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 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.