Triglyceride accumulation is not a feature of the atherosclerotic plaque but triglyceride-rich lipoproteins also contain cholesterol esters and it is likely that some of these are directly atherogenic.
Hypertriglyceridaemia is associated with alterations in the metabolism of other lipoproteins, which may explain its relationship to CHD risk. It is often inversely related to HDL such that as triglycerides increase, HDL cholesterol concentrations decrease.
In hypertriglyceridaemic individuals there is a preponderance of small, dense LDL particles. A further explanation for the link between plasma triglyceride and CHD risk relates to the association between hypertriglyceridaemia and coagulation factors. Factor VII is an important component of the extrinsic coagulation system and in prospective studies has been shown to be an independent predictor of CHD. Increasing plasma triglycerides are positively correlated with the activity of factor VII and some of the day-to-day variation in factor VII coagulation activity is related to dietary fat intake.
Plasma triglyceride concentration is also positively correlated with activity of plasminogen activator inhibitor 1 (PAI-1). PAI-1 is an inhibitor of plasminogen activation and has been shown to be increased in young myocardial infarction patients.