Postprandial lipaemia and haemostatic factors

Factor VII activity (FVIIc), a reported risk factor for fatal coronary heart disease, increases transiently after a fat-rich meal. The response shows dose-response characteristics and peak FVIIc and triglyceride concentrations above fasting levels tend to be positively associated. The mechanism is incompletely understood, but appears to require factor IX and the presence in plasma of lipoprotein products of lipolytic activity. Factor XII is not apparently essential. The increase in FVIIc is due to raised activated factor VII (FVIIa) activity, but is not associated with increased thrombin production or changes in fibrinolytic activity. The response of FVIIa appears independent of the proportions of saturated, monounsaturated and polyunsaturated fatty acids in the dietary fat, although dietary stearic acid may be less effective than myristic acid. However, in one study in which deliberate efforts were made to force an increase in plasma free stearic acid, its plasma level was positively associated with postprandial FVIIc. Because FVIIa initiates the thrombotic response to rupture of an atheromatous plaque, a raised postprandial level may represent a transient rise in the likelihood of a clinically significant coronary thrombosis.