Certain prospective epidemiologic studies (such as the Northwick Park Heart Study and the Prospective Cardiovascular Munster Study) have reported elevated factor VII coagulant activity to be an independent risk factor for heart disease. Interestingly, recent follow-up studies have indicated that factor VII coagulant activity is a much better risk predictor for fatal heart attacks than for non-fatal events. Because coagulation factor VII is the enzyme that initiates the blood clotting cascade, it is reasonable to suppose that high levels of plasma factor VII could be important in hypercoagulable states. However, this question has been controversial due to differences in methodology used to measure factor VII activity in different laboratories, and uncertainty about what is actually being measured in such assays. In particular, assays of factor VII coagulant activity measure, to varying extents, the levels of both factor VII (the inert precursor) and factor VIIa (the active enzyme) in plasma. New assay techniques based on a genetically engineered mutant of tissue factor (the protein cofactor for factor VIIa) now permit direct measurement of trace quantities of factor VIIa in plasma without interference from the large excess of factor VII. This has confirmed earlier predictions that trace amounts of pre-existing factor VIIa are a normal constituent of plasma. Currently, a number of studies are directly examining the relationship between elevated plasma factor VIIa levels and thrombotic diseases.
|Translated title of the contribution||Activated factor VII in plasma: A risk factor for heart disease?|
|Number of pages||6|
|Journal||Sang Thrombose Vaisseaux|
|State||Published - Mar 1 1996|
ASJC Scopus subject areas