title: Deletion polymorphism in angiotensin converting enzyme gene associated with carotid wall thickening in a healthy male population.
abstract: BACKGROUND
  Intimal thickening is an adaptive process of the arterial wall, presumably related to atherogenesis. Sex and interethnic differences in intimal thickening, as demonstrated histologically on autoptic material, would indicate a strong genetic control on this process. An insertion/deletion (ID) polymorphism in the angiotensin-converting enzyme (ACE) gene has been shown to be an independent risk factor for cardiovascular disease, especially in subjects otherwise at low risk for coronary heart disease. The aim of the present study was to evaluate the relationship between intimal plus medial thickness (IMT) and ACE-I/D genotype.
  
  
  METHODS
  132 healthy male subjects from Southern Italy were enrolled. IMT has been evaluated from high resolution B-mode echo-Doppler images. Blood lipids and glucose were measured using standard methods. Cigarette consumption was recorded by questionnaire. ACE genotypes were analysed by polymerase chain reaction.
  
  
  RESULTS
  Blood lipids, blood pressure and percentage of smokers were similar in the three groups. IMT was greatest in DD subjects, lowest in II subjects and intermediate in heterozygotes. The association between the presence of the D allele and IMT values was statistically significant. Significance was maintained after the elimination of subjects with carotid atherosclerotic plaques.
  
  
  CONCLUSIONS
  The present data suggest that the ACE gene seems to be a candidate gene that strongly influences the IMT of the arterial wall and might therefore be involved in the individual's predisposition to the development of atherosclerosis.
authors.affiliation: University of Reggio Calebria, Dipartimento di Medicina Sperimentale e Clinica, Catanzaro, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Pujia
authors.forename: C
authors.initials: C
authors.lastname: Motti
authors.forename: C
authors.initials: C
authors.lastname: Irace
authors.forename: C
authors.initials: C
authors.lastname: Cortese
authors.forename: L
authors.initials: L
authors.lastname: Biagiotti
authors.forename: P L
authors.initials: PL
authors.lastname: Mattioli
authors.forename: G
authors.initials: G
authors.lastname: Federici
authors.forename: A
authors.initials: A
authors.lastname: Gnasso
mesh_terms: D000328:Adult; D001161:Arteriosclerosis / Q000235:genetics* / Q000473:pathology; D016893:Carotid Stenosis / Q000235:genetics* / Q000473:pathology; D002872:Chromosome Deletion; D003324:Coronary Artery Disease / Q000235:genetics / Q000473:pathology; D005352:Fibromuscular Dysplasia / Q000235:genetics / Q000473:pathology; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology; D006801:Humans; D007558:Italy; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012016:Reference Values; D012307:Risk Factors; D017539:Tunica Intima / Q000473:pathology
chemical_list: D007703:Peptidyl-Dipeptidase A