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Quantifying Triglyceride-Rich Lipoprotein Atherogenicity, Associations With Inflammation, and Implications for Risk
Elias Björnson1, Martin Adiels2, Anders Gummesson3
1Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Insights
Triglyceride-rich lipoproteins (TRL/remnants) are approximately 4 times more likely to cause coronary heart disease (CHD) than low-density lipoprotein (LDL) particles. This finding suggests adjusting risk predictions for TRL/remnant cholesterol levels may improve accuracy.
Area of Science:
- Cardiovascular Genetics
- Lipid Metabolism
- Atherosclerosis Research
Background:
- Triglyceride-rich lipoproteins and remnants (TRL/remnants) are causally linked to coronary heart disease (CHD), but the extent of this risk is not fully quantified.
- Understanding the atherogenicity of different lipoprotein particles is crucial for accurate cardiovascular risk assessment.
Purpose of the Study:
- To quantify the per-particle atherogenicity of TRL/remnants compared to low-density lipoprotein (LDL).
- To investigate the causal relationship between TRL/remnants and systemic inflammation.
- To determine if differences in atherogenicity impact the association of non-high-density lipoprotein cholesterol (non-HDL-C) with CHD.
Main Methods:
- Utilized Mendelian randomization analysis on 1,357 UK Biobank participants with genome-wide association studies.
- Ranked single nucleotide polymorphisms (SNPs) into 10 clusters based on their effect on TRL/remnant cholesterol versus LDL cholesterol.
- Estimated coronary heart disease odds ratios (ORs) per unit increase in apolipoprotein B (apoB) and non-HDL-C, and assessed TRL/remnant association with inflammation biomarkers.
Main Results:
- TRL/remnants were estimated to be at least 3.9 times more atherogenic than LDL particles on a per-particle basis.
- Coronary heart disease risk increased across SNP clusters with greater TRL/remnant-C effects.
- TRL/remnants showed causal links with inflammation, but this did not fully explain their heightened atherogenicity.
Conclusions:
- TRL/remnants are substantially more atherogenic than LDL particles, approximately 4 times.
- The varying atherogenicity of lipoprotein components necessitates considering the proportion of TRL/remnant-C for precise non-HDL-C based CHD risk prediction.
Background:
Triglyceride-rich lipoproteins and remnants (TRL/remnants) have a causal, but not yet quantified, relationship with coronary heart disease (CHD): myocardial infarction plus revascularization.
Objectives:
The authors sought to estimate TRL/remnant per-particle atherogenicity, investigate causal relationships with inflammation, and determine whether differences in the atherogenicity of TRL/remnants and low-density lipoprotein (LDL) impact the causal association of non-high-density lipoprotein cholesterol (non-HDL-C) with CHD.
Methods:
Single nucleotide polymorphisms (SNPs) (N = 1,357) identified by genome-wide association in the UK Biobank were ranked into 10 clusters according to the effect on TRL/remnant-C vs LDL-C. Mendelian randomization analysis was used to estimate for each SNP cluster CHD ORs per 10 mg/dL apolipoprotein B (apoB) and per 0.33 mmol/L non-HDL-cholesterol, and to evaluate association of TRL/remnants with biomarkers of systemic inflammation.
Results:
SNPs in cluster 1 predominantly affected LDL-C, whereas SNPs in cluster 10 predominantly affected TRL/remnant-C. CHD risk per genetically predicted increase in apoB and in non-HDL-C rose across clusters. ORs per 10 mg/dL higher apoB was 1.15 (95% CI: 1.11-1.19) in cluster 1 vs 1.70 (95% CI: 1.52-1.90) in cluster 10. Comparing ORs between these TRL/remnant-predominant and LDL-predominant clusters, we estimated that TRL/remnants were at least 3.9 (95% CI: 2.8-5.4) times more atherogenic than LDL on a per-particle basis. For non-HDL-C, CHD ORs per 0.33 mmol/L rose from 1.15 (95% CI: 1.11-1.19) for cluster 1 to 1.40 (95% CI: 1.30-1.50) for cluster 10. TRL/remnants exhibited causal relationships with inflammation, but this did not explain their greater atherogenicity.
Conclusions:
TRL/remnants are about 4 times more atherogenic than LDL. Variation in the causal association of non-HDL-C with CHD indicates that adjustment for percentage TRL/remnant-C may be needed for accurate risk prediction.
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