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(Circulation. 2004;109:2337-2342.)
© 2004 American Heart Association, Inc.

Basic Science Reports

Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

Andreas Skyschally, PhD; Michael Haude, MD; Hilmar Dörge, MD; Matthias Thielmann, MD; Alexej Duschin, BSc; Anita van de Sand, BSc; Ina Konietzka, BSc; Astrid Büchert, BSc; Stephanie Aker, DMV; Parwis Massoudy, MD; Rainer Schulz, MD; Raimund Erbel, MD, FESC; Gerd Heusch, MD, FESC

From the Institut für Pathophysiologie (A.S., A.D., A.v.d.S., I.K., A.B., S.A., R.S., G.H.) und Abteilung für Kardiologie (M.H., R.E.), Zentrum für Innere Medizin, Klinik für Thorax- und Kardiovaskuläre Chirurgie (M.T., P.M.), Universitätsklinikum Essen, Essen; and the Klinik und Poliklinik für Thorax-, Herz-, und Gefäßchirurgie (H.D.), Georg-August-Universität, Göttingen, Germany.

Correspondence to Prof Dr med Dr hc Gerd Heusch, Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstraße 55, 45122 Essen, Federal Republic of Germany. E-mail gerd.heusch{at}uni-essen.de

Received January 18, 2002; de novo received December 2, 2003; revision received January 28, 2004; accepted February 2, 2004.

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.

Methods and Results— Microembolization was induced by injecting microspheres (42-µm 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.

Key Words: microcirculation • inflammation • ischemia • myocardial contraction

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