002097:C-Reactive Protein / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005340:Fibrinogen / Q000096:biosynthesis / Q000737:chemistry / Q000378:metabolism*; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011379:Prognosis; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012306:Risk; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000378:metabolism; D013997:Time Factors; D014463:Ultrasonography
D015415:Biomarkers; D000685:Serum Amyloid A Protein; D005340:Fibrinogen; D002097:C-Reactive Protein