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Objectives: The aim of this study was to retrospectively evaluate the sensitivity of noninvasive surveillance (physical examination, echocardiography) of rejection in accurately predicting histologically documented rejection episodes. Additionally, the usefulness of routine scheduled biopsy and its safety in pediatric patients was explored., Background: Endomyocardial biopsy has been utilized as the standard for rejection surveillance after heart transplantation in adults, but its role in documenting clinically suspected rejection and in routine surveillance of pediatric patients has not been agreed upon., Methods: Heart transplantation was performed in 14 neonates and 21 children. The immunosuppressive regimen consisted of cyclosporine, azathioprine and prednisone. All patients underwent routine noninvasive rejection surveillance that included clinical examination and echocardiography. In the neonates, biopsy was performed quarterly beginning 6 months after transplantation, after cessation of prednisone therapy. In the children, biopsy was performed 15 times in the 1st year. A minimum of five biopsy samples were interpreted using the Working Formulation for Heart Transplant Rejection., Results: In the neonates, 37 biopsies were performed. Evidence of rejection was present in only three biopsy samples obtained during eight episodes (38%) of clinically suspected rejection. In 29 biopsies performed when rejection was not clinically suspected, each biopsy was free of cellular infiltrate. In the children, 291 biopsies were performed. Evidence of rejection was present in only seven biopsies (41%) from 17 episodes of clinically suspected rejection. Cellular rejection was discovered during routine rejection surveillance biopsies in asymptomatic patients in 23 (8.4%) of 274 biopsies., Conclusions: In neonates with clinically suspected rejection, endomyocardial biopsy identified which patients did not require rejection therapy. Endomyocardial biopsy surveillance did not detect any unsuspected cases of rejection. In children, noninvasive rejection surveillance was less reliable even in asymptomatic patients, suggesting that periodic endomyocardial biopsy should be utilized.

Quinidine syncope and factors associated with it are well known among adult patients treated for cardiac arrhythmias. To define factors that may influence the occurrence of syncope in children taking quinidine, the clinical, anatomic, electrocardiographic, roentgenographic and pharmacologic data were compared in six patients with syncope (Group A) and 22 patients without syncope (Group B). There was a significant (chi-square = 10.2, p = 0.001) relation between heart disease and quinidine syncope: all six Group A (syncopal) patients had heart disease whereas 15 of the 22 Group B (non-syncopal) patients had no structural heart disease. In contrast, no significant difference was noted between Group A and Group B patients in mean age (11.4 versus 11.4 years), mean quinidine serum concentration (2.9 versus 2.3 micrograms/ml), mean corrected QT interval before quinidine (0.43 versus 0.40 second) or mean corrected QT interval during quinidine therapy (0.46 versus 0.46 second) or between those taking digitalis and those not. Two of the six Group A (syncopal) patients died during therapy, one 6 days after initiating therapy and one suddenly at home 6 months after beginning quinidine. Another two of the six Group A patients exhibited hypokalemia (both 2.9 mEq/liter) at the time of syncope, 2 weeks and 6 months, respectively, after initiation of quinidine therapy; both survived. Syncope occurred within 8 days of initiation of quinidine therapy in three of the six patients. Sustained ventricular tachycardia was observed during quinidine associated arrhythmia in three of six patients with syncope; nonsustained ventricular tachycardia or complex ventricular ectopic activity while on this therapy was observed before syncope in the other three patients in Group A.(ABSTRACT TRUNCATED AT 250 WORDS)