Comparing In vivo T2* and T2 Measurements in Tissues of Liver and Heart in thalassemia

Introduction: Cardiac complications secondary to iron overload are the leading cause of death in thalassemia major (TM). Cardiovascular magnetic resonance (CMR) can provide a noninvasive means of measuring the amount of tissue iron. With CMR, tissue iron is detected indirectly by the effect on relaxation times of hydrogen nuclei in the presence of ferritin and hemosiderin iron. The iron results in shortening of proton relaxation times and both CMR T2* and T2 have been validated as non-invasive means for assessment of iron overload in tissues of liver and heart. (1,2,3,4,5,6). A recent study (6) has shown that both liver T2* and T2 can accurately measure hepatic iron overload in thalassemia. We have demonstrated the linear correlation between myocardial T2 and T2* in patients with iron overload (7) indicating that iron loading becomes the dominant effect in determining the CMR T2* and T2 in the heart. However, there is currently little data on comparing this relationship of T2*/T2 between tissues of liver and heart. Although the mechanisms of iron-enhanced relaxation may be similar in these two human organs, the exact manner can differ due to biological differences.