Sumeray M S, Montgomery H E, Humphries S E
Hatter Institute for Cardiovascular Studies, University College London School of Medicine, UK.
Cardiovasc Drugs Ther. 1998 Jul;12(3):261-5. doi: 10.1023/a:1007713715744.
Fibrinogen is generally considered to be an important mediator of clot formation. However, its effects on clots and perhaps other more direct effects may also make it a powerful mediator in the genesis and progression of atheromatous disease. Indeed, raised fibrinogen levels may pose as great a cardiovascular risk as classical risk factors such as elevated blood pressure or cholesterol levels. The plasma fibrinogen level of any given individual, and its associated cardiovascular risk, is dependent upon an interaction between environmental and intrinsic (genetic) factors. Most environmental factors associated with elevated fibrinogen levels are also potent cardiovascular risk factors (e.g., cigarette smoking). Less is known of the role played by genetic factors. However, as research into the genotypic influences on both basal and "stimulated" fibrinogen production continues, high-risk groups may be identified that may benefit from therapeutic intervention aimed at lowering plasma fibrinogen.
纤维蛋白原通常被认为是血栓形成的重要介质。然而,它对血栓的影响以及可能的其他更直接的作用,也可能使其成为动脉粥样硬化疾病发生和发展的有力介质。事实上,纤维蛋白原水平升高所带来的心血管风险可能与血压升高或胆固醇水平升高等经典风险因素一样大。任何特定个体的血浆纤维蛋白原水平及其相关的心血管风险,取决于环境因素和内在(遗传)因素之间的相互作用。大多数与纤维蛋白原水平升高相关的环境因素也是强大的心血管风险因素(例如,吸烟)。关于遗传因素所起的作用,人们了解得较少。然而,随着对基因型对基础和“刺激后”纤维蛋白原产生的影响的研究不断深入,可能会确定出一些高危人群,他们可能会从旨在降低血浆纤维蛋白原的治疗干预中受益。