Copyright © 1999 by the European Society of Cardiology.
Angiotensin I-converting enzyme gene polymorphism, coronary artery disease and myocardial infarction. An angiographically controlled study
a Department of Medicine, Division of Endocrinology, Metabolism and Clinical Biochemistry, University of Tübingen, Tübingen, Germany
b Department of Medicine, Division of Cardiology, University of Tübingen, Tübingen, Germany
revised January 20, 1999; accepted February 3, 1999
Abstract
Objectives We investigated the association between insertion/deletion polymorphism of the angiotensin I-converting enzyme (ACE) gene, the presence and extent of coronary artery disease, and myocardial infarction.
Background The D allele of the ACE gene has been associated with coronary artery disease and myocardial infarction, but this association has been challenged in epidemiological studies.
Methods Nine hundred and sixty-nine men and 341 women undergoing coronary angiography were studied. The ACE genotypes were assessed by polymerase chain reaction from genomic deoxyribonucleic acid, homozygosity for the D allele was controlled using an insertion-specific primer. Coronary artery disease was defined by angiographic criteria, the extent of coronary artery disease by the number of coronary arteries with
50% lumen narrowing.
Results The ACE genotypes did not differ in terms of age, sex, body mass index, blood pressure, plasma lipids or lipoproteins. We found no association between the ACE genotypes and coronary artery disease (odds ratio, 95% confidence interval in DD genotypes for coronary artery disease in men 0·97, 0·701·36; in women 1·56, 0·952·57), extent of coronary artery disease (men 1·17, 0·851·61; women 1·24, 0·652·34), or myocardial infarction among the patients with coronary artery disease (men 1·07, 0·781·48; women 0·95, 0·501·76). The ACE genotype was not associated with coronary artery disease or myocardial infarction in hypertensives (n=771; odds ratio for coronary artery disease 0·93, 0·651·34; odds ratio for myocardial infarction 0·94, 0·661·33), or in patients
60 years (n=649; odds ratio for coronary artery disease 1·05, 0·721·52; odds ratio for myocardial infarction 0·96, 0·631·47).
Conclusion ACE insertion/deletion gene polymorphism is associated neither with the prevalence nor the extent of coronary artery disease, nor with myocardial infarction in this relatively large sample of Caucasian men and women. Genotyping for ACE insertion/deletion polymorphism is not useful in assessing the individual risk of coronary artery disease or myocardial infarction.
Key Words: ACE gene polymorphism, coronary heart disease, myocardial infarction
f1 Correspondence : Dr Martin Pfohl, BG-Kliniken Bergmannsheil, Universitätsklinik, Medizinische Klinik und Poliklinik, Bürkle-de-la-Camp-Platz 1, D-44789 Bochum, Germany.
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