The Use of Steroids As a Potentiator of Hypothermic Myocardial Preservation in Man.

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.