Effect of apolipoprotein E polymorphism on statin-induced decreases in plasma lipids and cardiovascular events.

Abstract

Hypercholesterolemia or dyslipidemia is an independent risk factor for cardiovascular disease and statins (inhibitors of a key enzyme of cholesterol synthesis, 3-hydroxymethyl glutaryl coenzyme A reductase) are the drugs of choice for decreasing plasma cholesterol. It has been estimated that genetic factors can explain 40%-60% of final cholesterol concentrations and approximately 70% of the efficacy of statin treatment. The gene most often analyzed in the context of statin efficacy is the gene for apolipoprotein E (APOE). This review summarizes evidence of the association between variations in the APOE gene locus and the response of plasma lipids to statin therapy. Although the results are not consistent, carriers of the APOE4 allele seems to be less responsive to statins than carriers of APOE2 and APOE3 alleles. This effect is partially context-dependent (gene-gender interactions; gene-nutrition and gene-smoking interactions have not yet been studied) and the absolute differences vary between different population groups.

• Authors: Jaroslav A Hubacek, Michal Vrablik
• Journal: Drug metabolism and drug interactions (Drug Metabol Drug Interact) Vol. 26 Issue 1 Pg. 13-20 ( 2011) ISSN: 0792-5077 [Print] Germany
• PMID: 21557673 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Apolipoproteins E
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Lipids
• Cholesterol

Topics

• Alleles
• Apolipoproteins E (genetics)
• Cardiovascular Diseases (etiology, prevention & control)
• Cholesterol (blood)
• Humans
• Hydroxymethylglutaryl-CoA Reductase Inhibitors (pharmacology)
• Hypercholesterolemia (complications, drug therapy)
• Lipids (blood)
• Pharmacogenetics
• Polymorphism, Genetic
• Risk Factors