title: Detection of acutely impaired microvascular reperfusion after infarct angioplasty with magnetic resonance imaging.
abstract: BACKGROUND
  Despite the reopening of the infarct-related artery (IRA) with infarct angioplasty, complete microvascular reperfusion does not always ensue.
  
  
  RESULTS
  We performed cardiovascular MRI (CMR) in 20 acute myocardial infarction (AMI) patients within 24 hours of successful infarct angioplasty and 10 control patients without obstructive coronary artery disease on a clinical 1.5-T CMR scanner. Three-month follow-up CMR in AMI patients evaluated the impact of abnormal reperfusion on recovery of function. Infarction was localized by delayed contrast hyperenhancement and impaired systolic thickening. Microvascular perfusion was assessed at rest by first-pass perfusion CMR after a bolus of gadolinium-DTPA by use of the time to 50% maximum myocardial enhancement. Whereas contrast wash-in was homogeneous in control patients, AMI patients exhibited delays in the hypokinetic region subtended by the IRA compared with remote segments in 19 of 20 patients, with a mean contrast delay of 0.9+/-0.1 seconds (95% CI, 0.6 to 1.2 seconds). At follow-up, the mean recovery of systolic thickening was lower in segments with a contrast delay of 2 seconds or more (10+/-7% versus 39+/-4%, P<0.001). A contrast delay > or =2 seconds and infarction >75% transmurally were independent predictors of impaired left ventricular systolic thickening at 3 months (P=0.002 for severe contrast delay, P=0.048 for >75% for transmural infarction).
  
  
  CONCLUSIONS
  CMR detects impaired microvascular reperfusion in AMI patients despite successful infarct angioplasty, which when severe is associated with a lack of recovery of wall motion.
authors.affiliation: Alfred and Baker Heart Research Institute, Heart Centre, Alfred Hospital, Melbourne, Australia. andrew.taylor@baker.edu.au
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Taylor
authors.forename: Nidal
authors.initials: N
authors.lastname: Al-Saadi
authors.forename: Hassan
authors.initials: H
authors.lastname: Abdel-Aty
authors.forename: Jeanette
authors.initials: J
authors.lastname: Schulz-Menger
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Messroghli
authors.forename: Matthias G
authors.initials: MG
authors.lastname: Friedrich
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D000077144:Clopidogrel; D003131:Combined Modality Therapy; D003326:Coronary Circulation; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D008279:Magnetic Resonance Imaging; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000628:therapy*; D015425:Myocardial Reperfusion; D011446:Prospective Studies; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000077466:Tirofiban; D016896:Treatment Outcome; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016277:Ventricular Function, Left
chemical_list: D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D007140:Immunoglobulin Fab Fragments; D014443:Tyrosine; D006493:Heparin; D000077144:Clopidogrel; D000077466:Tirofiban; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab