Lipoprotein lipase gene polymorphisms in Croatian patients with coronary artery disease

Goran Ferencak1, Daria Pasalić, Branka Grsković

  • 1Clinical Institute of Laboratory Diagnosis, Clinical Hospital Center and Zagreb University School of Medicine, Zagreb, Croatia. gferen@mef.hr

Insights

Lipoprotein lipase gene variations influence coronary artery disease (CAD) risk and lipid profiles. The N291S polymorphism showed a significant association with CAD, while other variants impacted lipid levels in Croatian patients.

Area of Science:

  • Genetics
  • Cardiovascular Disease
  • Biochemistry

Background:

  • Elevated triglycerides and reduced high-density lipoprotein (HDL) are key risk factors for coronary artery disease (CAD).
  • Lipoprotein lipase (LPL) plays a crucial role in lipid metabolism, making its gene a potential target for studying CAD predisposition.
  • Genetic variations in the LPL gene may influence an individual's susceptibility to CAD and their lipid profiles.

Purpose of the Study:

  • To investigate the association between specific LPL gene polymorphisms (-93T/G, D9N, N291S, and S447X) and the risk of CAD.
  • To determine the impact of these LPL gene polymorphisms on lipid levels (triglycerides, HDL, HDL2-cholesterol, apolipoprotein A-I) in Croatian patients with and without confirmed CAD.
  • To explore potential interactions between LPL gene variants, lipid profiles, and CAD risk.

Main Methods:

  • Genotyping of four LPL gene polymorphisms (-93T/G, D9N, N291S, S447X) in Croatian patients.
  • Case-control study design comparing patients with and without angiographically confirmed CAD.
  • Analysis of lipid profiles, including triglycerides, HDL-cholesterol, HDL2-cholesterol, and apolipoprotein A-I levels.
  • Statistical analysis to assess the association between LPL polymorphisms and CAD risk, adjusting for lipid levels.

Main Results:

  • The N291S polymorphism was significantly associated with increased CAD risk (OR = 0.36; p = 0.048), an association moderately affected by lipid adjustment.
  • Non-carriers of the -93T/G and D9N polymorphisms exhibited significantly higher HDL2-cholesterol and apolipoprotein A-I levels within the CAD group.
  • The S447X mutation was linked to lower triglyceride and higher HDL2-cholesterol levels in the control group.
  • No significant differences in lipid levels were observed for the N291S variant between carriers and non-carriers.

Conclusions:

  • LPL gene polymorphisms, particularly N291S, may play a role in the genetic predisposition to coronary artery disease.
  • Specific LPL gene variants are associated with variations in lipid profiles, potentially influencing CAD risk.
  • Further research is warranted to elucidate the complex interplay between LPL genetics, lipid metabolism, and cardiovascular disease development.

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