ACE inhibition attenuates radiation-induced cardiopulmonary damage. Issue 1 (January 2015)

• Record Type: Journal Article
• Authors: van der Veen, Sonja J.; Ghobadi, Ghazaleh; de Boer, Rudolf A.; Faber, Hette; Cannon, Megan V.; Nagle, Peter W.; Brandenburg, Sytze; Langendijk, Johannes A.; van Luijk, Peter; Coppes, Robert P.
• Is Part Of: Radiotherapy and oncology. Volume 114:Issue 1(2015:Jan.)
• Page Start: 96
• Page End: 103
• Publication Date: 2015-01
• Subjects: Oncology -- Periodicals; Radiotherapy -- Periodicals; Tumors -- Periodicals; Medical Oncology -- Periodicals; Neoplasms -- radiotherapy -- Periodicals; Radiotherapy -- Periodicals; Radiothérapie -- Périodiques; Cancérologie -- Périodiques; Tumeurs -- Périodiques; Electronic journals; 616.9940642
• DOI: 10.1016/j.radonc.2014.11.017
• Languages: English
• ISSNs: 0167-8140

Abstract

<abstract xml:lang="en" abstract-type="author" id="ab005"> <title id="st155">Abstract</title> <sec> <title id="st105">Background and purpose</title> <p id="sp0005">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.</p> </sec> <sec> <title id="st110">Material and methods</title> <p id="sp0010">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.</p> </sec> <sec> <title id="st115">Results</title> <p id="sp0015">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.</p> </sec> <sec> <title id="st120">Conclusion</title> <p id="sp0020">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.</p> </sec> </abstract>