title: Relationship of creatine kinase-myocardial band release to Thrombolysis in Myocardial Infarction perfusion grade after intracoronary stent placement: an ESPRIT substudy.
abstract: BACKGROUND
  The etiology of creatine kinase-myocardial band (CK-MB) release after percutaneous coronary intervention (PCI) remains unclear. The goal of this study was to evaluate the relationship of both epicardial and tissue level perfusion at the completion of stent placement to CK-MB release after the procedure. Given the high rates of Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow after PCI, we hypothesized that abnormalities in tissue level perfusion would instead explain CK-MB release.
  
  
  METHODS
  Data were drawn from the angiographic substudy of the Enhanced Suppression of the Platelet IIb/IIIa Receptor With Integrilin Therapy (ESPRIT) trial of eptifibatide versus placebo in patients undergoing planned coronary stent implantation. In the substudy, cinefilms of 65 patients were analyzed by an angiographic core laboratory blinded to enzymatic and clinical outcomes.
  
  
  RESULTS
  The release of CK-MB was not associated with TIMI grade 3 flow or the corrected TIMI frame count; 100% of patients had TIMI grade 3 flow at the completion of PCI. In contrast, tissue level perfusion using the TIMI myocardial perfusion grade (TMPG) was related to postintervention CK-MB release: patients with a closed myocardium (TMPG 0/1) or delayed myocardial perfusion (TMPG 2) had an average CK-MB release 2.2 +/- 2.7 times the upper limit of normal (n = 34), whereas those patients with normal myocardial perfusion (TMPG 3, n = 24) had CK-MB 0.8 +/- 0.6 times the upper limit of normal (P =.01). Although no patients with TMPG 3 sustained death/myocardial infarction/urgent target vessel revascularization or thrombotic bailout, 17.7% of patients with TMPG 0/1/2 did by 48 hours (P =.037).
  
  
  CONCLUSIONS
  Impaired tissue level perfusion as assessed by the TMPG and not epicardial coronary blood flow is associated with CK-MB elevation after PCI. These data provide a pathophysiologic link between impaired tissue level perfusion, post-PCI infarction, and adverse clinical outcomes.
authors.affiliation: Harvard Clinical Research Institute, 900 Commonwealth Ave, 2nd Floor, Boston, MA 02215, USA. mgibson@perfuse.org
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gibson
authors.forename: Sabina A
authors.initials: SA
authors.lastname: Murphy
authors.forename: Susan J
authors.initials: SJ
authors.lastname: Marble
authors.forename: David J
authors.initials: DJ
authors.lastname: Cohen
authors.forename: Eric A
authors.initials: EA
authors.lastname: Cohen
authors.forename: Henry K
authors.initials: HK
authors.lastname: Lui
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Young
authors.forename: Michael M
authors.initials: MM
authors.lastname: Kitt
authors.forename: Todd J
authors.initials: TJ
authors.lastname: Lorenz
authors.forename: James E
authors.initials: JE
authors.lastname: Tcheng
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000097:blood / Q000378:metabolism*; D052279:Creatine Kinase, MB Form; D004311:Double-Blind Method; D000077542:Eptifibatide; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000201:enzymology* / Q000628:therapy; D015425:Myocardial Reperfusion; D010455:Peptides / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D015607:Stents
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D000077542:Eptifibatide