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Lack of association of polymorphisms of the angiotensin converting enzyme and angiotensinogen genes with nonfamilial hypertrophic or dilated cardiomyopathy.

Authors: Yamada, Y  Ichihara, S  Fujimura, T  Yokota, M 
Citation: Yamada Y, etal., Am J Hypertens. 1997 Aug;10(8):921-8.
Pubmed: (View Article at PubMed) PMID:9270088

Although several genes or genetic loci that are either responsible for or confer susceptibility to familial hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM) have been identified, genetic defects that underlie nonfamilial HCM or DCM remain to be characterized. An allelic association study for the angiotensin converting enzyme (ACE) and angiotensinogen genes has now been performed with 71 patients with nonfamilial HCM, 88 patients with nonfamilial DCM, and 122 healthy control subjects in the Japanese population. The distribution of ACE genotypes for an insertion/deletion (I/D) polymorphism in intron 16 did not differ significantly among control subjects and patients with HCM or DCM. Similarly, the distributions of angiotensinogen genotypes for methionine-235-threonine (M235T) and threonine-174-methionine (T174M) polymorphisms did not differ significantly among the three groups. Echocardiographic parameters that are indicators of the severity or progression of disease did not differ significantly among ACE I/D or angiotensinogen M235T and T174M genotypes in the two patient groups. Finally, no additive or synergistic effect of any combined genotypes or haplotypes of the ACE and angiotensinogen polymorphisms on the association with HCM or DCM was detected. Results indicate that the ACE I/D and angiotensinogen M235T and T174M polymorphisms are not related to HCM or DCM in the Japanese population, and that variants of these polymorphisms do not contribute to the genesis or progression of these cardiomyopathies.

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CRRD Object Information
CRRD ID: 1566491
Created: 2006-02-15
Species: All species
Last Modified: 2006-02-15
Status: ACTIVE



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