Several markers including erythrocyte survival, reticulocyte count, schistocyte count, as well as serum levels of hemoglobin, indirect bilirubin, LDH, and haptoglobin have been applied to estimating the severity of intravascular hemolysis.3–7,21–28 Among these markers, serum LDH has been widely used to estimate the severity of intravascular hemolysis in patients with cardiac valve prostheses, because close relation between serum LDH and half-life of 51Cr-labeled erythrocyte was demonstrated in patients with ball-valve prosthesis and valvular disease.,7,22 However, serum LDH is interfered with by other pathologic or artificial processes, including the release of LDH from cardiac muscle, skeletal muscle, and malignant cells. Moreover, hemolysis in vitro during blood preparations (eg, during centrifugation, blood storage, or blood drawing) affects serum LDH levels. To clarify the diagnostic accuracy of various hemolytic markers, hemolytic markers were compared with total peak flow velocity as a shear stress on the erythrocytes. Although the patients with high erythrocyte creatine levels exhibited higher total peak flow velocity as compared to those with normal erythrocyte creatine levels, there was no significant difference in total peak flow velocity between patients with abnormal high LDH levels and normal LDH levels. In contrast to a good correlation between erythrocyte creatine and total peak flow velocity, serum LDH level was not related to total peak flow velocity. Interestingly, high LDH level was associated with elevation of myoglobin and myosin light chain 1 isoform in patients with prosthetic valves. Myoglobin is a cytoplasmic protein found in cardiac and skeletal muscles that binds oxygen. It is not a specific marker for cardiac muscle but can be used as a very sensitive maker of myocardial damage when combined with other specific cardiac muscle markers.,29Myosin light chain 1 isoform is a myocardial contractile protein that is released into circulating blood during myocyte necrosis, and is used as a specific marker of myocardial damage.30Thus, slight and significant increase in myoglobin and myosin light chain 1 isoform reflects the presence of limited cardiac muscle injury in patients with high LDH level. These findings indicate that an increase in serum LDH is ascribable not only to intravascular hemolysis but also to subtle cardiac muscle damage in patients with prosthetic valves, which compromise the reliability of diagnostic performance of LDH, particularly in the early postoperative stage. In contrast, there was no significant difference in the cardiac muscle markers between patients with high erythrocyte creatine and normal erythrocyte creatine. Considering the fact that erythrocyte creatine is not related to plasma creatine31 and is assayed in packed erythrocytes, erythrocyte creatine is not interfered substantially with cardiac muscle damage and hemolysis in vitro during blood preparations. Haptoglobin is thought to be a sensitive marker for intravascular hemolysis. However, since haptoglobin did not correlate with any of the hemodynamic parameters, it is not favorable for quantitative assessment of intravascular hemolysis in patients with prosthetic valves. Reticulocyte count is also a conventional marker, used as an erythropoietic or hemolytic marker, but it does not have a sufficient sensitivity to detect mild hemolysis.