Circulation, Vol 90, 669-676, Copyright © 1994 by American Heart Association
F Cambien, O Costerousse, L Tiret, O Poirier, L Lecerf, MF Gonzales, A Evans, D Arveiler, JP Cambou and G Luc
BACKGROUND: The angiotensin-converting enzyme (ACE) plays an important role
in the production of angiotensin II and the degradation of bradykinin, two
peptides involved in cardiovascular homeostasy. Presence of a polymorphism
in the ACE gene (ACE Ss) has been postulated from segregation analysis of
plasma ACE in families. This putative polymorphism, which strongly affects
the plasma and cellular levels of ACE, probably by modulating ACE gene
transcription, has not yet been identified at the molecular level; however,
an insertion/deletion polymorphism is present in the 16th intron of the ACE
gene (ACE I/D) and appears to be a very good marker for ACE Ss. The
biological role of ACE suggests that the ACE gene polymorphism could affect
the predisposition to myocardial infarction (MI). METHODS AND RESULTS: We
have recently shown, in a large case-control study (ECTIM), that the marker
allele D of the ACE gene, which is associated with higher levels of ACE in
plasma and cells, was more frequent in male patients with MI than in
control subjects, especially in patients considered at low risk. ACE
activity has now been measured from frozen aliquots of plasma in a large
subsample of the ECTIM study (n = 1086). Plasma ACE level did not differ
between patients and control subjects in the older age group (> or = 55
years) but was higher in patients than in control subjects in the younger
age group (< 55 years); P < .005 after adjustment on ACE I/D and
other risk factors. In patients, plasma ACE levels decreased with age (R =
-.225, P < 10(-4)), but in control subjects no such trend was observed.
In the low-risk group (ApoB < 1.25 mg/dL, body mass index < 26 kg/m2,
and not treated with hypolipidemic drugs), plasma ACE level was increased
in patients when compared with control subjects among homozygotes and
heterozygotes for the ACE I allele (P < .015). Analysis of the
distribution of plasma ACE by using commingling analysis conditional on the
marker genotype ACE I/D enabled us to infer the frequencies and effects of
the postulated ACE Ss genotypes. The results suggest that the higher plasma
ACE levels in patients than in control subjects in the younger age group
were due to a difference in frequency of the postulated S allele (.47
versus .36). CONCLUSIONS: These results extend our previous findings and
indicate that plasma ACE level may be a risk factor for MI, independent of
the ACE I/D polymorphism.
ARTICLES
Plasma level and gene polymorphism of angiotensin-converting enzyme in relation to myocardial infarction
INSERM SC7, Paris, France.
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