title: AMPD1 (C34T) polymorphism and clinical outcomes in patients undergoing myocardial revascularization.
abstract: BACKGROUND
  C34T variant of adenosine monophosphate deaminase 1 (AMPD1) gene has been associated with a prolonged survival in heart failure and coronary artery disease, hypothetically linked to an enhanced production of adenosine.
  
  
  METHODS
  Since adenosine administration is a promising approach for the prevention of the ischemia-reperfusion in myocardial revascularization, the aim of this study was to investigate whether the AMPD1 (-) allele is associated with a favorable prognosis after coronary revascularization. In addition, we assessed the association between AMPD1 polymorphism and plasma adenosine levels.
  
  
  METHODS
  We investigated a total of 161 patients receiving coronary revascularization (70 percutaneous transluminal coronary angioplasty and 91 coronary artery bypass graft). They were investigated for a composite endpoint including recurrent angina, non-fatal MI, target vessel revascularization, heart failure and cardiac death. Plasma adenosine was also measured by high-performance liquid chromatography methods on a subset of 25 patients.
  
  
  RESULTS
  During the follow-up period (7.0+/-0.3 months), the overall combined endpoint accounted for 17 events (10 cardiac-related deaths, 6 revascularization procedures and 1 congestive heart failure). The composite endpoint was 9.8% for AMPD1 (-) allele carriers vs. 11.5% for non-carriers (log-rank statistic, p=n.s.). In the logistic analysis only low (</=40%) ejection fraction was an independent predictor of adverse events (p=0.01, OR=3.8, 95% CI 1.3-11.4). Plasma adenosine levels were similar for AMPD1 (-) allele patients (n=7) as compared for AMPD1 (+) allele (n=18) subjects (290.5+/-31.0 vs. 303.3+/-28.5 nM, p=n.s.).
  
  
  CONCLUSIONS
  Our results indicate that AMPD1 (-) allele is not associated with a more favorable outcome after coronary revascularization. Alternative cardioprotective pathways of the AMPD1 gene-involving an enhanced chronic long-term production of adenosine-might be responsible for survival.
authors.affiliation: Institute of Clinical Physiology, Pisa, Italy. andreas@ifc.cnr.it
authors.forename: Maria Grazia
authors.initials: MG
authors.lastname: Andreassi
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Botto
authors.forename: Franco
authors.initials: F
authors.lastname: Laghi-Pasini
authors.forename: Samantha
authors.initials: S
authors.lastname: Manfredi
authors.forename: Bruno
authors.initials: B
authors.lastname: Ghelarducci
authors.forename: Andrea
authors.initials: A
authors.lastname: Farneti
authors.forename: Marco
authors.initials: M
authors.lastname: Solinas
authors.forename: Andrea
authors.initials: A
authors.lastname: Biagini
authors.forename: Eugenio
authors.initials: E
authors.lastname: Picano
mesh_terms: D000659:AMP Deaminase / Q000235:genetics*; D000241:Adenosine / Q000097:blood; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics* / Q000628:therapy*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D000659:AMP Deaminase; D000241:Adenosine