Beyond coagulation : Fibrinogen as a cause of cardiovascular surgical disease

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 card...

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Bibliographic Details
Published in:Cardiovascular drugs and therapy 1998-07, Vol.12 (3), p.261-265
Main Authors: SUMERAY, M. S, MONTGOMERY, H. E, HUMPHRIES, S. E
Format: Article
Language:English
Subjects:
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Blood Coagulation Disorders - complications
Blood Coagulation Disorders - physiopathology
Blood Coagulation Disorders - therapy
Cardiology. Vascular system
Cardiovascular Diseases - etiology
Cardiovascular Diseases - physiopathology
Cardiovascular Diseases - surgery
cholesterol
Cigarettes
Coagulation
Drugs
Environmental factors
Fibrinogen - genetics
Fibrinogen - physiology
Genotype
Humans
hypertension
intervention
Medical sciences
Risk Factors
surgery
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Summary: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.
ISSN:0920-3206
1573-7241
DOI:10.1023/A:1007713715744