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Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist

Cancer cachexia is defined as a multifactorial syndrome of involuntary weight loss characterized by an ongoing loss of skeletal muscle mass and progressive functional impairment. It is postulated that cardiac dysfunction/atrophy parallels skeletal muscle atrophy in cancer cachexia. Cardiotoxic chemo...

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Autores principales: Kazemi-Bajestani, Seyyed M. R., Becher, Harald, Fassbender, Konrad, Chu, Quincy, Baracos, Vickie E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053562/
https://www.ncbi.nlm.nih.gov/pubmed/24627226
http://dx.doi.org/10.1007/s13539-014-0137-y
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author Kazemi-Bajestani, Seyyed M. R.
Becher, Harald
Fassbender, Konrad
Chu, Quincy
Baracos, Vickie E.
author_facet Kazemi-Bajestani, Seyyed M. R.
Becher, Harald
Fassbender, Konrad
Chu, Quincy
Baracos, Vickie E.
author_sort Kazemi-Bajestani, Seyyed M. R.
collection PubMed
description Cancer cachexia is defined as a multifactorial syndrome of involuntary weight loss characterized by an ongoing loss of skeletal muscle mass and progressive functional impairment. It is postulated that cardiac dysfunction/atrophy parallels skeletal muscle atrophy in cancer cachexia. Cardiotoxic chemotherapy may additionally result in cardiac dysfunction and heart failure in some cancer patients. Heart failure thus may be a consequence of either ongoing cachexia or chemotherapy-induced cardiotoxicity; at the same time, heart failure can result in cachexia, especially muscle wasting. Therefore, the subsequent heart failure and cardiac cachexia can exacerbate the existing cancer-induced cachexia. We discuss these bilateral effects between cancer cachexia and heart failure in cancer patients. Since cachectic patients are more susceptible to chemotherapy-induced toxicity overall, this may also include increased cardiotoxicity of antineoplastic agents. Patients with cachexia could thus be doubly unfortunate, with cachexia-related cardiac dysfunction/heart failure and increased susceptibility to cardiotoxicity during treatment. Cardiovascular risk factors as well as pre-existing heart failure seem to exacerbate cardiac susceptibility against cachexia and increase the rate of cardiac cachexia. Hence, chemotherapy-induced cardiotoxicity, cardiovascular risk factors, and pre-existing heart failure may accelerate the vicious cycle of cachexia-heart failure. The impact of cancer cachexia on cardiac dysfunction/heart failure in cancer patients has not been thoroughly studied. A combination of serial echocardiography for detection of cachexia-induced cardiac remodeling and computed tomography image analysis for detection of skeletal muscle wasting would appear a practical and non-invasive approach to develop an understanding of cardiac structural/functional alterations that are directly related to cachexia.
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spelling pubmed-40535622014-06-12 Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist Kazemi-Bajestani, Seyyed M. R. Becher, Harald Fassbender, Konrad Chu, Quincy Baracos, Vickie E. J Cachexia Sarcopenia Muscle Review Cancer cachexia is defined as a multifactorial syndrome of involuntary weight loss characterized by an ongoing loss of skeletal muscle mass and progressive functional impairment. It is postulated that cardiac dysfunction/atrophy parallels skeletal muscle atrophy in cancer cachexia. Cardiotoxic chemotherapy may additionally result in cardiac dysfunction and heart failure in some cancer patients. Heart failure thus may be a consequence of either ongoing cachexia or chemotherapy-induced cardiotoxicity; at the same time, heart failure can result in cachexia, especially muscle wasting. Therefore, the subsequent heart failure and cardiac cachexia can exacerbate the existing cancer-induced cachexia. We discuss these bilateral effects between cancer cachexia and heart failure in cancer patients. Since cachectic patients are more susceptible to chemotherapy-induced toxicity overall, this may also include increased cardiotoxicity of antineoplastic agents. Patients with cachexia could thus be doubly unfortunate, with cachexia-related cardiac dysfunction/heart failure and increased susceptibility to cardiotoxicity during treatment. Cardiovascular risk factors as well as pre-existing heart failure seem to exacerbate cardiac susceptibility against cachexia and increase the rate of cardiac cachexia. Hence, chemotherapy-induced cardiotoxicity, cardiovascular risk factors, and pre-existing heart failure may accelerate the vicious cycle of cachexia-heart failure. The impact of cancer cachexia on cardiac dysfunction/heart failure in cancer patients has not been thoroughly studied. A combination of serial echocardiography for detection of cachexia-induced cardiac remodeling and computed tomography image analysis for detection of skeletal muscle wasting would appear a practical and non-invasive approach to develop an understanding of cardiac structural/functional alterations that are directly related to cachexia. Springer Berlin Heidelberg 2014-03-14 2014-06 /pmc/articles/PMC4053562/ /pubmed/24627226 http://dx.doi.org/10.1007/s13539-014-0137-y Text en © Springer-Verlag Berlin Heidelberg 2014
spellingShingle Review
Kazemi-Bajestani, Seyyed M. R.
Becher, Harald
Fassbender, Konrad
Chu, Quincy
Baracos, Vickie E.
Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title_full Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title_fullStr Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title_full_unstemmed Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title_short Concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
title_sort concurrent evolution of cancer cachexia and heart failure: bilateral effects exist
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053562/
https://www.ncbi.nlm.nih.gov/pubmed/24627226
http://dx.doi.org/10.1007/s13539-014-0137-y
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