title: Angiotensin II type 1 receptor A1166C gene polymorphism. Absence of an association with the risk of coronary artery disease and myocardial infarction and of a synergistic effect with angiotensin-converting enzyme gene polymorphism on the risk of these diseases.
abstract: OBJECTIVE
  There is evidence that interaction between angiotensin II type 1 receptor A1166C gene polymorphism and angiotensin I-converting enzyme Insertion/Deletion gene variation might have an effect on the risk of myocardial infarction. The study was carried out in a population of 2244 male Caucasians, whose coronary anatomy was defined by means of coronary angiography. We analysed the relationship, on the risk of ischaemic heart disease, of angiotensin II type 1 receptor A1166C gene variation, not only to myocardial infarction but also to coronary artery disease, and its potential interaction with angiotensin I-converting enzyme Insertion/Deletion gene polymorphism.
  
  
  RESULTS
  No association was detected between angiotensin II type 1 receptor A1166C gene polymorphism and coronary artery disease. Similarly, there was no link to myocardial infarction, either in the total population or in low risk groups. In addition, most importantly, we found no interaction between angiotensin II type 1 receptor A1166C gene variation and angiotensin I-converting Insertion/Deletion polymorphism, either in connection with the risk of coronary artery disease or myocardial infarction.
  
  
  CONCLUSIONS
  This angiotensin II type 1 receptor A1166C gene variation is not associated with any detectable increase in risk of ischaemic heart disease. The findings of the present study do not suggest that, as regards risk of coronary artery disease and myocardial infarction, there is interaction between gene polymorphism and angiotensin I-converting enzyme Insertion/Deletion gene variation.
authors.affiliation: Institut für Klinische Chemie und Pathobiochemie, Justus-Liebig-Universität Giessen, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Gardemann
authors.forename: Q D
authors.initials: QD
authors.lastname: Nguyen
authors.forename: J
authors.initials: J
authors.lastname: Humme
authors.forename: J
authors.initials: J
authors.lastname: Stricker
authors.forename: N
authors.initials: N
authors.lastname: Katz
authors.forename: H
authors.initials: H
authors.lastname: Tillmanns
authors.forename: F W
authors.initials: FW
authors.lastname: Hehrlein
authors.forename: M
authors.initials: M
authors.lastname: Rau
authors.forename: W
authors.initials: W
authors.lastname: Haberbosch
mesh_terms: D000368:Aged; D000804:Angiotensin II / Q000378:metabolism*; D003327:Coronary Disease / Q000201:enzymology / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011945:Receptors, Angiotensin / Q000235:genetics*; D012307:Risk Factors
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A