The D allele of the angiotensin-converting enzyme gene contributes towards blood LDL-cholesterol levels and the presence of hypertension

Atherosclerosis. 1999 Aug;145(2):267-71. doi: 10.1016/s0021-9150(99)00075-1.

Abstract

Coronary artery disease is a polygenic disease whose phenotypic manifestation depends on the interaction of the genetic background with a number of environmental factors. Recently, the gene coding for the angiotensin-converting enzyme (ACE) has been characterized and a deletion/insertion (D/I) polymorphism was defined. The prevalence of the three genotypes and their association with coronary artery disease (CAD) differ in different population groups. Mostly, the D allele was found as a significant risk factor for CAD, independently from other risk factors. In the present study, we determined the distribution of ACE alleles (D or I) in a cohort of healthy Israeli men and examined the correlation of the different genotypes with various CAD risk factors. We found LDL cholesterol levels to be highest in the DD genotype group, intermediate in the DI genotype group and lowest in the II genotype group. We also found higher blood pressure levels in subjects bearing the D allele compared to II homozygous subjects. In conclusion, it appears that the genetic influence of the D/I polymorphism on CAD manifests primarily through traditional risk factors.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Aged
  • Alleles*
  • Blood Pressure
  • Cholesterol, LDL / blood*
  • Coronary Artery Disease / blood
  • Coronary Artery Disease / genetics
  • DNA / analysis
  • DNA Transposable Elements / genetics
  • Gene Deletion
  • Gene Frequency
  • Genetic Markers
  • Genotype
  • Humans
  • Hypertension / blood
  • Hypertension / genetics*
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / blood
  • Peptidyl-Dipeptidase A / genetics*
  • Polymerase Chain Reaction
  • Risk Factors

Substances

  • Cholesterol, LDL
  • DNA Transposable Elements
  • Genetic Markers
  • DNA
  • Peptidyl-Dipeptidase A