RESUMO
INTRODUCTION: Phosphatidylserine is translocated from the inner to the outer leaflet of the plasma membrane in the early stages of apoptosis and necrosis and in reversibly injured cells. In rabbit hearts, ischemia followed by reperfusion results in exposure of phosphatidylserine on myocytes unaffected by apoptosis or necrosis. Lactadherin was recently introduced as a highly sensitive phosphatidylserine ligand. We hypothesized that ischemic myocardial cell damage can be identified by radio-labeled lactadherin and that the ischemic area at risk (AAR) can be visualized retrospectively after reperfusion. METHODS: Left anterior descending coronary artery in pigs was occluded for 20 minutes, 45 minutes or 45 minutes preceded by ischemic preconditioning. In all three groups, (99m)Tc-lactadherin was injected intravenously 30 minutes after reperfusion. The AAR was demarcated by Evans blue and the infarct size by 2,3,5,-triphenyltetrazodium chloride staining. RESULTS: The regional myocardial uptake of (99m)Tc-lactadherin closely correlated with the AAR (r=.83, P = .001). The area of (99m)Tc-lactadherin uptake was unaltered by a shorter duration of ischemia and ischemic preconditioning (P=.23) despite significantly different infarct development (P=.001). CONCLUSION: The results suggest that (99m)Tc-lactadherin can be used as a sensitive marker for AAR imaging when injected 30 minutes after reperfusion following acute ischemia.
