INTRODUCTION. Since the introduction of cardioplegic arrest, major advances have been made in preservation of myocardial function during open heart surgery. Despite variation in composition of cardioplegia, myocardial protection has been based primarily on use of high-potassium cold cardioplegic solutions. Although these solutions originally were designed to protect adult hearts, they have been adopted for pediatric cardiac surgery, but available laboratory data has been inconclusive to explain vulnerability of immature myocardium to cardiac surgery. Most reports suggest that developing mammalian hearts are more resistant to damaging effects of cardiac insults than adult hearts. However perioperative myocardial damage with low cardiac output remains the most common cause of morbidity and death after repair of congenital lesions and pediatric patients continue to need mechanical assist devices, as well as prolonged inotropic support or an open chest despite a technically faultless repair. Additionally cardiac damage from inadequate myocardial protection can prolong hospital stay and result in delayed myocardial fibrosis, leading to cardiac dysfunction months to years later. Therefore preservation of myocardial function in immature hearts assumes even greater importance, because a perioperative insult is both less well tolerated and more difficult to treat. Many techniques of pediatric myocardial protection have been extrapolated from adult hearts, but due to the structural, functional and metabolic differences between immature and mature myocardium, this strategy lack of scientific rigor. Cardioplegia should be tailored to the immature heart in the context of differences in age, cyanotic status, and pressure/volume overload, because all these variables influence the susceptibility to ischemia-reperfusion injury (...).
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