High fibrinogen levels have at least as great a predictive value as any other known risk factor, such as elevated LDL cholesterol, elevated triglycerides, obesity and diabetes. In persons with a family history of heart disease, fibrinogen levels are high. Fibrinogen levels are primarily genetically inherited, meaning that fibrinogen may be the genetic factor causing familial premature heart disease. Also, exposure to cold increases fibrinogen levels by 23 percent, and mortality from heart attack and stroke are higher in winter than in summer. Fibrinogen hinders blood flow and oxygen delivery by deforming red blood cells, causing red-cell aggregation and a thickening of the blood, all of which lead to diminished circulation.
Fibrinogen binds blood platelets together, thus initiating abnormal arterial blood clots.
Fibrinogen is then converted to fibrin, which is the final step in the blood-clotting cascade. Fibrinogen contributes to the development of atherosclerosis by incorporating itself into the arterial plaque. Further, fibrinogen and LDL cholesterol work together to generate atherosclerotic plaques. Fibrinogen initiates the atherosclerotic plaque, then converts to fibrin and serves as a scaffold for LDL cholesterol in the atherosclerotic plaque that slowly occludes an artery. Fibrinogen and its derivatives trigger a variety of other mechanisms thought to be involved in the atherosclerotic process.