title: Glucocorticoid treatment prevents progressive myocardial dysfunction resulting from experimental coronary microembolization.
abstract: BACKGROUND
  The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction.
  
  
  RESULTS
  Microembolization was induced by injecting microspheres (42-microm diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n=7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n=7) or 30 minutes after (n=5) microembolization. In addition, chronically instrumented dogs received either placebo (n=4) or methylprednisolone (n=4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0+/-2.1% (mean+/-SEM) at baseline to 5.8+/-0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0+/-0.7% at 4 to 6 hours after microembolization back to baseline (19.1+/-1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction.
  
  
  CONCLUSIONS
  Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.
authors.affiliation: Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Essen, Federal Republic of Germany.
authors.forename: Andreas
authors.initials: A
authors.lastname: Skyschally
authors.forename: Michael
authors.initials: M
authors.lastname: Haude
authors.forename: Hilmar
authors.initials: H
authors.lastname: Dörge
authors.forename: Matthias
authors.initials: M
authors.lastname: Thielmann
authors.forename: Alexej
authors.initials: A
authors.lastname: Duschin
authors.forename: Anita
authors.initials: A
authors.lastname: van de Sand
authors.forename: Ina
authors.initials: I
authors.lastname: Konietzka
authors.forename: Astrid
authors.initials: A
authors.lastname: Büchert
authors.forename: Stephanie
authors.initials: S
authors.lastname: Aker
authors.forename: Parwis
authors.initials: P
authors.lastname: Massoudy
authors.forename: Rainer
authors.initials: R
authors.lastname: Schulz
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
authors.forename: Gerd
authors.initials: G
authors.lastname: Heusch
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D003326:Coronary Circulation; D003327:Coronary Disease / Q000188:drug therapy* / Q000209:etiology; D003331:Coronary Vessels; D004285:Dogs; D006334:Heart Function Tests; D006439:Hemodynamics; D007269:Injections, Intra-Arterial; D008775:Methylprednisolone / Q000627:therapeutic use*; D008863:Microspheres; D009200:Myocardial Contraction / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000209:etiology; D009205:Myocarditis / Q000188:drug therapy* / Q000209:etiology; D009206:Myocardium / Q000737:chemistry / Q000473:pathology; D011292:Premedication; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000893:Anti-Inflammatory Agents; D014409:Tumor Necrosis Factor-alpha; D008775:Methylprednisolone