title: Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size.
abstract: BACKGROUND
  Ischemia/reperfusion injury worsens infarct size, a major determinant of morbidity and mortality after acute myocardial infarction (MI). We tested the hypothesis that reducing left ventricular wall stress with a percutaneous left atrial-to-femoral artery centrifugal bypass system while delaying coronary reperfusion limits myocardial injury in a model of acute MI.
  
  
  RESULTS
  MI was induced by balloon occlusion of the left anterior descending artery in adult male swine. In the MI group (n=4), 120 minutes of left anterior descending artery occlusion was followed by 120 minutes of reperfusion without mechanical support. In the mechanically supported group (MI+unload; n=4), percutaneous left atrial-to-femoral artery bypass was initiated after 120 minutes of ischemia, and left anterior descending artery occlusion was prolonged for an additional 30 minutes, followed by 120 minutes of reperfusion with device support. All animals were euthanized after reperfusion, and infarct size was quantified by triphenyltetrazolium chloride staining. Compared with baseline, mean left ventricular wall stress and stroke work were not changed at any point in the MI group but were decreased after reperfusion in the MI+unload group (mean left ventricular wall stress, 44 658 versus 22 963 dynes/cm(2); stroke work, 2823 versus 655 mm Hg·mL, MI versus MI+unload). Phosphorylation of reperfusion injury salvage kinase pathway proteins from noninfarcted left ventricular tissue was unchanged in the MI group but was increased in the MI+unload group. Compared with the MI group, total infarct size was reduced in the MI+unload group (49% versus 28%, MI versus MI+unload).
  
  
  CONCLUSIONS
  These data support that first unloading the left ventricle despite delaying coronary reperfusion during an acute MI reduces myocardial injury.
authors.affiliation: Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington St, Box 80, Boston, MA 02111, USA. Nkapur@tuftsmedicalcenter.org
authors.forename: Navin K
authors.initials: NK
authors.lastname: Kapur
authors.forename: Vikram
authors.initials: V
authors.lastname: Paruchuri
authors.forename: Jose Angel
authors.initials: JA
authors.lastname: Urbano-Morales
authors.forename: Emily E
authors.initials: EE
authors.lastname: Mackey
authors.forename: Gerard H
authors.initials: GH
authors.lastname: Daly
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Qiao
authors.forename: Natesa
authors.initials: N
authors.lastname: Pandian
authors.forename: George
authors.initials: G
authors.lastname: Perides
authors.forename: Richard H
authors.initials: RH
authors.lastname: Karas
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019560:Echocardiography, Three-Dimensional; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006353:Heart-Assist Devices; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D013314:Stress, Mechanical; D034421:Sus scrofa; D016277:Ventricular Function, Left / Q000502:physiology*
keywords: heart-assist devices; myocardial infarction; reperfusion injury