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C. Deroose

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    Poster Display Session (ID 63)

    • Event: ELCC 2017
    • Type: Poster Display Session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
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      164P - Heart radiation dose as a risk factor for dyspnea worsening after multimodality treatment for non-small cell lung cancer and pleural mesothelioma: An exploratory analysis (ID 500)

      12:30 - 13:00  |  Author(s): C. Deroose

      • Abstract

      The purpose of our study is to quantify the influence of heart dose on the early and late onset of dyspnea in a cohort of radiotherapy (RT)-treated non-small cancer patients (NSCLC) and malignant pleural mesothelioma (MPM) patients after multimodality treatment, according to the type of surgery.

      In 121 patients with multimodality-treated NSCLC and MPM the maximal dyspnea score (CTCAE 4.0) before RT and at an early (≤6 months) and a late (7-12 months) time point were obtained. Included patients needed to be clinically and radiologically progression-free 9 months after the end of RT. The difference (Δ) between the maximal dyspnea at ≤ 6 months and the pre-RT dyspnea or the maximal dyspnea at 7-12 months and the pre-RT dyspnea was calculated.

      Our results show that 44% (50/113) of patients developed an early worsening of at least 1 point in their dyspnea score (Δdyspnea ≥1) after the end of RT. As independent predictors of an early worsening, we identified the MHD (for Δdyspnea ≥1: OR = 1.032, p = 0.04) and the dyspnea score before RT (for Δdyspnea ≥1: OR = 0.40, p = 0.0001; for Δdyspnea ≥2: OR = 0.35, p = 0.05). At a later timepoint, only the dyspnea score before RT (OR: 0.40, p = 0.001) was identified as predictor of for Δdyspnea ≥1.

      Our results, albeit exploratory, suggest that heart dose may play a role in the early worsening of the dyspnea in a heterogeneous cohort of multimodality treated RT patients.

      Clinical trial identification:

      Legal entity responsible for the study:
      KUL UHasselt-ZOL-Jessa

      This study is part of the Limburg Clinical Research Program (LCRP) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk, province of Limburg, Flemish government, Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital. This work was partly funded by the European Union’s Seventh Framework Programme for research, technological development and demonstration under grant agreement no 601826 (REQUITE). CB is supported by the Cancer foundation Limburg and a grant from ‘Kom op tegen kanker’. AB is supported by a grant from the Stichting tegen kanker/Fondation contre le cancer (CA/2014/354) and by Kom op Tegen Kanker (Stand up to Cancer, The Flemish Cancer Society).

      All authors have declared no conflicts of interest.