title: Elevated levels of interleukin-1beta-converting enzyme and caspase-cleaved cytokeratin-18 in acute myocardial infarction.
abstract: BACKGROUND
  Systemic inflammation and apoptosis-specific immune activation play a major role in acute coronary syndromes (ACS) including acute myocardial infarction (AMI). The role of systemic and coronary obtained inflammatory plasma protein interleukin-1beta precursor (IL-1betap), IL-1beta-converting enzyme (ICE) and the apoptosis-specific caspase-cleaved cytokeratin-18 (ccCK-18) are not known in ACS.
  
  
  METHODS
  Plasma samples were obtained from stable angina (SA, n = 34), unstable angina (UA, n = 37) and patients with AMI (n = 39). Coronary blood was acquired by means of thrombectomy devices (X-sizer) in AMI patients. IL-1betap, ICE and ccCK-18 were determined by enzyme-linked immunosorbent assay (ELISA). Group comparisons were evaluated by parametric Tukey test. Multivariate logistic regression analysis was performed to determine predictive values of IL-1betap, ICE and ccCK-18 as compared to creatine kinase (CK) and troponin T (TnT) in order to relate these markers with the occurrence of myocardial damage.
  
  
  RESULTS
  IL-1betap, ICE and ccCK-18 were identified to be significantly altered in the peripheral blood of patients suffering from AMI as compared to SA and UA. ROC curves were plotted and revealed that ccCK-18 is a novel sensitive marker for the detection of myocardial damage as compared to TnT or CK. (AUC ccCK-18 0.925, TnT AUC 0.62 and CK AUC 0.858.) Moreover, ICE and ccCK-18 were significantly increased at the site of coronary occlusion as compared to peripheral blood samples in AMI patients (both P < 0.001).
  
  
  CONCLUSIONS
  Our data suggest that ACS is related to increased concentration of systemic soluble ICE and ccCK-18. Moreover, soluble ccCK-18 was identified to be a superior marker as compared to TnT or CK, for detection of myocardial damage.
authors.affiliation: Medical University of Vienna, Vienna, Austria.
authors.forename: C
authors.initials: C
authors.lastname: Adlbrecht
authors.forename: K
authors.initials: K
authors.lastname: Hoetzenecker
authors.forename: M
authors.initials: M
authors.lastname: Posch
authors.forename: S
authors.initials: S
authors.lastname: Steiner
authors.forename: C
authors.initials: C
authors.lastname: Kopp
authors.forename: S
authors.initials: S
authors.lastname: Hacker
authors.forename: J
authors.initials: J
authors.lastname: Auer
authors.forename: R
authors.initials: R
authors.lastname: Horvath
authors.forename: B
authors.initials: B
authors.lastname: Moser
authors.forename: G
authors.initials: G
authors.lastname: Roth
authors.forename: E
authors.initials: E
authors.lastname: Wolner
authors.forename: I M
authors.initials: IM
authors.lastname: Lang
authors.forename: H J
authors.initials: HJ
authors.lastname: Ankersmit
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood*; D020170:Caspase 1 / Q000097:blood*; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D006801:Humans; D053538:Keratin-18 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis*; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D053538:Keratin-18; D020107:Troponin T; D003402:Creatine Kinase; D020170:Caspase 1