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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2494.)
© 2000 American Heart Association, Inc.

Thrombosis

Dietary Factor VII Activation Does Not Increase Plasma Concentrations of Prothrombin Fragment 1+2 in Patients With Stable Angina Pectoris and Coronary Atherosclerosis

Else Marie Bladbjerg; Anna-Marie Münster; Peter Marckmann; Niels Keller; Jørgen Jespersen

From the Department of Thrombosis Research (E.M.B., A.-M.M., J.J.), The University of Southern Denmark, Esbjerg; the Department of Clinical Biochemistry (E.M.B., A.-M.M., J.J.) and the Department of Medicine (N.K.), Ribe County Hospital, Esbjerg; and the Research Department of Human Nutrition (P.M.), The Royal Veterinary and Agricultural University, Frederiksberg, Denmark.

Correspondence to Else Marie Bladbjerg, MSc, PhD, Department of Clinical Biochemistry, Ribe County Hospital, Østergade 80, DK-6700 Esbjerg, Denmark. E-mail emb{at}ribeamt.dk

Abstract—Studies in healthy subjects showed that blood coagulation factor VII (FVII) is activated postprandially after consumption of high-fat meals, but accompanying thrombin formation has not been demonstrated. In patients with coronary atherosclerosis, the arterial intima is supposed to present more tissue factor, the cofactor of FVII, to circulating blood; therefore, thrombin formation in response to FVII activation is more likely to occur in such patients. This hypothesis was tested in a randomized crossover study of 30 patients (aged 43 to 70 years) with stable angina pectoris and angiographically verified coronary atherosclerosis. They were served a low-fat (5% of energy from fat) breakfast and lunch and a high-fat (40% of energy from fat) breakfast and lunch on 2 different days. Venous blood samples were collected at 8:15 AM (fasting), 12:30 PM, 2:00 PM, 3:30 PM, and 4:45 PM and analyzed for triglycerides, activated FVII (FVIIa), FVII protein concentration (FVII:Ag), prothrombin fragment 1+2 (F1+2), and soluble fibrin. Triglyceride levels increased from fasting levels on both diets, but they increased most markedly on the high-fat diet. FVIIa and FVIIa/FVII:Ag increased with the high-fat diet and decreased with the low-fat diet. For both diets, FVII:Ag and F1+2 decreased slightly. No postprandial changes were observed for soluble fibrin. Postprandial mean values of triglycerides, FVIIa, FVII:Ag, and FVIIa/FVII:Ag were significantly higher for the high-fat diet than for the low-fat diet. Our findings confirm that high-fat meals cause immediate activation of FVII. The clinical implication is debatable because FVII activation was not accompanied by an increase in plasma F1+2 concentrations in patients with severe atherosclerosis. However, a local thrombin generation on the plaque surface cannot be excluded.

Key Words: atherosclerosis • cardiovascular diseases • coagulation • diet • thrombosis

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