Authors' recommendations: Coronary artery disease (CAD) results from impairment of blood flow through the coronary arteries, and is the leading cause of death in developed countries. Risk factors for CAD include inherited factors, systemic disorders, abnormal cholesterol levels, diabetes, obesity, physical inactivity, and smoking. Atherosclerosis, the accumulation of plaques in the walls of arteries, is the primary cause of CAD, and may be present for many years without symptoms. Plaques impede blood flow as they grow larger in size, or when they become dislodged and/or rupture. The rupture of plaques exposes clot-forming materials to the bloodstream, and plaque and clot materials may combine to block the blood vessel entirely. This prevents oxygen from reaching tissues beyond the blockage, resulting in damage or dysfunction of the tissue. Myocardial infarction (MI) typically results from the formation of a clot, or thrombus, in an atherosclerotic coronary artery. Approximately 1.5 million MIs occur in the United States each year. While many individuals survive MI, damage to the affected region of the heart is permanent. As vessel blockages consist of both plaque material and blood clots formed by the body's clotting mechanism, the coagulation cascade, factors involved in the coagulation cascade are an area of interest in research concerning causes of MI. Increase in the activity of FVII, an important component of the coagulation cascade, has been associated with CAD risk in some studies, although not all study results agree. FVII circulates in the blood in an inactive form, and is activated by other components of the coagulation cascade. Once activated, FVII contributes to the formation of blood clots. FVII is encoded by the coagulation factor VII (serum prothrombin conversion accelerator) (F7) gene. A genetic polymorphism in F7 called the p.Arg353Gln allele has been associated with decreased FVII activity in a number of studies. Due to this association and the tentative association between FVII levels and CAD, F7 p.Arg353Gln is the focus of study related to its potentially protective effect against CAD. As CAD is a very complex disorder, with a variety of clinical manifestations, studies investigating CAD range in focus and report different clinical endpoints. For this analysis, studies featuring MI as a clinical endpoint of CAD have been selected to facilitate meaningful comparison.

Project Status: Completed

Year Published: 2012

URL for published report: The report may be purchased from:http://www.hayesinc.com/hayes/crd/?crd=13729

English language abstract: An English language summary is available

Publication Type: Not Assigned

Country: United States

Organisation Name: HAYES, Inc.

Contact Address: 157 S. Broad Street, Suite 200, Lansdale, PA 19446, USA. Tel: 215 855 0615; Fax: 215 855 5218

Contact Name: saleinfo@hayesinc.com

Contact Email: saleinfo@hayesinc.com

Copyright: 2012 Winifred S. Hayes, Inc