title: Release of necrosis markers and cardiovascular magnetic resonance-derived microvascular perfusion in reperfused ST-elevation myocardial infarction.
abstract: BACKGROUND
  The association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown.
  
  
  METHODS
  We analyzed 163 patients with a first ST-elevation myocardial infarction and a patent infarct-related artery treated with thrombolysis (67%) or primary angioplasty (33%). Using first-pass perfusion CMR, abnormal perfusion was defined as a lack of contrast arrival into the infarct area in >1 segment. Troponin I, creatine kinase MB and myoglobin were measured upon arrival and at 6, 12, 24, 48 and 96 hours after reperfusion.
  
  
  RESULTS
  Abnormal perfusion was detected in 75 patients (46%) and was associated with a larger release of all 3 necrosis markers after reperfusion and higher peak values. This association was observed in the whole group and separately in patients treated with thrombolysis and primary angioplasty. Out of the 3 markers, troponin levels at 6 hours after reperfusion yielded the largest area under the receiver operating characteristic curve for prediction of abnormal perfusion (troponin: 0.69, creatine kinase MB: 0.65 and myoglobin: 0.58). In a comprehensive multivariate analysis, adjusted for clinical, angiographic, cardiovascular magnetic resonance parameters and all necrosis markers, high troponin levels at 6 hours after reperfusion (>median) independently predicted abnormal microvascular perfusion (OR 2.6 95%CI [1.2 - 5.5], p = .012).
  
  
  CONCLUSIONS
  In ST-elevation myocardial infarction, a larger release of cardiac necrosis markers soon after reperfusion therapy relates to abnormal perfusion. Troponin appears as the most reliable necrosis marker for an early detection of cardiovascular magnetic resonance-derived abnormal microvascular reperfusion.
authors.affiliation: Department of Cardiology, Hospital Clinico Universitario, Universidad de Valencia, Valencia, Spain. oliver.husser@gmail.com
authors.forename: Oliver
authors.initials: O
authors.lastname: Husser
authors.forename: Vicente
authors.initials: V
authors.lastname: Bodi
authors.forename: Juan
authors.initials: J
authors.lastname: Sanchis
authors.forename: Julio
authors.initials: J
authors.lastname: Nunez
authors.forename: Luis
authors.initials: L
authors.lastname: Mainar
authors.forename: Eva
authors.initials: E
authors.lastname: Rumiz
authors.forename: Maria P
authors.initials: MP
authors.lastname: Lopez-Lereu
authors.forename: Jose V
authors.initials: JV
authors.lastname: Monmeneu
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Forteza
authors.forename: Ricardo
authors.initials: R
authors.lastname: Oltra
authors.forename: Günter A J
authors.initials: GA
authors.lastname: Riegger
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Chorro
authors.forename: Angel
authors.initials: A
authors.lastname: Llacer
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography / Q000379:methods*; D052279:Creatine Kinase, MB Form / Q000097:blood; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D009206:Myocardium / Q000473:pathology; D009211:Myoglobin / Q000097:blood; D009336:Necrosis; D011379:Prognosis; D011446:Prospective Studies; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood
chemical_list: D015415:Biomarkers; D009211:Myoglobin; D014336:Troponin; D052279:Creatine Kinase, MB Form