title: Significant role of ADRB3 rs4994 towards the development of coronary artery disease.
abstract: BACKGROUND
  Coronary artery disease (CAD) is the most common type of heart disease and cause of heart attacks. It has been proposed that both the susceptibility to disease and the interindividual variability in response to treatment relates in part to genetic polymorphisms, particularly those polymorphisms for neurotransmitter and drug receptors. Common functional polymorphisms in β-adrenergic receptor genes (ADRB) have been associated with heart failure phenotypes. Therefore, the purpose of the present study was to explore the association of genetic variants in ADRB3 (C190T or Trp64Arg) ADRB1 (C1165G or Arg389Gly), and ADRA2A (C-1291G) with CAD.
  
  
  METHODS
  The present study recruited a total of 600 consecutive patients with angiographically confirmed CAD and 200 population-matched controls (173 men and 27 women) (mean age 54.10±8.30 years). The ADRB3 T190C, ADRA2A C-1291G, and ADRB1 C1165G polymorphisms were determined by PCR-restriction fragment length polymorphism. The putative functional effects were determined in the coding region of the ADRD3 gene by online web servers FASTSNP and F-SNP.
  
  
  RESULTS
  On comparing the genotype frequency distribution in CAD patients with that of healthy individuals, significant association was observed with the CC genotype of the ADRB3 T190C polymorphism (P=0.040, odds ratio=1.5). Also, at the allelic level the C allele of ADRB3 T190C conferred risk for CAD (P=0.005, odds ratio=1.7). The ADRA2A C-1291G and ADRB1 C1165G polymorphisms were not found to be a risk for CAD when compared with controls.
  
  
  CONCLUSIONS
  The present study finding suggests that ADRB3 C190T may also be involved in the complex pathophysiology of CAD.
authors.affiliation: Departments of aGenetics bCardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences (SGPGIMS), Lucknow, Uttar Pradesh, India.
authors.forename: Surendra
authors.initials: S
authors.lastname: Kumar
authors.forename: Avshesh
authors.initials: A
authors.lastname: Mishra
authors.forename: Anshika
authors.initials: A
authors.lastname: Srivastava
authors.forename: Tulika
authors.initials: T
authors.lastname: Mittal
authors.forename: Naveen
authors.initials: N
authors.lastname: Garg
authors.forename: Balraj
authors.initials: B
authors.lastname: Mittal
mesh_terms: D054458:Amplified Fragment Length Polymorphism Analysis; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000235:genetics* / Q000503:physiopathology; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010641:Phenotype; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D018341:Receptors, Adrenergic, alpha-2 / Q000235:genetics; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics; D022702:Receptors, Adrenergic, beta-3 / Q000235:genetics*; D012307:Risk Factors; D013318:Stroke Volume; D016277:Ventricular Function, Left
chemical_list: C547768:ADRA2A protein, human; C547787:ADRB1 protein, human; C568534:ADRB3 protein, human; D018341:Receptors, Adrenergic, alpha-2; D018342:Receptors, Adrenergic, beta-1; D022702:Receptors, Adrenergic, beta-3