Aprotinin Decreases Ischemic Damage During Coronary Revascularization

Background and Aim: This study sought to determine whether the favorable anti‐inflammatory effects of aprotinin might limit ischemic damage during the revascularization of ischemic myocardium. Methods: Twenty pigs underwent 90 minutes of coronary occlusion followed by 45 minutes of blood cardioplegi...

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Published inJournal of cardiac surgery Vol. 20; no. 6; pp. 519 - 523
Main Authors Lazar, Harold L., Bao, Yusheng, Tanzillo, Leslie, O'Gara, Paul, Reardon, Deborah, Price, David, Crowley, Richard, Cabral, Howard J.
Format Journal Article
LanguageEnglish
Published 350 Main Street , Malden , MA 02148-5020 , USA and 9600 Garsington Road , Oxford OX4 2XG , England Blackwell Science Inc 01.11.2005
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Summary:Background and Aim: This study sought to determine whether the favorable anti‐inflammatory effects of aprotinin might limit ischemic damage during the revascularization of ischemic myocardium. Methods: Twenty pigs underwent 90 minutes of coronary occlusion followed by 45 minutes of blood cardioplegic arrest and 180 minutes of reperfusion. Ten animals received a loading dose of aprotinin (40,000 kallikrein inhibiting units/kg) during the start of coronary occlusion followed by an infusion of 20,000 kallikrein inhibiting units/kg/hour. Ten other animals received no aprotinin. Summary statistics are expressed as the mean ± standard error. Results: The aprotinin‐treated animals required less cardioversions for ventricular arrhythmias (1.0 ± 0.7 vs. 3.6 ± 0.6; p < 0.001), accumulated less lung water (1.0 ± 0.2% change vs. 6.2 ± 0.9% change; p = 0.038), had more complete coronary relaxation to bradykinin (34.1 ± 5.9% change vs. 9.2 ± 3.5% change; p = 0.01), and had reduced infarct size (area necrosis/area risk = 20 ± 1.1% vs. 39 ± 1.2%; p = 0.003). Conclusions: Aprotinin limits ischemic injury during acute coronary revascularization by decreasing ventricular arrhythmias and lung edema, preserving endothelial function, and minimizing myocardial necrosis.
Bibliography:ark:/67375/WNG-3P15T169-W
ArticleID:JOCS136
istex:960BF5E459C8C9C51677348526F927067D383568
This work was presented at the 84th Annual Meeting of the American Association for Thoracic Surgery, April 25‐28, 2004, Toronto, Ontario, Canada.
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SourceType-Scholarly Journals-1
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ISSN:0886-0440
1540-8191
DOI:10.1111/j.1540-8191.2005.00136.x