We read with interest the recent paper by Hirata et al. entitled "Interpretation of reverse redistribution of 99m Tc-tetrofosmin in patients with acute myocardial infarction" [1]. The authors postulate that tetrofosmin reverse redistribution (RR) in patients with recent myocardial infarction (MI) reflects salvaged myocardium and they also present a possible mechanism for this finding. Regional wall motion study was performed to support this hypothesis. Although RR with a 99m Tc-labelled agent, in this clinical setting, has been previously reported [2], the tetrofosmin RR phenomenon was initially reported from our department [3,4]. Our results were included in the highlights of the EANM congress by I. Carrio in 1997 [5]. We compared early and late tetrofosmin images in thrombolysed acute MI patients with high patency grade of the infarct-related coronary artery 1 week and (in a subgroup of patients) 1 month post MI. Since early tetrofosmin images 1 week and 1 month post MI were similar and the RR found in the initial study was decreased or eliminated over 1 month of follow-up, we concluded that RR may reflect viable stunned myocardium.Although our results are in agreement with those of Hirata et al., we did not perform a wall motion study since we believe that it does not contribute in elucidating the main issue in this clinical setting, which is whether tetrofosmin RR directly reflects viable stunned myocardium or reflects other phenomena not related to the viable myocardial cells. Stunned myocardium in any case should be present and wall motion will improve over time in parallel with the decrease in the degree of the RR phenomenon. In order to explain tetrofosmin RR in this clinical setting we must examine four possible mechanisms:1. Early post-MI hyperperfusion and increased agent influx in the myocardial cells of the affected area, proportional to viability, is followed by faster wash-out. This mechanism can be excluded since tetrofosmin lacks the redistribution phenomenon observed with thallium-201.2. Tetrofosmin enters damaged cells which will undergo apoptosis. RR is produced since they cannot retain the tetrofosmin as long as normal cells. In this case the early tetrofosmin uptake in the follow-up study should be decreased proportionally to the magnitude of the RR. We also exclude this mechanism since, in a subgroup of these patients, a considerable initial RR which gradually completely recovers over time is combined with normal or near-normal early and late tetrofosmin uptake in the follow-up. Any significant decrease in early uptake between initial and follow-up study is not possible in this context and this is therefore completely uncoupled from the magnitude of the recovered RR. One such case is actually presented by Hirata et al. in Fig. 2. 3. One week post MI, although the epicardial vessel is open, the microvascular function has not yet been restored and the viable salvaged tissue is actually hypoperfused but can retain tetrofosmin like normal myocardium. An additional amount of the tetrofosmin is t...