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Apo A-I promoter polymorphism influences basal HDL-cholesterol and its response to pravastatin therapy

Carlos Lahoz1, Rocío Peña, Jose M Mostaza

  • 1Unidad de Arteriosclerosis, Hospital Carlos III, C/Sinesio Delgado 10, 28029 Madrid, Spain. clahoz@hciii.insalud.es

Atherosclerosis
|June 13, 2003
PubMed

Insights

Genetic variations in the apo A-I gene promoter influence baseline HDL-cholesterol and response to pravastatin. Specifically, A allele carriers show higher baseline HDL-C but do not increase it with statin treatment, unlike G allele homozygotes.

Area of Science:

  • Cardiovascular Genetics
  • Pharmacogenomics
  • Lipid Metabolism

Background:

  • Statins reduce cardiovascular events by lowering LDL-cholesterol and increasing HDL-cholesterol.
  • Genetic and environmental factors influence statin response, particularly HDL-cholesterol levels.
  • The role of genetic polymorphisms in HDL-C response to statins requires further investigation.

Purpose of the Study:

  • To investigate the impact of the apo A-I gene promoter G/A polymorphism on lipid and lipoprotein response to pravastatin treatment.
  • To determine if this genetic variation affects baseline HDL-C concentrations and statin-induced changes.

Main Methods:

  • A study of 397 hypercholesterolemic outpatients treated with 20 mg/day pravastatin for 16 weeks.
  • Genotyping for the G/A polymorphism in the apo A-I promoter region.
  • Analysis of lipid profiles, including HDL-C, in relation to genotype and treatment response.

Main Results:

  • A allele carriers exhibited 6.5% higher baseline HDL-C compared to G allele homozygotes (P=0.009).
  • Pravastatin treatment increased HDL-C in G allele homozygotes (4.9% increase) but not in A allele carriers (-0.3% change).
  • The difference in HDL-C response to pravastatin between genotypes was statistically significant (P=0.046).

Conclusions:

  • The G/A polymorphism in the apo A-I promoter region influences baseline HDL-C concentrations.
  • This genetic variation also affects the HDL-C response to pravastatin treatment, with G allele homozygotes showing a significant increase.
  • Individualized statin therapy may consider apo A-I genotype for optimizing HDL-C response.

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