124 Chapter 8 in oesophageal cancer patients) be explained by the differences in radiation dose distributions. In breast cancer, the LAD and left ventricle are located close to the target volume, whereas in EC, the distance between the target and these OARs is much larger. Concluding, although ischaemic events seemed a less frequently occurring complication in oesophageal cancer patients as compared to breast cancer patients, radiation dose to coronary arteries is associated with coronary events in EC patients as well. Therefore, radiation dose can and should be reduced in these subregions of the heart in EC cancer patients. Other and combined cardiac toxicities In Chapter 3, we showed that it was not possible to find an association with radiotherapy dose if we combined all types of cardiac toxicities. Clearly different toxicities originate from different biological mechanisms which might relate different to the radiation dose distribution to (subregions of) the heart. Combining toxicities as an endpoint in NTCP modelling is not a solution for low numbers of the separate events. Furthermore, many of the toxicities are related. For example, heart failure can be a consequence of an ischemic event, can be a consequence of pericardial effusion, as well as a valve disorder. The number of these “other” events were, and are in most of the oesophageal cancer papers, insufficient to draw firm conclusions on a dose response relationship. We tried to look further into heart failure and its mechanisms after radiotherapy for EC cancer. We expected myocardial fibrosis as described in the CROSS-SECT study would be a precursor for heart failure. However, local fibrosis as seen on imaging studies was not associated with cardiac functional parameters in the papers included in our review. Nor did we find associations with functional parameters indicating for example, left or right sided heart failure versus myocardial fibrosis in our CROSS SECT study. This can be explained by the limited number of patients included in these imaging studies and our CROSSECT study. An additional comment is that the effects seen, might have been too small to detect (sub)clinical consequences even in larger trials. Furthermore, we have to realize, that there are more (intrathoracic) critical organs at risk for radiation induced toxicity. In the retrospective study in chapter 3, we found that pulmonary toxicity and radiation dose was more important for overall
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