61 Myocardial fibrosis in esophageal cancer patients Introduction The clinical introduction of neo-adjuvant chemoradiotherapy (nCRT) prior to surgery provided an important survival benefit for esophageal cancer (EC) patients.[1] However, recent studies have shown that there is a substantial risk of cardiac toxicity and even mortality attributable to nCRT that potentially jeopardizes the benefit of nCRT.[2–5] Wang et al [6] reported grade ≥3 cardiac events in 18% of patients with EC who were treated with chemoradiotherapy. Radiation modality (hazard ratio: 1.7) or mean heart dose (hazard ratio: 1.03) were significantly associated with these complications. Moreover, patients who developed these cardiac complications had worse overall survival (OS: 5 years 38% vs 52%). The exact mechanism of toxicity underlying this increased risk of cardiac complications remains unknown. [7] Knowledge on these mechanisms might help reduce the toxicity risks, aiming to maximize the benefit of nCRT and ultimately improve survival in patients with EC. Various cardiac pathologies have been described because of thoracic irradiation. Shortly after radiotherapy, acute inflammatory effects could be observed.[8] Months to years after radiotherapy, chronic pericarditis, (major) coronary events, non-ischemic cardiomyopathies, conduction disorders and valve problems can occur.[9–11] Only limited data exists on the mechanism and extent of direct irradiation damage to the myocardium. Cardiac irradiation has been observed to cause reduced micro- vascularization and myocardial fibrosis in mice.[12] For detection of focal fibrosis, Cardiovascular Magnetic Resonance (CMR) with late Gadolinium Enhancement (LGE) is the gold standard in clinical practice.[13,14] After thoracic radiation therapy, LGE was a result of ischemic fibrosis after myocardial infarction, but also a sign of focal non- ischemic fibrosis in high-dose regions.[15,16] However, eye- balling fibrosis on LGE requires significant myocardial fibrosis to be present, and diffuse fibrosis is even harder to detect in the absence of normal myocardium. In these cases, T1 mapping, including extracellular volume (ECV) calculation, has the potential to make an important contribution to clinical risk stratification, because of its ability to enable detection and quantify myocardial fibrosis at a much earlier stage compared with LGE.[17,18] ECV has already been shown to correlate strongly with histologic collagen burden, and its levels have been found to correlate with increased risks of heart failure or cardiac death.[19] In a recent study by Takagi et al,[20] ECV changes in the myocardium were reported in EC patients after definitive CRT. 5
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