Correctly understand about residual cholesterol

Low density lipoprotein (LDL) is a typical atherogenic lipoprotein. As the main carrier of cholesterol in blood, in most people, it is the main carrier to transport cholesterol to the arterial wall, so as to start and promote the formation of lesions. However, there is increasing evidence that triglyceride rich lipoprotein (TRL) and its residues are also pathogenic factors of atherosclerotic cardiovascular disease (ASCVD). In the pathological process, its role is independent of LDL and can be used as a supplement to LDL.

Conceptually, all lipoproteins carrying the cholesterol "payload" and surface proteins, especially apoB100 and apoE, are potential contributors to focal cholesterol deposition and macrophage foam formation. Therefore, other members containing apoB lipoproteins may become intervention targets.

At present, the research to prove the importance of TRL residues in ASCVD is mainly based on genetics and epidemiology. However, there are still major obstacles in exploring and quantifying the contribution of residual particles to the formation of atherosclerosis. The lipid mass spectra of TRL residues present in the circulation are heterogeneous. So far, there are no biomarkers that can quantify the level of residues.

This is partly because circulating TRL residues are modified through metabolic processes (i.e. hydrolysis, cholesterol ester transfer protein mediated lipid exchange and liver receptor uptake), not only changing their lipid and protein levels.

Up to now, the following methods can be used for evaluation, including ultracentrifugation, immunoaffinity test, nuclear magnetic resonance (NMR) spectroscopy, calculation based on cholesterol measurement in different lipoprotein categories, and plasma triglyceride concentration divided by a factor. Because TRL cholesterol (trl-c) levels vary in proportion to the residue concentration, evaluating trl-c can provide an approximation of the residue level in the cycle. However, it is not an accurate or specific biomarker and must be used with caution.

Quispe et al. Used two methods to evaluate the contribution of residual cholesterol to the risk of ASCVD: multivariate model, in which residual cholesterol, LDL-C and apoB can be used as explanatory variables; Inconsistency analysis, percentage of residual cholesterol / LDL-C in the relevant population. Compared with the consistent group (the percentage of residual cholesterol and LDL-C was similar), the high residual cholesterol / low LDL-C group, rather than the low residual cholesterol / high LDL-C group, was associated with an increased risk of ASCVD (HR = 1.21, 95% CI: 1.08-1.35). The results of this observational study support the view that trl-c / residual cholesterol is another risk factor other than LDL-C. The findings are consistent with recent articles published by johannesen et al.

In addition, quispe et al. Also suggested that the risk associated with residual cholesterol is independent of the traditional risk factors LDL-C and apoB, which is still a statistically significant risk predictor even after adjusting for non-high density lipoprotein cholesterol (non-HDL-C). 

At present, the role of TRL and its residues in ASCVD has attracted more and more attention. It can not only be used as a part of the residual risk of patients who use statins to control the LDL level better, but also as an unsolved reason for the increased risk of asymptomatic patients.

It is worth noting that in assessing the effect of residual particles on atherosclerosis and as a potential intervention target, we still can not ignore that for many people, LDL is still the main driver of atherosclerosis.

 

Cindy