Sabeti Schila, Exner Markus, Mlekusch Wolfgang, Amighi Jasmin, Quehenberger Peter, Rumpold Helmut, Maurer Gerald, Minar Erich, Wagner Oswald, Schillinger Martin
Department of Angiology, Medical University of Vienna, Austria.
Stroke. 2005 Jul;36(7):1400-4. doi: 10.1161/01.STR.0000169931.96670.fc. Epub 2005 Jun 2.
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.
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).
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.
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.
纤维蛋白原是凝血级联反应中的关键因子，具有促炎特性，提示其在动脉粥样硬化形成中起关键作用。我们研究了纤维蛋白原是否能预测颈动脉粥样硬化的未来进展，分析纤维蛋白原水平是否能增加其他炎症参数的预后信息。
我们对1268例近期（12个月内）无脑血管疾病症状的连续患者进行了前瞻性研究。患者每隔6至9个月接受一次系列超声检查，将颈动脉狭窄程度分为0%至29%、30%至49%、50%至69%、70%至89%或90%至99%，或闭塞。在基线和随访时测定纤维蛋白原水平。根据纤维蛋白原水平计算颈动脉粥样硬化进展的风险，并对传统危险因素和其他炎症参数（C反应蛋白和血清淀粉样蛋白A）进行校正。
1268例患者中有117例（9.2%）在中位8个月（范围6至18个月）后出现颈动脉粥样硬化进展。与最低四分位数相比，随着基线纤维蛋白原四分位数的增加，动脉粥样硬化进展的校正风险比分别为1.83（P = 0.037）、2.09（P = 0.008）和2.45（P = 0.002）。随访时的纤维蛋白原水平也与疾病进展相关（P = 0.004）。然而，在进一步校正其他炎症参数后，这些关联减弱至无显著意义的水平。
升高的纤维蛋白原反映炎症活动水平，与颈动脉粥样硬化进展相关，正如之前其他炎症参数所显示的那样。然而，这种关联似乎与动脉粥样硬化疾病中炎症过程的程度非特异性相关，而非与纤维蛋白原的特定特性相关。
