Postprandial elevation of activated factor VII in young adults

The Northwick Park Heart Study found that factor VII (FVII) activity was a risk factor for ischemic heart disease, and other studies based on indirect assays of activated factor VII (FvIIa) found an elevation of FVIIa postprandially. We hypothesized that postprandial elevation of FVIIa would produce intermittent activation of factor X to Xa and, subsequently, prothrombin to thrombin. We chose to study postprandial activation of coagulation with a new assay specific for FVIIa that uses soluble tissue factor and with a prothrombin fragment 1+2 (F-1+2) assay to detect the activation of prothrombin by factor Xa. We fed a high-fat breakfast (30 g/m(2)) to 30 healthy volunteer subjects (30.8+/-9.8 years; range, 20 to 49 years) on no medication. Fasting blood samples were collected for FVIIa, FVII antigen (FVIIag), and F-1+2 as well as triglycerides and total and HDL cholesterol. A significant difference was found between fasting (2.82+/-1.49 ng/mL, mean+/-SD) and 6-hour postprandial (3.45+/-2.08 ng/mL) FVIIa levels (P<.004); FVIIag did not change significantly (mean, 0.89 U/mL fasting and 0.90 U/mL at 6 hours). In contrast, F-1+2 levels were slightly lower 6 hours postprandially than fasting (median, 0.39 versus 0.44 nmol/L, P<.02). Four-hour postprandial triglyceride levels correlated significantly (rho=0.51, P<.02) with B-hour postprandial FVIIag but not with 6-hour postprandial FVIIa. Postprandial F-1+2 levels (at 6 hours) correlated significantly (rho=0.39, P<.04) with fasting FVIIag levels but not with 6-hour postprandial FVIIa levels. Thus, the basal FVIIag level, in the fasting state, may be involved in control of the generation of F-1+2. We found a postprandial increase in FVIIa levels after a dietary fat load but did not find a concomitant postprandial burst of activation of factor X and prothrombin as measured by F-1+2. Further studies are to test whether postprandial FVIIa generation leads to enhanced activation of coagulation.