Fibrinogen and Atherosclerosis

Abstract

Cardiovascular disease has a multifactorial origin. Among these risk markers, fibrinogen is the most prominent. Interest in the role of fibrinogen in the atherogenic process is long-standing. In the 1960s, one of the first studies correlating fibrinogen and coronary artery disease was published. Since then, much evidence has been accumulating establishing elevated plasma levels of fibrinogen as an independent risk factor for coronary artery disease. As in acute myocardial infarction, fibrinogen is also elevated in cases of cerebrovascular accident and peripheral artery disease. It is noteworthy that fibrinogen levels are elevated in patients with transient ischemic attacks, suggesting that fibrinogen levels should be elevated before necrosis occurs. It is known that plasma fibrinogen is a dimer made up of alpha, beta and gamma chains, whose union is made through disulfide bonds. Measures to reduce plasma fibrinogen include diet, alcohol, physical activity, and drugs. Since fibrinogen is a risk factor for coronary artery disease, measures to reduce its levels should be adopted. In the future, with the evolution of genetic studies, the detection of individuals predisposed to hyperfibrinogenemia may be performed. It is up to pharmaceutical research to continue the investigation of effective and easy-to-use drugs to reduce fibrinogen levels.