title: Association between UCP2 A55V polymorphism and risk of cardiovascular events in patients with multi-vessel coronary arterial disease.
abstract: BACKGROUND
  UCP2 (uncoupling protein 2) plays an important role in cardiovascular diseases and recent studies have suggested that the A55V polymorphism can cause UCP2 dysfunction. The main aim was to investigate the association of A55V polymorphism with cardiovascular events in a group of 611 patients enrolled in the Medical, Angioplasty or Surgery Study II (MASS II), a randomized trial comparing treatments for patients with coronary artery disease and preserved left ventricular function.
  
  
  METHODS
  The participants of the MASS II were genotyped for the A55V polymorphism using allele-specific PCR assay. Survival curves were calculated with the Kaplan-Meier method and evaluated with the log-rank statistic. The relationship between baseline variables and the composite end-point of cardiac death, acute myocardial infarction (AMI), refractory angina requiring revascularization and cerebrovascular accident were assessed using a Cox proportional hazards survival model.
  
  
  RESULTS
  There were no significant differences for baseline variables according genotypes. After 2 years of follow-up, dysglycemic patients harboring the VV genotype had higher occurrence of AMI (p=0.026), Death+AMI (p=0.033), new revascularization intervention (p=0.009) and combined events (p=0.037) as compared with patients carrying other genotypes. This association was not evident in normoglycemic patients.
  
  
  CONCLUSIONS
  These findings support the hypothesis that A55V polymorphism is associated with UCP2 functional alterations that increase the risk of cardiovascular events in patients with previous coronary artery disease and dysglycemia.
authors.affiliation: Sao Paulo University Medical School, São Paulo, Brazil.
authors.forename: Luciana
authors.initials: L
authors.lastname: Gioli-Pereira
authors.forename: Paulo Cjl
authors.initials: PC
authors.lastname: Santos
authors.forename: Luisa S
authors.initials: LS
authors.lastname: Sugaya
authors.forename: Noely E
authors.initials: NE
authors.lastname: Ferreira
authors.forename: José Eduardo
authors.initials: JE
authors.lastname: Krieger
authors.forename: Alexandre C
authors.initials: AC
authors.lastname: Pereira
authors.forename: Whady A
authors.initials: WA
authors.lastname: Hueb
mesh_terms: D000368:Aged; D019943:Amino Acid Substitution; D002318:Cardiovascular Diseases / Q000235:genetics*; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D044882:Glucose Metabolism Disorders / Q000150:complications; D006801:Humans; D015994:Incidence; D007473:Ion Channels / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D024101:Mitochondrial Proteins / Q000235:genetics*; D009203:Myocardial Infarction / Q000150:complications; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012307:Risk Factors; D000071246:Uncoupling Protein 2; D016277:Ventricular Function, Left
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604389:UCP2 protein, human; D000071246:Uncoupling Protein 2
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