title: Relationship of angiotensin-converting enzyme gene polymorphism to carotid wall thickness in middle-aged men.
abstract: The insertion/deletion (I/D) polymorphism of the human angiotensin-converting enzyme (ACE) gene is a major determinant of circulating ACE levels. The D allele has been suggested to be a potent risk factor for coronary artery disease; however, the effect of the ACE gene on carotid atherosclerosis remains controversial. We therefore studied the relationship between the ACE gene I/D polymorphism and carotid artery intima-media thickness (IMT). A random sample of 300 men aged 50-59 years living in southern Finland were selected, and 233 agreed to participate (74%). Data were collected in 219 subjects. Quantitative B-mode ultrasonography was used to measure the maximum near and far wall IMT of right and left common, bifurcation, and internal carotid artery. The mean maximum IMT (overall mean) was calculated as the mean of 12 maximum IMTs at 12 standard sites. Patients with an IMT higher than 1.7 mm in at least one of 12 standard sites were assumed to have carotid atherosclerosis. The I/D polymorphism was determined by polymerase chain reaction. Overestimation of the frequency of the DD genotype was eliminated by insertion-specific primer and the inclusion of 5% dimethylsulfoxide. No significant differences were found in carotid wall thickness between the three genotypes; the overall mean IMT were 1.18 +/- 0.30, 1.22 +/- 0.24, and 1.08 +/- 0.40 mm in genotypes of II, ID, and DD, respectively. Similarly, the ACE genotypes and allele frequencies did not differ significantly between the subjects with and those without carotid atherosclerosis. There was no association in the subgroups among only nonsmoking subjects or subjects without chronic medication. The present data indicate that the I/D polymorphism of the ACE gene is not related to carotid IMT and is unlikely to play a major role in carotid atherosclerosis.
authors.affiliation: Department of Clinical Chemistry, Tampere University Hospital, Finland.
authors.forename: X H
authors.initials: XH
authors.lastname: Huang
authors.forename: A
authors.initials: A
authors.lastname: Loimaala
authors.forename: A
authors.initials: A
authors.lastname: Nenonen
authors.forename: M
authors.initials: M
authors.lastname: Mercuri
authors.forename: I
authors.initials: I
authors.lastname: Vuori
authors.forename: M
authors.initials: M
authors.lastname: Pasanen
authors.forename: P
authors.initials: P
authors.lastname: Oja
authors.forename: G
authors.initials: G
authors.lastname: Bond
authors.forename: T
authors.initials: T
authors.lastname: Koivula
authors.forename: T P
authors.initials: TP
authors.lastname: Hiltunen
authors.forename: T
authors.initials: T
authors.lastname: Nikkari
authors.forename: T
authors.initials: T
authors.lastname: Lehtimäki
mesh_terms: D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D005838:Genotype; D006801:Humans; D007438:Introns; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011897:Random Allocation; D017384:Sequence Deletion; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography
chemical_list: D007703:Peptidyl-Dipeptidase A