title: Preprocedural statin therapy, inflammation, and myocardial injury in low-risk stable coronary artery disease patients submitted to coronary stent implantation.
abstract: OBJECTIVE
  Evaluate if statin therapy prior to elective coronary stent implantation (CSI) reduces the plasma levels of markers of inflammation and of myocardial necrosis in low-risk stable coronary artery disease patients (CAD).
  
  
  BACKGROUND
  The elevation of markers of inflammation and of myocardial necrosis after percutaneous coronary intervention may interfere with clinical outcome. Among acute coronary syndrome patients, statins improve clinical outcomes when used before CSI-mostly due to reduction of CSI-related myocardial infarction. However, little is known concerning preprocedural statin therapy on the reduction of these markers in stable patients at low-risk.
  
  
  METHODS
  In this prospective, observational study, 100 patients (n = 50 on statin therapy vs. n = 50 not on statin) with stable coronary artery disease underwent elective CSI. Inflammatory (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor-α and matrix metalloproteinase-9) and myocardial necrosis markers (troponin I and CK-MB) were determined before and 24 hr after CSI.
  
  
  RESULTS
  All patients presented a significant increase of CRP and IL-6 after CSI. However, this increase was attenuated in patients on statin therapy prior to CSI than those without statin therapy: 75% vs. 150% (P < 0.001) and 192% vs. 300% (P < 0.01). The other pro-inflammatory markers were similar for both sets of patients. Troponin I and CK-MB did not change after CSI regardless of previous statin therapy or not.
  
  
  CONCLUSIONS
  Pretreatment with statin attenuates procedural inflammation, denoted by markedly lower increases of CRP and IL-6 levels, in elective CSI within low-risk stable CAD patients. Periprocedural myocardial injury was irrelevant and was not affected by preprocedural statin therapy in this population.
authors.affiliation: Acute Coronary Care Division, Cardiovascular Disease Institute of São José do Rio Preto.
authors.forename: Gilmar V
authors.initials: GV
authors.lastname: Greque
authors.affiliation: Acute Coronary Care Division Heart Institute (InCor), Medical School, University of São Paulo.
authors.forename: Carlos V
authors.initials: CV
authors.lastname: Serrano
authors.affiliation: Laboratory Clinic Analysis Division Heart Institute (InCor), Medical School, University of São Paulo.
authors.forename: Célia M
authors.initials: CM
authors.lastname: Strunz
authors.affiliation: Acute Coronary Care Division Heart Institute (InCor), Medical School, University of São Paulo.
authors.forename: Alexandre
authors.initials: A
authors.lastname: Soeiro
authors.affiliation: Laboratory of Hemodynamics Division of the Base Hospital Sao Jose of Preto, Medical School, University of Sao Jose do Rio Preto.
authors.forename: Márcio
authors.initials: M
authors.lastname: Santos
authors.affiliation: Laboratory of Hemodynamics Division of the Base Hospital Sao Jose of Preto, Medical School, University of Sao Jose do Rio Preto.
authors.forename: Flávio
authors.initials: F
authors.lastname: Pivateli
authors.affiliation: Laboratory of Hemodynamics Division, Cardiovascular Disease Institute of São José do Rio Preto.
authors.forename: José Luis B
authors.initials: JL
authors.lastname: Jacob
authors.affiliation: Cardiology Department Division of Albert Einstein Hospital, Sao Paulo, Brazil.
authors.forename: Antonio Eduardo P
authors.initials: AE
authors.lastname: Pesaro
authors.affiliation: Acute Coronary Care Division Heart Institute (InCor), Medical School, University of São Paulo.
authors.forename: José Carlos
authors.initials: JC
authors.lastname: Nicolau
authors.affiliation: Acute Coronary Care Division Heart Institute (InCor), Medical School, University of São Paulo.
authors.forename: Roberto
authors.initials: R
authors.lastname: Kalil-Filho
mesh_terms: D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000628:therapy*; D052279:Creatine Kinase, MB Form / Q000097:blood; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009336:Necrosis; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000295:instrumentation*; D011446:Prospective Studies; D012307:Risk Factors; D015607:Stents; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D019210:Troponin I; D002097:C-Reactive Protein; D052279:Creatine Kinase, MB Form
keywords: coronary stent implantation; inflammatory markers; myocardial damage; stable coronary artery disease; statin