title: Plasma angiotensin-converting enzyme activity and carotid wall thickening.
abstract: BACKGROUND
  Mechanisms underlying the previously reported association between a deletion polymorphism in the gene encoding for angiotensin-converting enzyme (ACE) and the risk of myocardial infarction in low-risk subjects are unclear. The purpose of this case-control study was to examine the relation of plasma ACE activity to intimal-medial thickness of the carotid wall measured ultrasonographically in an apparently healthy population.
  
  
  RESULTS
  We determined plasma ACE activity in 80 pairs of subjects without any history of ischemic heart disease or any treatment of hypertension and diabetes. Cases and control subjects were defined on the basis of intimal-medial thickness measured in the common carotid arteries by B-mode ultrasound and were matched for sex, sonographer, and the presence of atheromatous plaques. Subjects were selected from a sample of 434 men and 602 women between 60 and 69 years old participating in an ongoing study on vascular aging (EVA). Subjects with intimal-medial thickening (cases) showed a slight but not significant increase in plasma ACE activity in comparison with control subjects (P < .16). However, after exclusion of subjects receiving lipid-lowering drugs, the mean plasma ACE activity became significantly higher in cases than in control subjects (29.9 +/- 7.7 U/L versus 27.5 +/- 8.0 U/L; n = 54 pairs, P < .03). The mean case-control difference in plasma ACE activity was further increased when analysis was restricted to pairs without carotid atheromatous plaques (n = 42 pairs). After adjustment for body mass index, smoking, and systolic blood pressure, the odds ratio for having carotid wall thickening based on 1 SD difference in log ACE was 2.29 (95% confidence interval, 1.16 to 4.52; P < .02).
  
  
  CONCLUSIONS
  The results of the study suggest that chronic exposure to high levels of plasma ACE could be involved in structural changes of the arterial wall.
authors.affiliation: INSERM U258, Hôpital Broussais, Paris, France.
authors.forename: C
authors.initials: C
authors.lastname: Bonithon-Kopp
authors.forename: P
authors.initials: P
authors.lastname: Ducimetière
authors.forename: P J
authors.initials: PJ
authors.lastname: Touboul
authors.forename: J M
authors.initials: JM
authors.lastname: Fève
authors.forename: E
authors.initials: E
authors.lastname: Billaud
authors.forename: D
authors.initials: D
authors.lastname: Courbon
authors.forename: V
authors.initials: V
authors.lastname: Héraud
mesh_terms: D000368:Aged; D000375:Aging / Q000473:pathology; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000453:epidemiology; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood*; D012307:Risk Factors; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography
chemical_list: D007703:Peptidyl-Dipeptidase A