title: Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.
abstract: OBJECTIVE
  We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction.
  
  
  BACKGROUND
  The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling.
  
  
  METHODS
  I/D genotyping, predischarge adenosine-thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography.
  
  
  RESULTS
  Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean +/- SD] 33.7 +/- 22.5%, 29.5 +/- 19.2% and 22.2 +/- 16.0%, respectively [p = 0.022]; reversible defect size 18.0 +/- 16.0%, 12.1 +/- 11.6% and 8.2 +/- 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001).
  
  
  CONCLUSIONS
  DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.
authors.affiliation: Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
authors.forename: H A
authors.initials: HA
authors.lastname: Dakik
authors.forename: J J
authors.initials: JJ
authors.lastname: Mahmarian
authors.forename: M S
authors.initials: MS
authors.lastname: Verani
authors.forename: J A
authors.initials: JA
authors.lastname: Farmer
authors.forename: G
authors.initials: G
authors.lastname: Zhao
authors.forename: A J
authors.initials: AJ
authors.lastname: Marian
mesh_terms: D000241:Adenosine; D002317:Cardiovascular Agents; D003331:Coronary Vessels / Q000503:physiopathology*; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D011875:Radionuclide Angiography; D013794:Thallium Radioisotopes; D014654:Vascular Patency
chemical_list: D002317:Cardiovascular Agents; D013794:Thallium Radioisotopes; D007703:Peptidyl-Dipeptidase A; D000241:Adenosine