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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-09-2754.

Submitted September 13, 2002
Accepted January 27, 2003
Evaluation of myocardial iron by magnetic resonance imaging during iron chelation therapy with desferrioxamine. Indication of close relation between myocardial iron content and chelatable iron pool
Peter D Jensen*, Finn T Jensen, Thorkil Christensen, Hans Eiskjaer, Ulrik Baandrup, and Johan L Nielsen
Department of Hematology, Aarhus University Hospital, Aarhus, Denmark
Center for Nuclear Magnetic Resonance, Aarhus University Hospital, Aarhus, Denmark
Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark
Institute of Pathology, Aarhus University Hospital, Aarhus, Denmark
* Corresponding author; email: d222615{at}inet.uni2.dk.
Evaluation of myocardial iron during iron chelation therapy is not feasible by repeated endomyocardial biopsies owing to the heterogeneity of iron distribution and the risk of complications. Recently, we described a non-invasive method based on magnetic resonance imaging. Here the method is used for repeated estimation of the myocardial iron content during iron chelation with desferrioxamine in 14 adult non-thalassemic patients with transfusional iron overload. We investigated the repeatability of the method and the relation between the myocardial iron estimates and iron status. The repeatability coefficient (2xSD) was 2.8 µmol/g in the controls (day-to-day) and 4.0 µmol/g in the patients (within-day). Myocardial iron estimates were elevated in 10 of all 14 patients at first examination, but normalized in six after 6 to 18 months of treatment. If liver iron declined below 350 µmol/g all but one of the myocardial iron estimates were normal or nearly normal. At start (R2=0.69, P=.0014) and still after 6 months of iron chelation (R2=0.76, P=.001), the estimates were significantly and more closely related to the urinary iron excretion than to liver iron or serum ferritin levels. In conclusion, our preliminary data, which may only pertain to patients with acquired anemias, suggest the existence of a critical liver iron concentration, above which elevated myocardial iron is present, but its extent seems related to the size of the chelatable iron pool, as reflected by the urinary iron excretion. This further supports the concept of the labile iron pool as the compartment directly involved in transfusional iron toxicity.

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