Relationship of angiotensin-converting enzyme gene polymorphism to carotidwall thickness in middle-aged men

The insertion/deletion (I/D) polymorphism of the human angiotensin-converti ng 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 rem ains controversial. We therefore studied the relationship between the ACE g ene I/D polymorphism and carotid artery intima-media thickness (IMT). A ran dom sample of 300 men aged 50-59 years living in southern Finland were sele cted, and 233 agreed to participate (74%). Data were collected in 219 subje cts. Quantitative B-mode ultrasonography was used to measure the maximum ne ar and far wall IMT of right and left common, bifurcation, and internal car otid 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 at herosclerosis. The I/D polymorphism was determined by polymerase chain reac tion. Overestimation of the frequency of the DD genotype was eliminated by insertion-specific primer and the inclusion of 5% dimethylsulfoxide. No sig nificant 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 ge notypes and allele frequencies did not differ significantly between the sub jects with and those without carotid atherosclerosis. There was no associat ion in the subgroups among only nonsmoking subjects or subjects without chr onic medication. The present data indicate that the IID polymorphism of the ACE gene is not related to carotid IMT and is unlikely to play a major rol e in carotid atherosclerosis.