Early development of atherosclerosis results from a complex multifactorial process where lipoprotein anomalies play a predominant role. The metabolism of lipoproteins is regulated by numerous reactions between the structural components of the lipoproteins and the receptors and/or enzymes with which they interact. Among the well-characterized anomalies, the elevation of small and dense LDL and/or the diminution of HDL levels are in first line of the factors involved in the formation of atheromatous plaques. LDL play a direct role by penetrating the intima of the arteries and HDL play an reverse transport of cholesterol from cells to the liver. There has been a long debate concerning risk related to triglyceride rich lipoproteins (TGRL), and more particularly the increase in VLDL. However, a large number of studies have demonstrated that these ephemeral lipoproteins can acquire major atherogenic potential when their level is increased and/or they are associated with perturbed metabolism leading to an accumulation of remnants. Current investigation methods have shown that LDL and HDL-cholesterol levels are excellent markers of LDL and HDL concentrations. Inversely, triglyceride levels provide little information concerning the nature of the elevated TGRL and fasting hypertriglyceridemia, even if moderate, should therefore be considered as a warning sign of persistent atherogeneous remnants in the fasting state.