90 Chapter 6 findings suggest that myocardial fibrosis as induced by radiotherapy is a second mechanism in the development of AF in this irradiated population. Other investigators suggested that inflammatory reactions may also lead to AF [36].Indeed, if the interval between treatment and onset of the arrhythmia is short, local inflammation due to nCRT eventually leading to fibrosis could be one of the mechanisms. However, in this cross-sectional study with assessments of cardiac abnormalities 5 to 10 years after treatment this question remains unanswered. Development of AF is a clinically relevant adverse event. Patients with AF are at higher risk of developing a stroke. Moreover, AF may cause or enhance heart failure and patients require hospitalization more frequently. Moreover, AF patients have worse overall survival rates [37,38]. In the current study, we were not able to identify cardiac systolic or diastolic dysfunction secondary to myocardial fibrosis based on ultrasound measurements. This could be explained by the small sample size and the fact that many of the echocardiographic parameters were not assessable because of poor acoustic windows. Therefore, we were not able to analyse sufficient parameters for an adequate diastolic function assessment nor to perform strain imaging. Another reason could be the selection bias as we only included long term survivors. Surprisingly, we did not find a difference in coronary calcifications as measured by the CAC-score between the two treatment groups. In this study population, known prognostic factors such as hypertension, age and diabetes were associated with higher calcium scores. Nor did we find any relationship between radiation dose and CAC score. This might also be explained by the small sample size and the fact that we analysed long-term survivors, whereas patients with cardiovascular risk factors might have experienced cardiac complications and mortality sooner after treatment[34]. In addition, most coronary arteries are located in lower dose regions as opposed to the radiation dose in e.g., breast cancer patients. Therefore, coronary problems might be less important in this patient group. In the current study, the relaxation time after ventricle contraction (QTc interval) and the width of the QRS complex were significantly shorter in the irradiated group (table 2). We did not find a good explanation for the changes in QTc time. This can be caused by differences in heart rate, prior infarctions, or the use of cardiac medication. The shorter QRS complex can, however, be caused by myocardial fibrosis (ECV values) as detected on MRI as described earlier in a large, otherwise
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