Low prevalence of XXXX in @entity2395 major assessed by late @entity2287 enhancement cardiovascular magnetic resonance.

@entity1 @entity712 @entity296 @entity82 @entity1002 @entity2395 @entity299 @entity2287 @entity68
BACKGROUND: @entity712 remains a major cause of mortality in thalassaemia major. The possible role of @entity299 in @entity2395 major in the genesis of @entity712 is not clear. It is also unclear whether @entity299 might arise as a result of @entity712 . METHODS: We studied 45 @entity1 with thalassaemia major who had a wide range of current cardiac @entity68 loading and included @entity1 with prior and current @entity712 . Myocardial @entity68 was measured using T2* cardiovascular magnetic resonance (CMR), and following this, late @entity2287 enhancement (LGE) was used to determine the presence of macroscopic @entity296 . RESULTS: The median myocardial T2* in all @entity1 was 22.6 ms (range 5.3-58.8 ms). @entity82 was detected in only one @entity1 , whose myocardial T2* was 20.1 ms and left ventricular ejection fraction 57%. No @entity82 was identified in 5 @entity1 with a history of @entity712 with full recovery, in 3 @entity1 with current @entity1002 undergoing treatment, or in 18 @entity1 with myocardial @entity68 loading with cardiacT2* < 20 ms at the time of scan. CONCLUSION: This study shows that macroscopic @entity296 is uncommon in @entity2395 major across a broad spectrum of myocardial @entity68 loading. Importantly, there was no macroscopic @entity82 in @entity1 with current or prior @entity712 , or in @entity1 with myocardial @entity68 loading without @entity712 . Therefore if @entity296 indeed contributes to @entity296 in @entity2395 , our data combined with the knowledge that the @entity296 of @entity68 overload can be reversed, indicates that any such @entity82 would need to be both microscopic and reversible.
