Myocardium utilizes more oxygen and glucose during tepid blood cardioplegic infusion in arrested heart

Abstract

The aims of this study were to evaluate myocardial metabolic activity during tepid blood cardioplegic infusion in the arrested heart in comparision with cold blood cardioplegia and to assess the early clinical outcomes of these patients. Thirty patients undergoing first elective coronary artery bypass grafting surgery were included and randomized to two groups (T for tepid and C for cold), 15 patients in each. Myocardial protection was similar in both groups except for the reinfusion of blood cardioplegia, which was 6°C in group C and 28°C in group T (same temperature as the body perfusion). The route of cardioplegic reinfusion was antegrade during the first reinfusion and retrograde during the second reinfusion. In order to assess myocardial metabolic activity, myocardial oxygen consumption (MVO2), myocardial glucose uptake, and myocardial lactate and acid production were all calculated. Arterial and coronary venous blood samples were obtained from the aortic root cannula and coronary sinus. During cardioplegic reinfusions in the ischemic period, the calculated values of myocardial oxygen extraction, oxygen consumption, and glucose uptake were higher in group T than in group C (P < 0.05). This difference was observed during both antegrade and retrograde delivery of cardioplegic solution. Myocardial lactate production was greater in group C than in group T during cardioplegic reinfusion, both antegradely and retrogradely (P < 0.05). In all patients, cardiopulmonary bypass was terminated in the first attempt. The clinical outcome was similar in both groups. The results of this study indicate that globally ischemic myocardium is able to utilize more oxygen and glucose during cardioplegic reinfusions at a tepid temperature in comparison to cold. In addition, the data showed evidence of less myocardial injury and better left ventricular function throughout the critical period of recovery from global ischemia for the heart protected by tepid cardioplegia. Copyright © 2005 by the International Heart Journal Association.