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Previous Volume 334:1023-1028 April 18, 1996 Number 16 Next

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ABSTRACT

Background Homozygous carriers of the D allele of the angiotensin-converting–enzyme (ACE) gene have been reported to be at increased risk for various cardiovascular disorders, including left ventricular hypertrophy. We investigated the potential role of the ACE gene in influencing left ventricular mass.

Methods Quantitative echocardiographic data and DNA samples were available for 2439 subjects from the Framingham Heart Study. ACE genotypes were determined by an assay based on the polymerase chain reaction. (The D allele of the ACE gene contains a deletion, whereas the I [insertion] allele does not.) Left ventricular mass and the prevalence of left ventricular hypertrophy, adjusted for clinical covariates, were analyzed according to genotype. Genetic linkage between the ACE locus and left ventricular mass was evaluated by quantitative analysis of pairs of siblings.

Results The ACE genotype was associated neither with left ventricular mass nor with the prevalence of left ventricular hypertrophy. Mean (±SE) left ventricular mass (adjusted for sex) among subjects carrying the DD, DI, and II genotypes was 165±1.6, 165±1.3, and 166±2.0 g, respectively (P = 0.90). The prevalence of left ventricular hypertrophy among the three genotype groups was 15.6 percent, 13.6 percent, and 15.6 percent, respectively (P = 0.36), and the adjusted relative risk of left ventricular hypertrophy associated with the DD genotype was 1.10 (95 percent confidence interval, 0.86 to 1.19). Linkage analysis in 759 pairs of siblings using both the ACE D/I marker and a microsatellite polymorphism at the neighboring locus for the human growth hormone gene failed to support any role of ACE in influencing left ventricular mass.

Conclusions The ACE genotype showed no association with echocardiographically determined left ventricular mass, nor did it confer an increased risk of left ventricular hypertrophy. We found no appreciable role of the ACE gene in influencing left ventricular mass.

Source Information

From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital (K.L., M.L., M.A.P.); the Department of Cardiology, Children's Hospital (K.L.); the Divisions of Cardiology and Clinical Epidemiology, Department of Medicine, Beth Israel Hospital (D.L.); Harvard Medical School (K.L., M.L., M.A.P., D.L.); the Department of Neurology (R.H.M.) and the Divisions of Epidemiology and Preventive Medicine, Department of Medicine (M.G.L., V.S.R., D.L.), Boston University Medical School; and the Lipid Metabolism Laboratory, U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University School of Medicine (J.M.O., E.J.S.) — all in Boston; the Framingham Heart Study, Framingham, Mass. (M.G.L., P.W.F.W., R.S.V., D.L.); the Department of Biometry and Genetics, Louisiana State University Medical Center, New Orleans (A.F.W.); and the National Heart, Lung, and Blood Institute, Bethesda, Md. (P.W.F.W., D.L.).

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

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Absence of Association or Genetic Linkage between the Angiotensin-Converting–Enzyme Gene and Left Ventricular Mass
Cambien F., Tiret L., Cheung B., Lindpaintner K., Larson M. G., Wilson A. F.
Extract | Full Text  
N Engl J Med 1996; 335:1070-1071, Oct 3, 1996. Correspondence

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