title: Prolonged CRP Increase After Percutaneous Coronary Intervention Is Associated with High Thrombin Concentrations and Low Platelet' Response to Clopidogrel in Patients with Stable Angina.
abstract: BACKGROUND
  Inflammation is involved in all stages of development of atherosclerotic plaques. Currently, percutaneous coronary intervention (PCI) is a widely used method of treatment of coronary artery disease (CAD) when combined with optimal medical therapy (OMT). However, there is still controversy over invasive versus optimal pharmacological treatment in stable CAD (SCAD). Systemic inflammatory response triggered by PCI may limit its effectiveness in patients with SCAD.
  
  
  OBJECTIVE
  We aimed to evaluate plasma CRP and its relation to thrombin generation and platelet reactivity both early after the procedure and in a one-month observation following successful PCI with stent implantation, in patients with SCAD and OMT, including statins.
  
  
  METHODS
  We conducted a prospective study, in which CRP, platelet activation, thrombin generation and time course of prothrombin activation were determined at baseline, 3-5 days and 30 days after successful PCI with stent implantation, in 50 consecutive patients with SCAD, on chronic statin therapy.
  
  
  RESULTS
  Early after PCI CRP increased by 176% as compared with baseline (p < 0.001) and one-month after angioplasty CRP was still 54% higher than before the procedure (p = 0.002). In multivariate model prolonged increase in CRP 1 month after PCI was independently associated with P2Y12-reactivity index (PRI) (p = 0.04) and maximum concentration of thrombin (p = 0.003), both measured 30 days after the procedure.
  
  
  CONCLUSIONS
  Post-procedural CRP increase, which persists at least one month in patients with SCAD, after elective PCI with stent implantation, is one of the main finding of our study. We demonstrated the relationship between prolonged post-PCI inflammatory reaction, reflected by elevated CRP, and increased thrombin generation and low platelets' response to clopidogrel, which may account for limited benefits of PCI in stable coronary patients. It may be advisable to assay post-procedural CRP in each patient with SCAD, who underwent PCI to predict those, with potentially low response to clopidogrel.
authors.affiliation: Department of Coronary Disease and Heart Failure, John Paul II Hospital, Jagiellonian University Medical College, Kraków, Poland.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Mostowik
authors.affiliation: Department of Coronary Disease and Heart Failure, John Paul II Hospital, Kraków, Poland.
authors.forename: Aleksander
authors.initials: A
authors.lastname: Siniarski
authors.affiliation: Department of Coronary Disease and Heart Failure, John Paul II Hospital, Kraków, Poland.
authors.forename: Renata
authors.initials: R
authors.lastname: Gołębiowska-Wiatrak
authors.affiliation: Department of Coronary Disease and Heart Failure, Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Kraków, Poland.
authors.forename: Jadwiga
authors.initials: J
authors.lastname: Nessler
authors.affiliation: Department of Coronary Disease and Heart Failure, Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Kraków, Poland.
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Gajos
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism*; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D004351:Drug Resistance; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D018836:Inflammation Mediators / Q000097:blood*; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects* / Q000295:instrumentation; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D010979:Platelet Function Tests; D011446:Prospective Studies; D012307:Risk Factors; D015607:Stents; D013917:Thrombin / Q000378:metabolism*; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D010975:Platelet Aggregation Inhibitors; D002097:C-Reactive Protein; D000077144:Clopidogrel; D013917:Thrombin; D013988:Ticlopidine