Background Epidemiologic studies have shown that left ventricularhypertrophy is often found in the absence of an elevated cardiacworkload. To investigate whether such hypertrophy is determinedin part by genetic factors, we studied the association betweenthis condition, as assessed by electrocardiographic criteria,and a deletion (D)-insertion (I) polymorphism of the angiotensin-converting-enzyme(ACE) gene.
Methods A population-based random sample of 711 women and 717men 45 to 59 years of age was studied cross-sectionally in Augsburg,Germany. Electrocardiographic indexes, including the Sokolow-Lyonindex, Minnesota Code 3.1, and the Rautaharju equations, wereused to detect left ventricular hypertrophy. The status of theACE gene with respect to the deletion-insertion allele was determinedby the polymerase chain reaction in all subjects with left ventricularhypertrophy and an identical number of control subjects withoutthe condition who were matched for age, sex, and blood-pressurestatus.
Results We identified 141 women and 149 men with evidence ofleft ventricular hypertrophy. Among these subjects, an excesswere homozygous for the D allele of the ACE gene (odds ratio,1.76; 95 percent confidence interval, 1.22 to 2.53; P = 0.003).The association of the DD genotype with left ventricular hypertrophywas stronger in men (odds ratio, 2.63; 95 percent confidenceinterval, 1.50 to 4.64; P<0.001) than in women and was mostprominent when blood-pressure measurements were normal (oddsratio, 4.05; 95 percent confidence interval, 1.76 to 9.28; P= 0.001). This association was evident for each of the scoresrecorded in the electrocardiographic testing for left ventricularhypertrophy.
Conclusions The findings suggest that left ventricular hypertrophyis partially determined by genetic disposition. They identifythe DD genotype of ACE as a potential genetic marker associatedwith an elevated risk of left ventricular hypertrophy in middle-agedmen.
Source Information
From the Medizinische Klinik II, University of Regensburg, Regensburg, Germany (H.S., S.R.H., G.A.J.R.); the Institut fur Epidemiologie (H.-W.H., M.S., U.K.) and the MEDIS Institut (S.P.), GSF Forschungszentrum, Munchen-Neuherberg, Germany; the Institut fur Epidemiologie und Sozialmedizin (H.-W.H., U.K.), University of Munster, Munster, Germany; and the Charles A. Dana Research Institute and Harvard-Thorndike Laboratory of Beth Israel Hospital, Department of Internal Medicine, Cardiovascular Division, Beth Israel Hospital and Harvard Medical School, Boston (B.H.L.). Presented in part at the 66th scientific sessions of the American Heart Association, Atlanta, November 8-11, 1993.
Address reprint requests to Dr. Schunkert at the Klinik and Poliklinik fur Innere Medizin II, Universitat Regensburg, Franz-Josef Strauss Allee, D-93053 Regensburg, Germany.
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van Bockxmeer, F. M., Mamotte, C. D. S., Gibbons, F. A., Burke, V., Taylor, R. R.
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Lechin, M., Quinones, M. A., Omran, A., Hill, R., Yu, Q.-T., Rakowski, H., Wigle, D., Liew, C.C., Sole, M., Roberts, R., Marian, A. J.
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Danser, A.H. J., Schalekamp, M. A.D.H., Bax, W. A., van den Brink, A. M., Saxena, P. R., Riegger, G. A.J., Schunkert, H.
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Markus, H. S., Barley, J., Lunt, R., Bland, J. M., Jeffery, S., Carter, N. D., Brown, M. M.
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