A Prospective Evaluation of an Angiotensin-Converting-Enzyme Gene Polymorphism and the Risk of Ischemic Heart Disease

doi:10.1056/NEJM199503163321103

Volume 332:706-712		March 16, 1995		Number 11

A Prospective Evaluation of an Angiotensin-Converting–Enzyme Gene Polymorphism and the Risk of Ischemic Heart Disease

Klaus Lindpaintner, M.D., Marc A. Pfeffer, M.D., Ph.D., Reinhold Kreutz, M.D., Meir J. Stampfer, M.D., Dr.P.H., Francine Grodstein, Sc.D., Fran LaMotte, B.S., Julie Buring, Sc.D., and Charles H. Hennekens, M.D., Dr.P.H.

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ABSTRACT

Background In a previous study, men with a history of myocardialinfarction were found to have an increased prevalence of homozygosityfor the deletional allele (D) of the angiotensin-converting–enzyme(ACE) gene. The D allele is associated with higher levels ofACE, which may predispose a person to ischemic heart disease.We investigated the association between the ACE genotype andthe incidence of myocardial infarction, as well as other manifestationsof ischemic heart disease, in a large, prospective cohort ofU.S. male physicians.

Methods In the Physicians' Health Study, ischemic heart diseaseas defined by angina, coronary revascularization, or myocardialinfarction developed in 1250 men by 1992. They were matchedwith 2340 controls according to age and smoking history. Zygosityfor the deletion–insertion (D–I) polymorphism ofthe ACE gene was determined by an assay based on the polymerasechain reaction. Data were analyzed for both matched pairs andunmatched samples, with adjustment for the effects of knownor suspected risk factors by conditional and nonconditionallogistic regression, respectively.

Results The ACE genotype was not associated with the occurrenceof either ischemic heart disease or myocardial infarction. Theadjusted relative risk associated with the D allele was 1.07(95 percent confidence interval, 0.96 to 1.19; P = 0.24) forischemic heart disease and 1.05 (95 percent confidence interval,0.89 to 1.25; P = 0.56) for myocardial infarction, if an additivemode of inheritance is assumed. Additional analyses assumingdominant and recessive effects of the D allele also failed toshow any association, as did the examination of low-risk subgroups.

Conclusions In a large, prospectively followed population ofU.S. male physicians, the presence of the D allele of the ACEgene conferred no appreciable increase in the risk of ischemicheart disease or myocardial infarction.

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From the Divisions of Cardiovascular Diseases (K.L., M.A.P., R.K.) and Preventive Medicine (F.L., J.B., C.H.H.), and the Channing Laboratory (M.J.S., F.G.), Department of Medicine, Brigham and Women's Hospital; the Department of Cardiology, Children's Hospital (K.L.); the Department of Ambulatory Care and Prevention, Harvard Medical School (J.B., C.H.H.); and the Departments of Epidemiology and Nutrition, Harvard School of Public Health (M.J.S., C.H.H.) — all in Boston.

Address reprint requests to Dr. Lindpaintner at the Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115.

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N Engl J Med 1995; 333:458-460, Aug 17, 1995. Correspondence

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