POSTPRANDIAL ELEVATION OF ACTIVATED FACTOR-VII IN YOUNG-ADULTS

Citation
R. Kapur et al., POSTPRANDIAL ELEVATION OF ACTIVATED FACTOR-VII IN YOUNG-ADULTS, Arteriosclerosis, thrombosis, and vascular biology, 16(11), 1996, pp. 1327-1332
Citations number
31
Categorie Soggetti
Cardiac & Cardiovascular System","Peripheal Vascular Diseas
ISSN journal
10795642
Volume
16
Issue
11
Year of publication
1996
Pages
1327 - 1332
Database
ISI
SICI code
1079-5642(1996)16:11<1327:PEOAFI>2.0.ZU;2-C
Abstract
The Northwick Park Heart Study found that factor VII (FVII) activity w as a risk factor for ischemic heart disease, and other studies based o n indirect assays of activated factor VII (FvIIa) found an elevation o f FVIIa postprandially. We hypothesized that postprandial elevation of FVIIa would produce intermittent activation of factor X to Xa and, su bsequently, prothrombin to thrombin. We chose to study postprandial ac tivation of coagulation with a new assay specific for FVIIa that uses soluble tissue factor and with a prothrombin fragment 1+2 (F-1+2) assa y 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 p ostprandial (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 postprandiall y than fasting (median, 0.39 versus 0.44 nmol/L, P<.02). Four-hour pos tprandial triglyceride levels correlated significantly (rho=0.51, P<.0 2) with B-hour postprandial FVIIag but not with 6-hour postprandial FV IIa. Postprandial F-1+2 levels (at 6 hours) correlated significantly ( rho=0.39, P<.04) with fasting FVIIag levels but not with 6-hour postpr andial FVIIa levels. Thus, the basal FVIIag level, in the fasting stat e, may be involved in control of the generation of F-1+2. We found a p ostprandial increase in FVIIa levels after a dietary fat load but did not find a concomitant postprandial burst of activation of factor X an d prothrombin as measured by F-1+2. Further studies are to test whethe r postprandial FVIIa generation leads to enhanced activation of coagul ation.