Iron overload is characterized by excessive accumulation of iron in various organs, including the liver and the heart [1,2]. This condition may lead to serious complications, including hepatic fibrosis, cirrhosis, hepatocellular carcinoma or heart failure [3,4,5]. Iron overload can be caused by a variety of factors, including genetic disorders such as hereditary hemochromatosis or chronic transfusion therapy for conditions such as thalassemia or sickle cell disease [6], [7], [8], [9]. Cardiovascular magnetic resonance (CMR) T2* analysis is currently the reference standard for the diagnosis and management of iron overload cardiomyopathy [5], offering the advantages of rapid and reliable non-invasive acquisition [10] and generalizability of its values between different CMR scanners [11]. Tissue T2* relaxation time decreases with increasing iron concentration, providing reproducible quantification of iron deposition, and therefore disease severity [12]. This allows treating physicians to tailor treatment to the individual patient, with the ability to adjust treatment regimens through repeat CMR examination, resulting in better non-invasive patient monitoring [13]. In addition to cardiac T2* quantification, hepatic T2* values can also be assessed [14,15]. Detection of hepatic iron overload could then reveal inherited diseases such as hemochromatosis, which is known to have a high prevalence of approximately 1 case per 300 individuals in Europe, the United States and Australia [16].

We hypothesized that routinely performed CMR T2* analysis may identify a substantial number of patients with abnormal cardiac and/or hepatic values indicating iron overload, which might have clinical implications for the individual patient. To date, there is a lack of adequately powered studies addressing the routine assessment of potential cardiac and hepatic iron overload as an incidental finding on CMR T2* mapping.

To address this gap, the purpose of this study was to assess the diagnostic capabilities of CMR in the detection of incidental hepatic and cardiac iron overload by T2* mapping.