Recent advances in cardiovascular magnetic resonance (CMR) have revolutionised the monitoring and therapy of patients with beta-thalassaemia. Thalassaemia mainly affects patients in a broad belt stretching from the Mediterranean to South-East Asia and throughout the world in lower prevalence following immigration [1]. For clinical purposes, beta-thalassaemia is divided into beta-thalassaemia major, intermedia and minor, based on phenotypic severity including transfusion requirement. Originally described by Thomas Cooley in 1925, beta-thalassaemia major (TM) causes profound anaemia due to absence or severe reduction in the production of the beta globin chains of adult haemoglobin. Patients require lifelong transfusions from infancy to prevent death and other complications including bony deformities due to marrow expansion, growth retardation, splenomegaly and susceptibility to infections. Without transfusion, the majority of children die before the age of 5 [1, 2]. Such transfusion-dependent patients develop iron overload both as a result of transfusional iron (200–250 mg per unit of blood) and inappropriately high intestinal iron absorption. Untreated, this causes progressive ironinduced damage to the heart, liver, pancreas and other endocrine organs. In the heart, iron accumulates predominantly in ventricular myocardium, affecting the mitochondrial respiratory chain which leads to reduction of contractility and the development of cardiac failure [3–5]. Beta-thalassaemia intermedia (TI) describes patients of intermediate severity. Symptoms may not be apparent until much later in life but these patients can also develop hepatosplenomegaly and skeletal abnormalities due to marrow expansion and extramedullary haematopoiesis. Transfusion may be needed but even without this, iron overload can occur due to increased gastrointestinal absorption. Beta thalassaemia minor patients are usually asymptomatic and may be only mildly anaemic, but have potential to pass the mutant gene to their children. Until recently, survival in transfusion-dependent thalassaemia patients was poor and even as late as 2000, 50% of UK patients died before the age of 35 years [6]. Heart disease (predominantly heart failure and arrhythmia) remains the leading cause of death, responsible for 71% of the deaths in TM [7]. The iron chelating agent deferoxamine, which has been the mainstay of therapy, was introduced in 1975 and two newer oral chelators, deferiprone and deferasirox have been introduced since. Over the last decade, there has been an improvement in survival, in Editorial comment to: Mavrogeni et al. (2008) Magnetic resonance evaluation of liver and myocardial iron deposition in thalassemia intermedia and b-thalassemia major. Int J Cardiovasc Imaging. doi:10.1007/s10554-008-9332-2.