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The use of steroids as a potentiator of hypothermic myocardial preservation in man

1979; Elsevier BV; Volume: 26; Issue: 6 Linguagem: Inglês

10.1016/0022-4804(79)90059-3

1095-8673

L Levinský, George Schimert, Thomas Z. Lajos, Arthur B. Lee, András L. Korényi-Both, Adrian O. Vladutiu, Mario Montes, John H. Siegel,

Anesthesia and Neurotoxicity Research

Profound hypothermic preservation (15–18°C) of the arrested myocardium offers the best protection against ischemic changes and potassium cardioplegia potentiates this preservation by allowing a more dynamic postbypass recovery, but at the cost of increased intra- and extracellular edema and mitochondrial injury. This study assesses the protective value of a steroid in the perfusion solution, methylprednisolone sodium succinate (1 g/liter), in the presence of profound hypothermic (myocardial T < 20°C) potassium (K = 26 meq/liter) cardioplegia. In a randomized prospective blinded study two groups (control A and steroid B) of 10 patients undergoing a minimum of three coronary bypass grafts were compared by clinical, cardiodynamic, electron microscopic biopsy, and mixed venous lactate and creatine phosphokinase (CK-MB) isoenzyme studies. The mean anoxic arrest time and number of grafts per patient were comparable. Although the CK-MB isoenzyme levels were lower in the postoperative period in the Solu-Medrol group, this was not statistically significant. The clinical course of the two groups was similar, however the control group of patients required a far greater degree and duration of inotropic support to attain comparable recovery trajectories to the Solumedrol group of patients. Critical ultrastructural differences in the steroid-treated group were better mitochondrial preservation, increased perimitochondrial glycogen stores, and a reduction in intracellular edema. These results suggest that steroids may enhance stabilization of cellular metabolic processes under conditions of hypothermic potassium cardioplegia.