title: The DD genotype of the angiotensin converting enzyme gene independently associates with CMR-derived abnormal microvascular perfusion in patients with a first anterior ST-segment elevation myocardial infarction treated with thrombolytic agents.
abstract: BACKGROUND
  The role of the angiotensin converting enzyme (ACE) gene on the result of thrombolysis at the microvascular level has not been addressed so far. We analyzed the implications of the insertion/deletion (I/D) polymorphism of the ACE gene on the presence of abnormal cardiovascular magnetic resonance (CMR)-derived microvascular perfusion after ST-segment elevation myocardial infarction (STEMI).
  
  
  METHODS
  We studied 105 patients with a first anterior STEMI treated with thrombolytic agents and an open left anterior descending artery. Microvascular perfusion was assessed using first-pass perfusion CMR at 7+/-1 days. CMR studies were repeated 184+/-11 days after STEMI. The ACE gene insertion/deletion (I/D) polymorphism was determined using polymerase chain reaction amplification.
  
  
  RESULTS
  Overall genotype frequencies were II-ID 58% and DD 42%. Abnormal perfusion (> or = 1 segment) was detected in 56% of patients. The DD genotype associated to a higher risk of abnormal microvascular perfusion (68% vs. 47%, p=0.03) and to a larger extent of perfusion deficit (median [percentile 25 - percentile 75]: 4 [0-6] vs. 0 [0-4] segments, p=0.003). Once adjusted for baseline characteristics, the DD genotype independently increased the risk of abnormal microvascular perfusion (odds ratio [95% confidence intervals]: 2.5 [1.02-5.9], p=0.04). Moreover, DD patients displayed a larger infarct size (35+/-17 vs. 27+/-15 g, p=0.01) and a lower ejection fraction at 6 months (48+/-14 vs. 54+/-14%, p=0.03).
  
  
  CONCLUSIONS
  The DD genotype associates to a higher risk of abnormal microvascular perfusion after STEMI.
authors: Cardiology Department, Hospital Clinico Universitario, Universidad de Valencia, Valencia, Spain. vicentbodi@hotmail.com
authors: Vicente
authors: V
authors: Bodi
authors: Juan
authors: J
authors: Sanchis
authors: Julio
authors: J
authors: Nunez
authors: Salvador F
authors: SF
authors: Aliño
authors: Maria J
authors: MJ
authors: Herrero
authors: Francisco J
authors: FJ
authors: Chorro
authors: Luis
authors: L
authors: Mainar
authors: Maria P
authors: MP
authors: Lopez-Lereu
authors: Jose V
authors: JV
authors: Monmeneu
authors: Ricardo
authors: R
authors: Oltra
authors: Fabian
authors: F
authors: Chaustre
authors: Maria J
authors: MJ
authors: Forteza
authors: Oliver
authors: O
authors: Husser
authors: Günter A
authors: GA
authors: Riegger
authors: Angel
authors: A
authors: Llacer
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D005343:Fibrinolytic Agents / Q000494:pharmacology; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012306:Risk; D016896:Treatment Outcome
chemical_list: D005343:Fibrinolytic Agents; D007703:Peptidyl-Dipeptidase A