title: Angiotensinogen T174M and M235T gene polymorphisms are associated with the extent of coronary atherosclerosis.
abstract: BACKGROUND
  The relations of the angiotensinogen (AGT) T174M and M235T gene polymorphisms to the risk of coronary heart disease (CHD) have been investigated in only a few studies with conflicting results.
  
  
  RESULTS
  Therefore, we analysed the relationship of the AGT gene polymorphisms to the presence and extent of CHD in 2250 male Caucasians whose coronary anatomy was defined by means of coronary angiography. The relative frequencies of the T and M alleles of the T174M and of the M235T gene variation did not significantly differ between patients without or with single-, double- or triple-vessel disease and between subjects without or with myocardial infarction (MI). In contrast the mean CHD score--defined by Gensini--was higher within MM homozygotes of the T174M gene variation than within TT genotypes; TM subjects had intermediate values. In M235T genotypes, mean CHD scores were similar in the total sample and in older individuals (> or = 62 years), whereas in younger individuals (< 62 years) a higher CHD score was found within AGT 235 T allele carriers than within MM homozygotes. In younger individuals with high apoAI plasma levels, the mean CHD score was clearly higher within TT homozygotes of the M235T gene variation than within MM genotypes; MT subjects had intermediate values. An interaction between both angiotensinogen gene polymorphisms on the extent of CHD or on the risk of non-fatal MI were not observed when the M allele of AGT T174M was combined either with the T allele or the TT genotype of M235T.
  
  
  CONCLUSIONS
  The present study strengthens the hypothesis of an association of both angiotensinogen gene polymorphisms with the extent of coronary heart disease.
authors.affiliation: Institut für Klinische Chemie und Pathobiochemie, Klinikum der Justus-Liebig-Universität Giessen, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Gardemann
authors.forename: J
authors.initials: J
authors.lastname: Stricker
authors.forename: J
authors.initials: J
authors.lastname: Humme
authors.forename: Q D
authors.initials: QD
authors.lastname: Nguyen
authors.forename: N
authors.initials: N
authors.lastname: Katz
authors.forename: M
authors.initials: M
authors.lastname: Philipp
authors.forename: H
authors.initials: H
authors.lastname: Tillmanns
authors.forename: F W
authors.initials: FW
authors.lastname: Hehrlein
authors.forename: W
authors.initials: W
authors.lastname: Haberbosch
mesh_terms: D000483:Alleles; D000808:Angiotensinogen / Q000097:blood / Q000235:genetics*; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D003062:Codon; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000235:genetics*; D005787:Gene Frequency; D005819:Genetic Markers; D005838:Genotype; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D003062:Codon; D005819:Genetic Markers; D000808:Angiotensinogen