Figure 9.

TRL remnants clinical tips: atherogenicity and analytical approach. The role of the postprandial phase in atherogenesis cannot be overemphasized. (A). In fact, as pointed out earlier, delays in the turnover of TRL remnants produce particles that, as shown to the left, can enter the artery wall and bind to heparan sulfate proteoglycans. Together with LDLs, apo B48 as well as apoB100 TRL remnants can accumulate in the arterial intima and result in the production of foam cells. Indeed, remnants, although less concentrated than LDLs can carry two or three times more cholesterol per particle. The take-home message is that TGs are just a marker for the presence of cholesterol-enriched particles which are per se atherogenic. From a molecular as well as pathological standpoint, TGs are neutral. (B). Since TRL remnants are so heterogeneous, so far there is no gold standard for their measurement in clinical practice. However, several practical approaches should be taken into consideration, as shown in the figure to the right. TG/HDL-C remains to be the cheapest way to ascertain the presence of metabolic syndrome dyslipidemia and a surrogate marker for the presence of small-dense LDLs. The Martin algorithm and others are more useful than the classical Friedewald formula to estimate VLDL cholesterol and remnants. Non-HDL cholesterol is also another approximation to the problem and so are new assays for remnant-like lipoprotein particles that are immunological in nature. NMR is not available to everybody and has some pitfalls anyway. The figure was partly generated using Servier Medical Art, provided by Servier, licensed under a Creative Commons Attribution 3.0 unported license.