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Ann Thorac Surg 2000;69:1914-1919
© 2000 The Society of Thoracic Surgeons
a Course of Interventional Medicine (E1), Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan
Address reprint requests to Dr Sawa, Course of Interventional Medicine (E1), Department of Surgery, Osaka University Graduate School of Medicine, 2–2 Yamada-oka, Suita, Osaka 565–0871, Japan
e-mail: sawa{at}surg1.med.osaka-u.ac.jp
Background. Blood cardioplegia (BCP) is widely used for myocardial protection during open heart operation. However, BCP may have a chance to induce neutrophil-mediated myocardial injury during aortic cross-clamping. We clinically evaluated the myocardial protective effect of leukocyte-depleted blood cardioplegia (LDBCP) for initial and intermittent BCP administration in pediatric patients.
Methods. Fifty patients undergoing open heart operation for congenital heart disease between January 1997 and March 1999 were reviewed. Twenty-five were administered LDBCP for myocardial protection during ischemic periods (LDBCP group), and the remaining 25 were given BCP without leukocyte depletion (BCP group).
Results. The difference in plasma concentrations of malondialdehyde between coronary sinus effluent blood and arterial blood just after reperfusion in the LDBCP group (1.68 ± 0.56 µmol/L) was significantly lower than that in the BCP group (2.35 ± 0.62 µmol/L; p < 0.01). The LDBCP group showed significantly lower plasma concentrations of human heart fatty acid-binding protein at 50 minutes after reperfusion (LDBCP group, 103.5 ± 38.7 IU/L; BCP group, 144.8 ± 48.8 IU/L; p < 0.01) and the peak value of creatine kinase-MB during the first 24 postoperative hours (LDBCP group, 17.0 ± 8.5 IU/L; BCP group, 26.0 ± 11.6 IU/L; p < 0.01) than did the BCP group. The maximum dose of catecholamine was significantly smaller in the LDBCP group (LDBCP group, 3.20 ± 2.18 µg · kg-1 · min-1; BCP group, 5.60 ± 2.83 µg · kg-1· min-1; p < 0.01).
Conclusions. These results suggest the usefulness of LDBCP for protection from the myocardial injury that can be induced by BCP administration during aortic cross-clamping.
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