title: Effect of intensive atorvastatin therapy on periprocedural PDCD4 expression in CD4+ T lymphocytes of patients with unstable angina undergoing percutaneous coronary intervention.
abstract: OBJECTIVE
  To investigate the effects of intensive atorvastatin therapy on programmed cell death 4 (PDCD4) expression by CD4+ T lymphocytes in patients with unstable angina who received percutaneous coronary intervention (PCI).
  
  
  METHODS
  Patients with unstable angina were randomized to pretreatment with either an intensive dose (80 mg/day, n = 33) or a conventional dose (20 mg/day, n = 33) of atorvastatin. Circulating CD4+ T cells were subsequently obtained prior to PCI, and also 18-24 h after PCI, using a magnetic cell sorting system. Fluorescence-based quantitative real-time PCR was then used to measure levels of PDCD4 mRNA in the isolated CD4+ T lymphocytes, and Western blot analysis was used to detect levels of PDCD4. Serum levels of interleukin (IL)-10 and TNF-α were quantified using enzyme-linked immunosorbent assays.
  
  
  RESULTS
  Of the 66 patients with unstable angina that were examined, levels of PDCD4 mRNA and protein were found to dramatically decrease in patients who received an intensive dose of atorvastatin following PCI (p < 0.05). In contrast, serum levels of TNF-α significantly increased following PCI in both the intensive dose group and the conventional dose group, with the latter being higher than the former (p < 0.05). Serum IL-10 levels also markedly increased following PCI for the two groups. However, higher values were associated with the intensive dose group (p < 0.05).
  
  
  CONCLUSIONS
  Intensive atorvastatin treatment reduced the post-PCI myocardial inflammatory response in patients with unstable angina, possibly by inhibiting PDCD4 expression in CD4+ T lymphocytes.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, PR China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Su
authors.forename: Lang
authors.initials: L
authors.lastname: Li
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.forename: You
authors.initials: Y
authors.lastname: Zhou
authors.forename: Jiangyou
authors.initials: J
authors.lastname: Wang
authors.forename: Yuhan
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000628:therapy*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D016753:Interleukin-10 / Q000378:metabolism; D008297:Male; D062645:Percutaneous Coronary Intervention; D011758:Pyrroles / Q000008:administration & dosage*; D012333:RNA, Messenger / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000378:metabolism*; D019210:Troponin I / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C114487:PDCD4 protein, human; D011758:Pyrroles; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002097:C-Reactive Protein; D000069059:Atorvastatin; D052279:Creatine Kinase, MB Form