Most of our lifetime we spend in the postprandial state. Postprandial trigl
yceridemia may represent a procoagulant state involving disturbances of bot
h blood coagulation and fibrinolysis, in particular due to elevation of the
plasma levels of activated factor VII (VIIa) and plasminogen activator inh
ibitor (PAI-1). Therefore. disturbances of the hemostatic system might, at
least partly, account for by the link between hypertriglyceridemia and coro
nary heart disease (CHD). - Factor VIIa is the first enzyme of the blood co
agulation system and serves a priming function for triggering of the clotti
ng cascade. The coagulant activity of factor VII (VIIc, total activity of f
actor VII in plasma) was identified as an independent predictor of myocardi
al infarction in initially healthy middle-aged men. and particularly of Fat
al coronary events. and both serum cholesterol and triglyceride concentrati
ons correlated positively with the VIIc level. Addition of fat to diet has
been consistently shown to cause a rapid conversion of the factor VII zymog
en into its active form (VIIa) whereas the concentration of total protein i
s unaffected. Postprandial activation of factor VII is dependent on lipolyt
ic activity and it is mainly supported by large triglyceride-rich lipoprote
in of the VLDL class. Studies in vivo with specific coagulation factor-defi
cient patients indicate that factor IX is essential for the postprandial ac
tivation of factor VII. The basal generation of thrombin seems to be unaffe
cted by increased plasma levels of VIIa. However, since VIla-tissue factor
complex is responsible for the initiation of the coagulation cascade, incre
ased generation of VIIa in the post prandial state would increase the poten
tial for thrombin production in the event of plaque rupture. - Plasminogen
activator inhibitor-1 (PAI-1) is the major physiological inhibitor of the p
lasminogen activators in the circulation and thereby the: principal inhibit
or of the fibrinolytic system. Postprandial triglyceridemia has been observ
ed in many. not all. studies to increase PAI-1 plasma levels, which would f
urther strengthen the chances of thrombotic occlusion of a vessel after rup
ture of an atherosclerotic plaque.