Abstract
Dextro-transposition of the great arteries is a critical cyanotic congenital heart defect in which neonatal survival depends on effective intercirculatory mixing. Balloon atrial septostomy (BAS) improves atrial-level mixing; however, many infants remain dependent on prostaglandin E1 (PGE1) following the procedure, reflecting a disconnect between successful anatomical intervention and physiological adaptation. This review synthesizes the underlying physiology, available clinical evidence, and practical considerations for PGE1 management following BAS. Available data indicate that postprocedural systemic oxygen saturation and restrictive atrial or ventricular physiology are the strongest predictors of ongoing PGE1 requirement. Early discontinuation, often prompted by procedural success, is often associated with rebound hypoxemia, suggesting that physiological stabilization may lag anatomical intervention. The continuation of PGE1 appears safe and serves as supportive management during the transitional cardiopulmonary period rather than as a marker of procedural failure or a determinant of surgical timing. A physiology-guided, individualized approach to PGE1 discontinuation is therefore recommended. Prospective multicenter studies are needed to refine clinical criteria and optimize preoperative stabilization and outcomes.
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