Abstract
There is increasing evidence that fasting hypertriglyceridaemia identifies individuals who are at increased risk for coronary artery disease. It is probable that this reflects the effects of the smaller triglyceride-bearing lipoproteins. It may also reflect increased levels of postprandial lipoproteins. There is considerable theoretical and experimental evidence to support an atherogenic role for the smaller, triglyceride-rich postprandial lipoproteins. Cross-sectional studies in humans also indicate that those with coronary disease have increased levels of postprandial lipids, probably in the remnants of chylomicrons. Recently we have completed a study examining the progression of coronary atherosclerosis angiographically. The study showed that the progression was linearly related to the numbers of chylomicron remnant particles, as reflected by the quantity of apoB48 in Sf20-60 lipoproteins, in the postprandial circulation. This paper reviews these studies, the physiology of postprandial lipoprotein metabolism and the therapeutic implications of this information.