title: The different mechanisms of periprocedural myocardial infarction and their impact on in-hospital outcome.
abstract: BACKGROUND
  CK-MB levels exceeding 3 times the upper limit of normal (ULN) following percutaneous coronary intervention (PCI), defining periprocedural myocardial infarction (PMI), are associated with worse outcomes. This study assessed the incidence and mechanisms of PMI and their impact on in-hospital stay.
  
  
  RESULTS
  Over a 12-year period (1996-2007), 272 cases of PMI (overall incidence, 3.5%) were analyzed among 310 consecutive cases of periprocedural myocardial necrosis (PMN; CK-MB > ULN). Mean numbers of treated segments and stents per procedure were 1.87 ± 0.99 and 1.43 ± 1.01, respectively. Mean stent length per procedure was 29.50 ± 19.30 mm. Following analysis of angiogram, procedural data, delay between PCI and necrosis, and mechanisms of PMN were classified as follows: cryptogenic (by exclusion, 41.5%), immediate failure, side-branch occlusion (14.0% each), stent thrombosis (10.6%), prolonged ischemia (9.2%), delayed failure (8.1%), post coronary artery bypass graft (1.5%), and non-target lesion related MI (1.1%). Significantly more stents were used in stent thrombosis, prolonged ischemia during PCI, and cryptogenic cases. In-hospital mortality was 8.1% for PMN and 8.8% for periprocedural MI, decreasing from non-target lesion related MI (25.0%) to mechanisms linked to stent thrombosis (20.7%), immediate failure (17.5%), delayed failure (7.7%), cryptogenic causes (6.1%), and prolonged ischemia (3.4%). Multivariate analysis confirms that in-hospital mortality is influenced by stent thrombosis, age, ejection fraction, and extent of coronary artery disease.
  
  
  CONCLUSIONS
  The precise mechanism of PMI was determined in about 60% of our series. Stent thrombosis and immediate failure had the poorest in-hospital outcomes.
authors.affiliation: Department of Cardiology, Université Catholique de Louvain, University Hospital of Mont-Godinne, Belgium, Av. Gaston Therasse, 15530 Yvoir, Belgium. xavier.muschart@uclouvain.be
authors.forename: Xavier
authors.initials: X
authors.lastname: Muschart
authors.forename: Alisson
authors.initials: A
authors.lastname: Slimani
authors.forename: Jacques
authors.initials: J
authors.lastname: Jamart
authors.forename: Patrick
authors.initials: P
authors.lastname: Chenu
authors.forename: Vincent
authors.initials: V
authors.lastname: Dangoisse
authors.forename: Laurence
authors.initials: L
authors.lastname: Gabriel
authors.forename: Antoine
authors.initials: A
authors.lastname: Guédès
authors.forename: Baudouin
authors.initials: B
authors.lastname: Marchandise
authors.forename: Erwin
authors.initials: E
authors.lastname: Schröder
mesh_terms: D000368:Aged; D054059:Coronary Occlusion / Q000150:complications; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology; D052279:Creatine Kinase, MB Form / Q000097:blood; D005260:Female; D017052:Hospital Mortality; D006801:Humans; D007297:Inpatients; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology* / Q000628:therapy*; D009336:Necrosis / Q000150:complications; D062645:Percutaneous Coronary Intervention; D011859:Radiography; D012189:Retrospective Studies; D015607:Stents / Q000009:adverse effects; D013927:Thrombosis / Q000150:complications; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D052279:Creatine Kinase, MB Form