Circulation, Vol 89, 952-954, Copyright © 1994 by American Heart Association
C Bonithon-Kopp, P Ducimetiere, PJ Touboul, JM Feve, E Billaud, D Courbon and V Heraud
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. METHODS AND 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.
ARTICLES
Plasma angiotensin-converting enzyme activity and carotid wall thickening
INSERM U258, Hopital Broussais, Paris, France.
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