Abstract

ObjectivesWe conducted a prospective randomized controlled trial to compare del Nido (DN) and histidine-tryptophan-ketoglutarate (HTK) cardioplegia solution in pediatric patients undergoing intracardiac tetralogy of Fallot repair. MethodsOne hundred consecutive patients 12 years of age or younger, undergoing intracardiac repair of tetralogy of Fallot were randomized into DN (n = 50) and HTK (n = 50) groups. Cardioplegia strategy consisted of a single dose of DN (20 mL/kg) or HTK (6 mL/kg/min for 6 minutes). Primary outcome was cardiac index (CI). Secondary outcomes were ventricular arrhythmias post cross-clamp release, time to peripheral rewarming, duration of mechanical ventilation, inotropic score, intensive care unit and hospital stay, and serum levels of troponin-I, interleukin-6, and tumor necrosis factor-α. Ultrastructural changes in the myocardium were assessed. ResultsCI was significantly higher in the DN group compared with the HTK group at 6 (P = .005) and 24 hours (P < .001) after surgery. It was on an average 0.44 L/min/m2 higher in the DN group at any time point (P = .004). Time for complete cessation of electrical activity was longer in the HTK group (P = .01) and more patients in the HTK group had ventricular arrhythmias post cross-clamp release (P = .03). Duration of mechanical ventilation (P = .006), intensive care unit stay (P = .05), and hospital stay (P < .001) were lower in the DN group. Patients in the DN group had lower troponin I levels 24 hours after cardiopulmonary bypass (P < .001). Electron microscopic studies showed more myocardial edema (P = .02) and myofibrillar disarray (P = .04) in the HTK group along with lower glycogen stores (P = .04). DN cardioplegia was more cost-effective than HTK cardioplegia (P < .001). ConclusionsDN cardioplegia was associated with better preservation of CI, less duration of mechanical ventilation, shorter intensive care unit and hospital stays, lower inotropic scores, and less release of troponin-I. Electron microscopy showed less myocardial edema and better preservation of the myofibrillar architecture and glycogen stores in the DN group.

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