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REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #5 2023

EXPLORE Dyslipidaemia
AN OVERVIEW OF POPULATION
HEALTH AND DEMOGRAPHIC
INFORMATION FOR EVERY COUNTRY
OF THE WORLD BASED ON THE GBD
DATABASE HERE.

CLICK HERE
FOR THE LINK TO FULL ARTICLE

Triglyceride-rich lipoprotein remnants, low-density lipoproteins, and risk of
coronary heart disease: A UK Biobank study.
Björnson E, et al. Eur Heart J. 2023 Jun 26;ehad337. doi: 10.1093/eurheartj/ehad337. Online ahead of print.

Triglyceride-rich lipoproteins (TRL), and more specifically
cholesterol content of TRL and their ‘remnants’, may be causally Single nucleotide polymorphisms (SNPs)
related to coronary heart disease (CHD). Remnant lipoproteins The most common type of genetic
can penetrate the subendothelial space in artery walls and bind variation among people. Each SNP represents a
to proteoglycans, thereby initiating cholesterol deposition and difference in a single DNA building block, a nucleotide.
foam cell formation. They are most commonly found in the DNA between
genes and act as biological markers to locate genes

The authors examined the strength of the relationship of TRL that are associated with disease.
with risk of CHD compared with LDL by examining the UK
Biobank population for single-nucleotide polymorphisms (SNPs) associated with TRL/remnant cholesterol and LDL-C.

In a multivariable Mendelian randomization analysis, TRL/remnant-C was strongly and independently associated with CHD in a
model adjusted for apoB. In another multivariable model, TRL/remnant-C and LDL-C also exhibited independent associations with
CHD with odds ratios per 1 mmol/L higher cholesterol of 2.59 (95% CI: 1.99–3.36) and 1.37 (95% CI: 1.27–1.48), respectively.

The authors discuss the importance in
understanding the role of lipoproteins in
atherosclerosis. First, TRL/remnant-C was a
strong predictor of CHD risk independent of
apoB and LDL-C. Second, two major SNP
clusters were identified that had differing
genetic effects on TRL/remnant-C relative to
LDL-C. Third, the increment in CHD risk per
particle (per apoB) was approximately two-
fold greater in the SNP cluster with the larger
effect on TRL/remnants. These observations
suggest that TRL/remnant particles have a
substantially greater atherogenicity than
LDL. Causes of this increased atherogenicity
are not clear yet. Implications for risk
assessment and intervention strategies need
to be assessed in future studies.

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