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Myocardial iron loading by magnetic resonance imaging T2* in good prognostic myelodysplastic syndrome patients on long‐term blood transfusions
Author(s) -
Chacko Joseph,
Pennell Dudley J.,
Tanner Mark A.,
Hamblin Terry J.,
Wonke Beatrix,
Levy Terry,
Thomas Peter W.,
Killick Sally B.
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06695.x
Subject(s) - medicine , gastroenterology , chelation therapy , magnetic resonance imaging , ferritin , myelodysplastic syndromes , anemia , serum ferritin , blood transfusion , deferiprone , thalassemia , cardiology , surgery , radiology , bone marrow
Summary Magnetic resonance imaging (MRI) was used to quantify myocardial iron loading by T2* in 11 transfusion‐dependent good prognostic myelodysplastic syndrome (MDS) patients. Myocardial T2*, left ventricular function and hepatic T2* were measured simultaneously. Patients had been on transfusion therapy for 13–123 months and had serum ferritin levels of 1109–6148 μ g/l at the time of study. Five patients had not commenced iron chelation and had been transfused with a median of 63 red cell units and had a median serum ferritin level of 1490 μ g/l. Six patients were on iron chelation and had been transfused with a median of 112 red cell units and had a median serum ferritin level of 4809 μ g/l. Hepatic iron overload was mild in two, moderate in seven and severe in two patients. The median liver iron concentration was 5·9 mg/g dry weight in chelated patients and 9·5 mg/g in non‐chelated patients ( P = 0·17; not significant). Myocardial T2* indicated absent iron loading in 10/11 patients (91%; 95% confidence interval 62–98%) and borderline‐normal in one patient. Left ventricular function was normal in all patients. No correlation was observed between increasing serum ferritin levels, hepatic iron overload and myocardial T2*. A long latent period relative to hepatic iron loading appears to predate the development of myocardial iron loading in transfusion‐dependent MDS patients.