73 Myocardial fibrosis in esophageal cancer patients Increased rates of (major) coronary events after thoracic radiotherapy are frequently reported, and in breast cancer and Hodgkin lymphoma patients a clear doseresponse relationship has been demonstrated.[36,37] However, rather than the coronary artery flow territories, the changes in segmental ECV in the nCRT group follow the dose distribution (figure 4).[38,39] CMR with LGE was used in several other studies to detect fibrosis due to myocardial ischemia. A recent imaging study in 20-years survivors of Hodgkin disease found LGE in 29% of the patients, and the vast majority showed an enhancement pattern matching with myocardial infarction. [15] In our study only one patient (6%) experienced an occult myocardial infarction after nCRT. However, we found intramural LGE in 4 patients (24%), a pattern that can be observed in non-ischemic cardiomyopathies.[13] Umezawa et al. [16] analyzed patients with EC approximately 1 year after definitive chemoradiation (CRT) (60-70 Gy). In 46% of the patients, intramural LGE was detected. The lower rates of LGE in our cohort may be attributed to the lower radiation dose in the neoadjuvant setting. The relation that Umezawa et al.[16] found between the presence of LGE in the LV myocardial segments and radiation dose supports this. The researchers described 15% LGE in segments that received a radiation dose between 40 Gy and 60 Gy and 21% if the segmental dose exceeded 60 Gy. How radiation-induced myocardial damage develops over time is unknown. A prospective Japanese study performed in EC patients treated with definitive CRT demonstrated an increase in native T1 of 7% (p < 0.05) and 5% (p >0.05) and in ECV of 24% (p < 0.05) and 14% (p > 0.05) in the basal septum (irradiated area) at 0.5 and 1.5 years follow up respectively, compared to baseline[20]. In addition, post-contrast T1 values showed a significant decrease at 1.5 year when compared to baseline. The apical lateral wall was measured as control (non-irradiated volume) and did not show differences over time. An explanation for the initial increase of ECV might be the presence of myocardial inflammation shortly after radiotherapy, as also suggested by the authors.[12,40] It is known that in case of myocardial inflammation, ECV can lead to an overestimation of the extent of myocardial fibrosis.[41] This cross-sectional study has two limitations. Firstly, the cohort size is limited. As a consequence, we could not determine risk factors that might affect ECV changes after radiotherapy, or correlate elevated ECV with cardiac function measures. Secondly, patients who already died prior to the study were not in the cohort. Since cardiac toxicity is known to negatively influence overall survival,[2] our study is indeed likely affected by a selection bias, which might have led to an underestimation of the risk of myocardial toxicity. 5
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