Dietary factor VII activation does not increase plasma concentrations of prothrombin fragment 1+2 in patients with stable angina pectoris and coronary atherosclerosis

Studies in healthy subjects showed that blood coagulation factor VII (FVII) is activated postprandially after consumption of high-fat meals, but accom panying thrombin formation has not been demonstrated. In patients with coro nary atherosclerosis, the arterial intima is supposed to present more tissu e factor, the cofactor of FVII, to circulating blood; therefore, thrombin f ormation in response to FVII activation is more likely to occur in such pat ients. This hypothesis was tested in a randomized crossover study of 30 pat ients (aged 43 to 70 years) with stable angina pectoris and angiographicall y verified coronary atherosclerosis. They were served a low-fat (5% of ener gy from fat) breakfast and lunch and a high-fat (40% of energy from fat) br eakfast 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 lev els increased from fasting levels on both diets, but they increased most ma rkedly on the high-fat diet. FVIIa and FVIIa/FVII:Ag increased with the hig h-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 FVI Ia/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 activat ion of FVII. The clinical implication is debatable because FVII activation was not accompanied by an increase in plasma F1+2 concentrations in patient s with severe atherosclerosis. However, a local thrombin generation on the plaque surface cannot be excluded.