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Previous Volume 330:1634-1638 June 9, 1994 Number 23 Next

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ABSTRACT

Background Epidemiologic studies have shown that left ventricular hypertrophy is often found in the absence of an elevated cardiac workload. To investigate whether such hypertrophy is determined in part by genetic factors, we studied the association between this 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 717 men 45 to 59 years of age was studied cross-sectionally in Augsburg, Germany. Electrocardiographic indexes, including the Sokolow-Lyon index, Minnesota Code 3.1, and the Rautaharju equations, were used to detect left ventricular hypertrophy. The status of the ACE gene with respect to the deletion-insertion allele was determined by the polymerase chain reaction in all subjects with left ventricular hypertrophy and an identical number of control subjects without the condition who were matched for age, sex, and blood-pressure status.

Results We identified 141 women and 149 men with evidence of left ventricular hypertrophy. Among these subjects, an excess were 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 hypertrophy was stronger in men (odds ratio, 2.63; 95 percent confidence interval, 1.50 to 4.64; P<0.001) than in women and was most prominent when blood-pressure measurements were normal (odds ratio, 4.05; 95 percent confidence interval, 1.76 to 9.28; P = 0.001). This association was evident for each of the scores recorded in the electrocardiographic testing for left ventricular hypertrophy.

Conclusions The findings suggest that left ventricular hypertrophy is partially determined by genetic disposition. They identify the DD genotype of ACE as a potential genetic marker associated with an elevated risk of left ventricular hypertrophy in middle-aged men.

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.

Full Text of this Article

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