Lectin-like oxidized-LDL receptor-1 (LOX-1) polymorphisms influence cardiovascular events rate during statin treatment

Int J Cardiol. 2007 Jun 25;119(1):41-7. doi: 10.1016/j.ijcard.2006.07.045. Epub 2006 Oct 13.

Abstract

Background: Oxidized-LDL (ox-LDL) are involved in atherothrombosis by induction of endothelial dysfunction and thrombosis. The specific receptor lectin-like oxidized-LDL receptor-1 (LOX-1) is expressed in endothelial cells, monocytes and platelets. LOX-1 gene allelic variants (3'UTR/T) have been related with cardiovascular events and reduced anti-platelet activity induced by statins.

Objectives: To detect whether LOX-1 polymorphisms could affect statins effectiveness in cardiovascular prevention.

Patients/methods: The present was a retrospective study performed in 751 white hypercholesterolemic subjects treated with increasing doses of atorvastatin (n=382, 247 male, 135 female) or simvastatin (n=369, 244 male, 125 female) up to 4 years, whose LDL target was 3.36 mmol/L according to the National Cholesterol Education Program, Adult Treatment Panel III (NCEP-ATPIII). Single nucleotide polymorphism were evaluated by allelic discrimination assays (PCR), lipid profile by enzymatic-colorimetric methods and C-reactive protein (CRP) by a nephelometric technique.

Results: Twenty-three non-ST elevation (NSTEMI) and eleven ST-elevation myocardial infarction (STEMI) were encountered in the observational period without differences between treatments (p=0.175) and sex (p=0.139). Each symptomatic subject (10 reaching the appropriate LDL target and 24 with still undesirable LDL) had the 3'UTR/T allelic variant (adjusted O.R. 4.63, 95% C.I. 3.46-6.70, p<0.0001). Among patients not reaching LDL target the C allele resulted protective with respect to T carriers (p<0.00001). Also, similar changes of CRP resulted in different event rate between T and C carriers (p<0.001) in the whole cohort.

Conclusions: In the studied population LOX-1 genetic variants influence cardiovascular risk reduction induced by statins also in patients not reaching the LDL target. The previously described LOX-1-related antithrombotic actions of both statins employed could have a specific role in what observed, suggesting a genetic influence in statins LDL-lowering partially related actions.

MeSH terms

  • Aged
  • Anticholesteremic Agents / administration & dosage*
  • Atorvastatin
  • C-Reactive Protein / metabolism
  • Cholesterol, LDL / blood
  • Coronary Artery Disease / drug therapy*
  • Coronary Artery Disease / epidemiology
  • Coronary Artery Disease / genetics*
  • Drug Resistance / genetics
  • Female
  • Heptanoic Acids / administration & dosage*
  • Heterozygote
  • Humans
  • Hypercholesterolemia / drug therapy
  • Hypercholesterolemia / epidemiology
  • Hypercholesterolemia / genetics
  • Male
  • Middle Aged
  • Polymorphism, Genetic
  • Pyrroles / administration & dosage*
  • Retrospective Studies
  • Risk Factors
  • Scavenger Receptors, Class E / genetics*
  • Simvastatin / administration & dosage
  • Thrombosis / drug therapy
  • Thrombosis / epidemiology
  • Thrombosis / genetics

Substances

  • Anticholesteremic Agents
  • Cholesterol, LDL
  • Heptanoic Acids
  • OLR1 protein, human
  • Pyrroles
  • Scavenger Receptors, Class E
  • C-Reactive Protein
  • Atorvastatin
  • Simvastatin