Metabolic changes and myocardial injury during cardioplegia: A pilot study

Background. The timing, nature, and severity of both increased cardiac trop onin I (cTn-I) levels and myocardial injury during ischemic arrest with car dioplegia are unknown. To define them more accurately, we studied myocardia l metabolic activity and the release of markers of myocardial cell injury i nto the coronary sinus before, during, and after cardioplegia. Methods. We simultaneously measured creatine kinase, creatine kinase-MB, cT n-I, lactate, phosphate, and blood gases in coronary sinus and systemic art erial blood from 12 patients before cardiopulmonary bypass, after removal o f the aortic cross-clamp, and after discontinuation of cardiopulmonary bypa ss. We also measured coronary sinus flow and transmyocardial fluxes of all analytes and calculated myocardial oxygen consumption, myocardial carbon di oxide production, and myocardial energy expenditure. Results. Myocardial lactate release increased 10-fold after removal of the aortic cross-clamp (p = 0.012) and was accompanied by a surge in myocardial phosphate uptake (p = 0.056). These events were associated with only parti al cardioplegia-induced suppression of myocardial oxygen consumption (p = 0 .0047), myocardial carbon dioxide production (p = 0.0022), and myocardial e nergy expenditure (p = 0.0029). Simultaneously, coronary sinus cTn-I levels increased from a mean of 0.76 to 2.43 ng/mL after removal of the aortic cr oss-clamp, and 2.51 ng/mL after cardiopulmonary bypass (p = 0.014), leading to an increase in arterial cTn-I concentration from 0.18 to 0.98 and 3.01 ng/mL (p = 0.0002). Thus, cTn-I release across the myocardium was absent at baseline, became detectable (p = 0.012) after removal of the aortic cross- clamp, and correlated with cross-clamp and pump times. Similar changes occu rred with creatine kinase-MB. Conclusions. Metabolic myocardial stress occurs during ischemic arrest with cardioplegia and is associated with inadequate suppression of metabolism a nd with a surge in cTn-I and creatine kinase-MB release, which is maximal a fter removal of the aortic cross-clamp. These changes are likely to represe nt structural myocardial cell injury. (C) 2001 by The Society of Thoracic S urgeons.