Iron Overload Cardiomyopathy in Myelodysplastic Syndrome: A Fatal Outcome After 20 Years of Chronic Transfusions

Iron overload cardiomyopathy (IOC) results from excess iron accumulation in the myocardium, usually because of genetic disorders or secondary hemochromatosis by multiple blood transfusions.

A 42-year-old man with refractory heart failure was referred to our hospital. He had a history of myelodysplastic syndrome, requiring 112 U of blood transfusions over 16 years. Severe left ventricular dysfunction, elevated ferritin levels, and myocardial iron deposition confirmed by endomyocardial biopsy led to the diagnosis of IOC. Despite intensive management, the patient was discharged after death.

Early IOC typically starts with asymptomatic diastolic dysfunction. Noninvasive modalities (eg, N-terminal pro-B-type natriuretic peptide, T2-star magnetic resonance imaging) are crucial for early detection. Iron chelation therapy may reverse cardiac dysfunction in the early phase but is less effective in advanced phases, highlighting the need for timely intervention.

Early detection, cardiac monitoring, and close collaboration between hematologists and cardiologists are essential to prevent IOC progression.