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Absence of Association or Genetic Linkage between the Angiotensin-Converting–Enzyme Gene and Left Ventricular Mass

Open access
Lindpaintner, Klaus, Lee, MinAe, Larson, Martin G., Rao, V. Srinivas, Pfeffer, Marc A., Ordovas, Jose M., Schaefer, Ernst J., Wilson, Alexander F., Wilson, Peter W.F., Vasan, Ramachandran S., Myers, Richard H., Levy, Daniel·1996·New England Journal of Medicine

Abstract

BACKGROUND: Homozygous carries 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.

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Metadata

Authors
Lindpaintner, K., Lee, M., Larson, M. G., Rao, V. S., Pfeffer, M. A., Ordovas, J. M., Schaefer, E. J., Wilson, A. F., Wilson, P. W. F., Vasan, R. S., Myers, R. H., & Levy, D.
Venue
New England Journal of Medicine
Published
1996-04-18
Volume
334
Issue
16
Pages
1023-1028
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W4233429344
Cited by
180
References
6
FWCI
19.37
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Absence of Association or Genetic Linkage between the Angiotensin-Converting–Enzyme Gene and Left Ventricular Mass. https://app.cochat.ai/papers/10.1056/nejm199604183341604
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Lindpaintner, K., Lee, M., Larson, M. G., Rao, V. S., Pfeffer, M. A., Ordovas, J. M., Schaefer, E. J., Wilson, A. F., Wilson, P. W. F., Vasan, R. S., Myers, R. H., & Levy, D. (1996). Absence of Association or Genetic Linkage between the Angiotensin-Converting–Enzyme Gene and Left Ventricular Mass. New England Journal of Medicine. https://doi.org/10.1056/nejm199604183341604

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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