Physiological Interaction of Heart and Lung in Thoracic Irradiation

Journal Article · Sat Dec 01 00:00:00 EST 2012 · International Journal of Radiation Oncology, Biology and Physics

DOI:https://doi.org/10.1016/J.IJROBP.2012.07.2362· OSTI ID:22149690

Ghobadi, Ghazaleh; Veen, Sonja van der ^[1]; Bartelds, Beatrijs ^[2]; Boer, Rudolf A. de ^[3]; Dickinson, Michael G. ^[2]; Jong, Johan R. de ^[4]; Faber, Hette; Niemantsverdriet, Maarten ^[1]; Brandenburg, Sytze ^[5]; Berger, Rolf M.F. ^[2]; Langendijk, Johannes A. ^[1]; Coppes, Robert P. ^[1]

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1. Department of Radiation Oncology, University of Groningen, University Medical Center Groningen, Groningen (Netherlands)
2. Center for Congenital Heart Disease, Beatrix Children Hospital, University of Groningen, University Medical Center Groningen, Groningen (Netherlands)
3. Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen (Netherlands)
4. Department of Nuclear Medicine and Molecular Imaging, University of Groningen, University Medical Center Groningen, Groningen (Netherlands)
5. Kernfysisch Versneller Instituut, University of Groningen, Groningen (Netherlands)

Introduction: The risk of early radiation-induced lung toxicity (RILT) limits the dose and efficacy of radiation therapy of thoracic tumors. In addition to lung dose, coirradiation of the heart is a known risk factor in the development RILT. The aim of this study was to identify the underlying physiology of the interaction between lung and heart in thoracic irradiation. Methods and Materials: Rat hearts, lungs, or both were irradiated to 20 Gy using high-precision proton beams. Cardiopulmonary performance was assessed using breathing rate measurements and F{sup 18}-fluorodeoxyglucose positron emission tomography ({sup 18}F-FDG-PET) scans biweekly and left- and right-sided cardiac hemodynamic measurements and histopathology analysis at 8 weeks postirradiation. Results: Two to 12 weeks after heart irradiation, a pronounced defect in the uptake of {sup 18}F-FDG in the left ventricle (LV) was observed. At 8 weeks postirradiation, this coincided with LV perivascular fibrosis, an increase in LV end-diastolic pressure, and pulmonary edema in the shielded lungs. Lung irradiation alone not only increased pulmonary artery pressure and perivascular edema but also induced an increased LV relaxation time. Combined irradiation of lung and heart induced pronounced increases in LV end-diastolic pressure and relaxation time, in addition to an increase in right ventricle end-diastolic pressure, indicative of biventricular diastolic dysfunction. Moreover, enhanced pulmonary edema, inflammation and fibrosis were also observed. Conclusions: Both lung and heart irradiation cause cardiac and pulmonary toxicity via different mechanisms. Thus, when combined, the loss of cardiopulmonary performance is intensified further, explaining the deleterious effects of heart and lung coirradiation. Our findings show for the first time the physiological mechanism underlying the development of a multiorgan complication, RILT. Reduction of dose to either of these organs offers new opportunities to improve radiation therapy treatment of thoracic tumors, potentially facilitating increased treatment doses and tumor control.

• OSTI ID: 22149690
• Journal Information: International Journal of Radiation Oncology, Biology and Physics, Vol. 84, Issue 5; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0360-3016
• Country of Publication: United States
• Language: English

Related Subjects

62 RADIOLOGY AND NUCLEAR MEDICINE
ACCURACY
ARTERIES
EDEMA
FIBROSIS
FLUORINE 18
FLUORODEOXYGLUCOSE
HEALTH HAZARDS
HEART
INFLAMMATION
INTERACTIONS
IRRADIATION
LUNGS
NEOPLASMS
PERFORMANCE
PHYSIOLOGY
POSITRON COMPUTED TOMOGRAPHY
PROTON BEAMS
RADIATION DOSES
RADIOTHERAPY
RATS
RELAXATION TIME
RESPIRATION
TOXICITY