Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins.

In addition to low-density lipoproteins, plasma chylomicrons and very-low-density lipoproteins (VLDL) contribute to atherogenesis. When triglyceride-rich particles bind to arterial endothelium and to deendothelialized areas, locally present lipoprotein lipase initiates triglyceride hydrolysis and decreases the size of the adhering particles. Additional changes in composition are brought about by the exchange of lipids between chylomicron/VLDL remnants and the cholesteryl ester-rich low- and high-density lipoproteins. These exchanges are mediated by lipid transfer proteins in plasma. Animal studies with doubly labeled lipoproteins show that the size of lipoprotein particles determines their rate of entering the artery and contributes to the formation of lesions. This model supports epidemiologic studies that have identified plasma triglycerides as a risk factor for atherogenesis. The model for a causal role of pre- and postprandial triglyceride-rich lipoproteins in atherogenesis suggests that measuring them may improve the assessment of cardiovascular risk factors.