Journal
RADIOTHERAPY AND ONCOLOGY
Volume 114, Issue 1, Pages 96-103Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.radonc.2014.11.017
Keywords
Thoracic tumors; Radiation-induced cardiac toxicity; Radiation-induced lung toxicity; ACE inhibition; Captopril
Funding
- Dutch Cancer Society [RUG-2007-3890]
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Background and purpose: In thoracic irradiation, the maximum radiation dose is restricted by the risk of radiation-induced cardiopulmonary damage and dysfunction limiting tumor control. We showed that radiation-induced sub-clinical cardiac damage and lung damage in rats mutually interact and that combined irradiation intensifies cardiopulmonary toxicity. Unfortunately, current clinical practice does not,include preventative measures to attenuate radiation-induced lung or cardiac toxicity. Here, we investigate the effects of the ACE inhibitor captopril on radiation-induced cardiopulmonary damage. Material and methods: After local irradiation of rat heart and/or lungs captopril was administered orally. Cardiopulmonary performance was assessed using biweekly breathing rate measurements. At 8 weeks post-irradiation, cardiac hemodynamics were measured, CT scans and histopathology were analyzed. Results: Captopril significantly improved breathing rate and cardiopulmonary density/structure, but only when the heart was included in the radiation field. Consistently, captopril reduced radiation-induced pleural and pericardial effusion and cardiac fibrosis, resulting in an improved left ventricular end-diastolic pressure only in the heart-irradiated groups. Conclusion: Captopril improves cardiopulmonary morphology and function by reducing acute cardiac damage, a risk factor in the development of radiation-induced cardiopulmonary toxicity. ACE inhibition should be evaluated as a strategy to reduce cardiopulmonary complications induced by radiotherapy to the thoracic area. (C) 2014 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 114 (2015) 96-103
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