title: Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention.
abstract: BACKGROUND
  C-reactive protein (CRP), a marker of inflammation, plays a role in the pathophysiology of atherosclerotic events. The relationship between CRP levels and myocardial necrosis assessed by troponin T (TnT) in patients undergoing percutaneous coronary intervention (PCI) has not been established. In addition, the long-term significance of TnT rise following PCI is not clear.
  
  
  OBJECTIVE
  To examine the relationship between CRP and the rise in TnT levels, and evaluate the long-term prognostic implications of TnT rise following PCI.
  
  
  METHODS
  A total of 1208 patients underwent successful nonemergent PCI. Baseline demographic characteristics, CRP and TnT levels were prospectively collected before and 12 h to 18 h following PCI. Long-term follow-up data over two years were available.
  
  
  RESULTS
  Among the patients studied (mean age 62 years), 64% presented with acute coronary syndrome. A PCI procedure was associated with a significant increase in TnT levels (higher than 0.1 microg/L) in 238 patients (20%). Multivariate logistic regression identified presentation with acute coronary syndrome or myocardial infarction, no statin use at the time of the procedure, increased CRP and increasing length of stent as independent predictors of TnT rise following PCI. Periprocedural TnT rise was not associated with adverse events in follow-up examinations (OR 1.09, 95% CI 0.73 to 1.65).
  
  
  CONCLUSIONS
  Myocardial necrosis commonly occurred in otherwise successful PCI and was particularly prevalent in the proinflammatory milieu of a recent myocardial infarction. This response was blunted with statin therapy. However, there was no long-term adverse sequelae of these troponin rises following otherwise uncomplicated PCI.
authors.affiliation: Department of Cardiovascular Sciences and Libin Cardiovascular Institute, University of Calgary, Calgary, Alberta.
authors.forename: Jaroslav
authors.initials: J
authors.lastname: Hubacek
authors.forename: Rashpal S
authors.initials: RS
authors.lastname: Basran
authors.forename: Fiona M
authors.initials: FM
authors.lastname: Shrive
authors.forename: Lana
authors.initials: L
authors.lastname: Shewchuk
authors.forename: David M
authors.initials: DM
authors.lastname: Goodhart
authors.forename: Todd J
authors.initials: TJ
authors.lastname: Anderson
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D016001:Confidence Intervals; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy*; D009206:Myocardium / Q000473:pathology*; D016017:Odds Ratio; D011379:Prognosis; D013997:Time Factors; D020107:Troponin T / Q000097:blood*
chemical_list: D000924:Anticholesteremic Agents; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D020107:Troponin T; D002097:C-Reactive Protein