New possibilities in scintigraphy detection of carbon monoxide cardiotoxicity

The blood clearance of Tc99m MIBI is rapid and biexponential, with an initial fast phase followed by a slow phase. The fundamental myocellular uptake mechanism involves passive distribution across plasma and mitochondrial membranes, and at equilibrium, sestamibi is sequestered within the mitochondria by the larger negative mitochondrial transmembrane potential. Reverse distribution into blood stream is stopped by the high membrane potential of the cardiac cells. Scintigraphic changes followed by the metabolic abnormalities in patients after acute carbon monoxide poisoning can be necrosis or only the transitory ischemia. It seems to detect accurately the extension of the early necrosis (unreversible) of the myocardium. Amiscan kit for the preparation of Tc99m-glucarate is being developed as a radiopharmaceutical diagnostic agent for the imaging of and diagnosis of acute myocardial necrosis. Cellular and subcellular uptake studies have shown that Tc99m-glucarate localizes in necrotic tissues binding primarily to the nucleoprotein sub-fractions and to a lesser extent to the DNA fractions. Glucarate is taken up rapidly by necrotic myocardium and cleared relatively rapidly from the circulation resulting in early, hight target-to-background ratios. In studies of Amiscan in patients with acute myocardial infarction, sensitivity was found to be 100% when Amiscan is administered within 9 hours of the onset of chest pain. In our preliminary study the scintigraphic scans using Tc99m-glucarate were performed in 10 patients after acute carbon monoxide poisoning. The study can confirm that some patients during acute CO poisoning have typical myocardial necrosis, but part of them have hibernating and/or stunned myocardium.