High fibrinogen levels are at least as great a predictor of cardiovascular disease as any other known risk factor such as elevated LDL cholesterol, elevated triglycerides, high blood pressure, obesity, and diabetes. Fibrinogen levels are high in persons with a family history of heart disease. The predisposition to high fibrinogen levels is genetically inherited, which suggests that fibrinogen may be the genetic factor that causes familial heart disease. As a result, mortality from heart attack and stoke is higher in winter than in summer. Fibrinogen hinders blood flow and oxygen delivery by deforming red blood cells, causing red cell aggregation, and thickening the blood by increasing its viscosity-all of which leads to diminished circulation.
Fibrinogen binds blood platelets together, thus initiating abnormal arterial blood clot formation.
Fibrinogen is then converted to fibrin, which is the final step in the blood clotting process. Fibrinogen contributes to atherosclerosis by incorporating itself into arterial plaque. Fibrinogen and LDL cholesterol work together to help generate atherosclerotic plaques after fibrinogen initiates the process. Fibrinogen is converted into fibrin, which serves as a scaffold for LDL cholesterol in the formation of the atherosclerotic plaques that slowly block arteries. Platelet aggregation inhibitors reduce the risk that fibrinogen will cause an abnormal blood clot.