81 Late cardiac toxicity in survivors of esophageal cancer Introduction Although cure rates of esophageal cancer (EC) patients have been improved since the introduction of neo-adjuvant chemoradiation (nCRT), radiation-induced cardiac toxicity might jeopardize the beneficial effect of this treatment. The CROSS trial showed a significant increase in survival rates for patients treated with nCRT prior to surgery compared to patients treated with surgery alone with acceptable acute and perioperative toxicity [1,2]. Quality of life was similar in both groups at one year after treatment [3]. Therefore, nCRT became the standard treatment for EC in large parts of the world. However, after thoracic radiotherapy for haematological malignancies, lung or breast cancer, radiation-induced cardiac and pulmonary toxicity has increasingly been acknowledged as a clinically relevant problem. [4–6]. SEER database studies including EC patients showed more cardiac deaths among irradiated patients as opposed to those treated with surgery [7,8]. Recent studies comparing, modern organ sparing radiotherapy techniques like IMRT or proton therapy with more conventional techniques found lower rates of all cause or cardiac morbidity and mortality [9–11]. Furthermore, higher (cardiovascular) postoperative complication rates were found in irradiated patients as well as patients treated with less advanced radiotherapy techniques [12–15]. These findings suggest that treatment-related cardiovascular morbidity is a clinically relevant problem in EC patients. In retrospective studies, high rates of atrial fibrillation, pericardial effusion, heart failure and cardiac wall motion disorders have been described [16–19]. However, so far, prospective imaging studies have not been systematically performed in EC patients. Moreover, information of the biological mechanisms resulting in cardiovascular toxicity is lacking. Therefore, assessment of subclinical cardiac toxicity using advanced cardiac imaging techniques may provide a better understanding of these mechanisms and may identify targets to prevent cardiac toxicity in the treatment of EC. Therefore, the main objective of this prospective hypothesis-generating crosssectional pilot study was to identify subclinical and clinical cardiopulmonary abnormalities in EC survivors after nCRT followed by resection and compared to patients treated with surgery alone. 6
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