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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Epidemiology of thrombotic-hemostatic factors and their associations with cardiovascular disease
T A Pearson1, J LaCava, H F Weil
1Mary Imogene Bassett Research Institute, Cooperstown, NY, USA.
Abundant evidence proves that thrombosis is involved in the acute presentation of coronary, cerebrovascular, and peripheral vascular diseases. However, the role of thrombotic factors in the development of the atherosclerotic lesions themselves has been more difficult to prove. This difficulty has been due, at least in part, to several methodologic issues in the study of hemostatic factors and cardiovascular disease (CVD). These include the possibility that associations between CVD and hemostatic factors may not be causal but rather due to confounding by other factors, acting as part of an extended causal pathway or requiring interaction with other risk factors or atherosclerotic disease, or may result from disease rather than causing the disease. In addition, several challenges remain in the measurement of hemostatic factors. Nonetheless, a growing number of studies have examined the association of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and fibrinolytic factors [tissue plasminogen activator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic activity]. Of these, only for fibrinogen is there significant, strong, and consistent evidence of a causal association. Given the preliminary nature of these associations, any association between dietary factors and hemostatic factors other than fibrinogen is difficult to invoke as evidence for a deleterious effect of diet on CVD risk via thrombogenic mechanisms.
Abundant evidence proves that thrombosis is involved in the acute presentation of coronary, cerebrovascular, and peripheral vascular diseases. However, the role of thrombotic factors in the development of the atherosclerotic lesions themselves has been more difficult to prove. This difficulty has been due, at least in part, to several methodologic issues in the study of hemostatic factors and cardiovascular disease (CVD). These include the possibility that associations between CVD and hemostatic factors may not be causal but rather due to confounding by other factors, acting as part of an extended causal pathway or requiring interaction with other risk factors or atherosclerotic disease, or may result from disease rather than causing the disease. In addition, several challenges remain in the measurement of hemostatic factors. Nonetheless, a growing number of studies have examined the association of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and fibrinolytic factors [tissue plasminogen activator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic activity]. Of these, only for fibrinogen is there significant, strong, and consistent evidence of a causal association. Given the preliminary nature of these associations, any association between dietary factors and hemostatic factors other than fibrinogen is difficult to invoke as evidence for a deleterious effect of diet on CVD risk via thrombogenic mechanisms.
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