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RECENT PUBLICATIONS ON RESIDUAL RISK

2017

Is inflammation a key determinant of the atherogenicity of remnant cholesterol?

Attention has refocused on remnant cholesterol, transported by triglyceride-enriched precursors to low-density lipoproteins, as a contributor to cardiovascular risk. There is compelling evidence from several Mendelian randomization studies that remnant cholesterol is causal in atherosclerotic cardiovascular disease, as well as supportive findings from cross-sectional and prospective studies. There is also biological plausibility for such a link, given that at least some of the group of remnant lipoproteins, such as intermediate density lipoproteins, which contain far more cholesterol per particle than LDL, are able to traverse the arterial wall to elicit changes that predispose to or exacerbate atherosclerosis. Added to this, new evidence indicates that there is an important inflammatory component to the atherogenicity of remnant cholesterol.
 
This study evaluated arterial wall inflammation and bone marrow activity using 18F-FDG PET/CT (18F- fluoro-2-deoxy-d-glucose positron emission tomography–computed tomography) and monocyte phenotype with flow cytometry in 17 patients with familial dysbetalipoproteinaemia (characterized by increased total cholesterol and triglyceride levels) and 17 matched controls. Compared with controls, there was a 20% increase in 18F-FDG uptake in the arterial wall, as well as increased lipid accumulation and higher expression of surface integrins (CD11b, CD11c, and CD18) in patients with familial dysbetalipoproteinaemia. In addition, data from the Copenhagen General Population Study validated the correlation between remnant levels and hematopoietic activity, as well as the strong correlation with leukocyte counts. These findings support an important inflammatory component to the atherogenicity of remnant cholesterol, contributing to the increased cardiovascular disease risk in these patients.
Remnant cholesterol elicits arterial wall inflammation and a multilevel cellular immune response in humans.

Bernelot Moens SJ, Verweij SL, Schnitzler JG et al