Cardiovascular Disease

LDL-TG’s Atherosclerosis Association

Out of tens of thousands of blood-based molecules and biomarkers, triglyceride-rich LDL molecules (LDL-TG) emerged as a direct cause of atherosclerotic coronary artery disease (ASCAD). 

LDL-C and Apo-B are widely known CVD risk factors, but it’s still unclear which specific risk factors underlie atherosclerosis, and to what extent. To investigate this, the authors applied a hypothesis-free Bayesian network analysis and genetic studies to 665 patients with suspected CAD.

The authors assessed simultaneous associations between genotypes, gene expression levels, circulating biomarkers, and CT-based atherosclerosis levels, finding that… 

  • LDL-TG was directly upstream from atherosclerosis in the Bayesian analysis.
  • LDL-TG was associated with atherosclerosis independent of well-known factors like age, sex, LDL-C and ApoB levels.
  • Genetic variations that “turned off” the hepatic lipase gene correlated with LDL-TG levels and atherosclerosis.
  • LDL-TG was positively linked to triglycerides, sd-LDL, and inflammatory markers.

What’s new? These findings are consistent with previous literature, but also reveal that LDL-TG has a central causal role in ASCAD, potentially as a result of abnormal hepatic lipase activity.  

The Takeaway 

The study suggests that triglyceride-rich LDL particles directly cause atherosclerotic CAD. With the recent introduction of a simple and fully automated method to measure LDL-TG levels, this biomarker may become an important tool in the clinical assessment of atherosclerosis. 

The analysis also showcases a promising new approach to evaluate genetic predisposition to ASCAD, and demonstrates how big “omics” data combined with AI has the potential to reveal novel treatment avenues.

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