title: Reduction of "no-reflow" phenomenon by intra-aortic balloon counterpulsation in a randomized magnetic resonance imaging experimental study.
abstract: OBJECTIVE
  Intra-aortic balloon counterpulsation (IABC) can improve post-myocardial infarction (MI) outcomes, but the mechanisms of such effect remain unclear. We hypothesized that IABC augmentation reduces the extent of microvascular obstruction after acute infarction.
  
  
  BACKGROUND
  Microvascular obstruction or "no-reflow" (MO) has been shown to negatively influence left ventricular (LV) remodeling after myocardial infarction (MI).
  
  
  METHODS
  Seventeen dogs underwent 90 min of coronary artery occlusion followed by reperfusion. Animals were then randomized to either IABC (n = 9) or control (n = 8); IABC augmentation was performed for 24 h after MI. Microvascular obstruction and infarct size by first-pass and delayed contrast-enhanced magnetic resonance imaging (MRI) were measured at 1 and 24 h after reperfusion and compared with postmortem infarct size and MO by microspheres.
  
  
  RESULTS
  Microvascular obstruction by MRI, expressed as percent LV mass, decreased significantly in IABC (4.9 +/- 2.2% to 3.6 +/- 1.5%) and increased in controls (3.4 +/- 0.5% to 4.9 +/- 1.1% from 1 to 24 h, respectively; p < 0.001). Similar results were found for MO defined by microspheres. In the control group, MO increased significantly, during 24 h of study (from 8.8 +/- 1.7% to 43.2 +/- 11.1% of infarcted myocardium; p < 0.05), whereas not important change was observed in the IABC group (from 21.3 +/- 7.1% to 25.8 +/- 14.7%; p < 0.05 vs. control at 24 h). Infarct size, measured by MRI, increased in both groups (13.2 +/- 1.8 to 15.5 +/- 2.1 from 1 to 24 h, respectively; p < 0.05).
  
  
  CONCLUSIONS
  Intra-aortic balloon counterpulsation augmentation performed after reperfusion improves myocardial perfusion at the tissue level, and reduces the extent of no-reflow caused by microvascular obstruction.
authors.affiliation: Department of Medicine, Division of Cardiology, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21287-6568, USA.
authors.forename: Luciano C
authors.initials: LC
authors.lastname: Amado
authors.forename: Dara L
authors.initials: DL
authors.lastname: Kraitchman
authors.forename: Bernhard L
authors.initials: BL
authors.lastname: Gerber
authors.forename: Ernesto
authors.initials: E
authors.lastname: Castillo
authors.forename: Raymond C
authors.initials: RC
authors.lastname: Boston
authors.forename: Joseph
authors.initials: J
authors.lastname: Grayzel
authors.forename: João A C
authors.initials: JA
authors.lastname: Lima
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004396:Coloring Agents; D003326:Coronary Circulation / Q000502:physiology*; D015908:Counterpulsation; D004195:Disease Models, Animal; D004285:Dogs; D007423:Intra-Aortic Balloon Pumping; D008279:Magnetic Resonance Imaging; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery; D015425:Myocardial Reperfusion; D011859:Radiography; D013778:Tetrazolium Salts; D016896:Treatment Outcome
chemical_list: D004396:Coloring Agents; D013778:Tetrazolium Salts; C009591:triphenyltetrazolium