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Ann Thorac Surg 1998;65:973-977
© 1998 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Boston Medical Center, Boston, Massachusetts, USA
b Boston University School of Medicine, Boston, Massachusetts, USA
Accepted for publication October 13, 1997.
Address reprint requests to Dr Lazar, Department of Cardiothoracic Surgery, Boston Medical Center, 88 E Newton St, Suite B404, Boston, MA 02118
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 myocardium.
Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to -1 = dyskinesia), and infarct size (area of necrosis versus area at risk).
Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively; 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 smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively; p < 0.0001).
Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.
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