© 1996 American Heart Association, Inc.
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Genotype Distribution of Angiotensin-Converting Enzyme Polymorphism in Australian Healthy and Coronary Populations and Relevance to Myocardial Infarction and Coronary Artery Disease
From the Department of Cardiovascular Medicine, University of New South Wales, Prince Henry/Prince of Wales Hospitals, Sydney, Australia.
Correspondence to Prof David Wilcken, Department of Cardiovascular Medicine, Clinical Sciences Building, Prince Henry Hospital, Little Bay, NSW 2036, Australia. E-mail x.l.wang@unsw.edu.au.
Abstract Angiotensin-converting enzyme is a
key component of the renin-angiotensin system that
plays an important role in cardiovascular regulation.
An association between the angiotensin-converting
enzyme insertion/deletion (I/D) polymorphism and increased
coronary risk has been found in some studies but not in others.
To explore this further in an Australian white population, we compared
the ACE genotype distribution in 550 patients aged 37 to 65
years with coronary artery disease documented by angiography
with the genotype distribution in 404 healthy school children
aged 6 to 13 years. We also explored associations in the patients
between the angiotensin-converting enzyme I/D
polymorphism and a history of myocardial infarction and
coronary artery disease severity assessed by the number of
major coronary arteries with more than 50% luminal
obstructions and by the Green Lane coronary score. The
frequencies of the angiotensin-converting enzyme
genotype in the coronary artery disease patients were
0.236 for I/I, 0.395 for I/D, and 0.369 for D/D genotypes. This
distribution with an excess of the D/D genotype was
significantly different (
2=23.69,
P<.0001) from that in the school children, in whom the
genotype distribution was in Hardy-Weinberg equilibrium (I/I,
0.21; I/D, 0.54; D/D, 0.25). There was also a significant excess of D/D
genotype among patients with a history of myocardial infarction
(2=9.42, P=.009), and there was the
same D/D excess in the subgroup of children (n=60) with two or more
grandparents who had had coronary artery disease. We found no
associations between the angiotensin-converting enzyme
polymorphism and the number of significantly stenosed
coronary arteries (2=2.069,
P=.91). We conclude that the D/D genotype is a
significant predictor for coronary artery disease events in the
Australian white population but is not a marker for angiographically
assessed coronary artery disease severity. The
angiotensin-converting enzyme
genotype–associated increased risk for coronary
events may be mediated more by angiotensin II–induced
coronary vasoconstriction than by an increase in
injury-related smooth muscle cell proliferation in the
coronary vasculature.
Key Words: ACE I/D polymorphism • myocardial infarction • coronary artery disease, severity • renin-angiotensin system
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