POSTPERICARDIOTOMY-SYNDROME IN PEDIATRIC HEART-TRANSPLANT RECIPIENTS - IMMUNOLOGICAL CHARACTERISTICS

Clinical features of postpericardiotomy syndrome (PPS) occur in pediat ric heart transplant recipients despite immunosuppression, which raise s questions about the mechanism of PPS. We studied the clinical and im munologic characteristics of 75 pediatric heart transplant patients, a ges 1.1 to 17.8 years (mean, 7.5 years); 7 had clinical evidence of PP S (PPS+), and 8 were without clinical features of PPS (PPS-). indicato rs of PPS included fever irritability, pericardial friction rub, leuko cytosis without other cause, and pericardial effusion. The onset of PP S was from 9 to 26 postoperative days (mean, 16 days). Immunosuppressi ve regimens were comparable up to the day of PPS diagnosis in PPS+ pat ients, and up to day 16 in PPS- patients (average onset of PPS in PPS patients). No differences were found between groups with respect to w eight-adjusted dosages of cyclosporin A, azathioprine, or corticostero ids. Mean cyclosporin A levels in PPS+ and PPS- patients were 142 +/- 88 ng/mL (mean +/- standard deviation) and 265 +/- 122 ng/mL (p=0.045) , respectively. Echocardiographic data on 3 PPS+ patients within 7 day of PPS diagnosis revealed pericardial effusions ranging from 5 to 24 mm. No data were available on the remaining 4 PPS+ patients. Minimal p ericardial effusions (<10 mml were seen in 4 PPS- patients during a co mparable time period. One PPS- patient required pericardiocentesis. En domyocardial biopsy rejection grade did not diifer between groups. Mea n pretransplant soluble interleukin-2 receptor levels did not differ b etween PPS+ and PPS- patients (758 +/- 410 vs 653 +/- 270 IU/mL); nor did the PPS+ pretransplant levels differ from levels obtained 1 or 2 m onths postoperatively (700 +/- 437 and 751 +/- 367 IU/mL, respectively ). Although pretransplant percentages of the standard T-cell (CD2, CD3 , CD4, CD8) and B-cell (DR and CD19) markers differed from posttranspl ant values, the changes could be explained by the immunosuppressive re gimen and did not differ between PPS+ and PPS- patients. In the PPS+ p atients, however, there were significant increases in the proportion o f activated helper T cells (CD4(+)/25(+)) and cytotoxic T cells (Leu-7 (+)/CD8(+)) following heart transplantation in comparison with pretran splant levels. We speculate that these changes in activation markers i n PPS+ patients suggest a possible role for cell-mediated immunity in the pathogenesis of PPS in this group of patients.