SOLUBLE COMPLEMENT RECEPTOR-TYPE-I LIMITS DAMAGE DURING REVASCULARIZATION OF ISCHEMIC MYOCARDIUM

Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic m yocardium. Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of card ioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble hu man complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no sol uble human complement receptor type I. Complement activation was measu red by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myo cardial tissue pH, wall motion scores (range, 4 = normal to -1 = dyski nesia), and infarct size (area of necrosis versus area at risk). Resul ts. After 180 minutes of reperfusion, hearts treated with soluble huma n complement receptor type I had significantly less complement activat ion than nontreated hearts (1.1% +/- 0.09% versus 7.8% +/- 0.04%, resp ectively; p < 0.002), less myocardial acidosis (-0.41 +/- 0.03 versus -0.72 +/- 0.03, respectively; p < 0.0001), higher wall motion scores ( 3.1 +/- 0.09 versus 1.67 +/- 0.16, respectively; p < 0.0001), and smal ler infarct size (24.6% +/- 2.0% versus 41% +/- 1.3%, respectively; p < 0.0001). Conclusions. Complement inhibition with soluble human compl ement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium. (C) 1998 by The Soci ety of Thoracic Surgeons.