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Cancer cachexia: getting to the heart of the matter

John D. Groarke, Susan Cheng, Lee W. Jones, Javid Moslehi
DOI: http://dx.doi.org/10.1093/eurheartj/eht424 First published online: 14 October 2013

This editorial refers to ‘Prevention of liver cancer cachexia-induced cardiac wasting and heart failure’, by J. Springer et al. doi:10.1093/eurheartj/eht302

In his Principles and Practices of Medicine, written over 100 years ago, William Osler described cachexia in stomach cancer as ‘progressive emaciation’ and ‘loss of strength disproportionate to loss of weight’.1 Today, cachexia is further defined as a multifactorial syndrome characterized by an ongoing loss of skeletal muscle mass that cannot be reversed by conventional nutritional support, leading to progressive functional impairment.2 Although the prevalence and severity vary across cancer types, cachexia occurs in the majority of patients with advanced oncological disease and is responsible for ∼ 20% of cancer deaths.3,4 The negative impact on functional capacity, quality of life, cancer treatment response, and prognosis in the oncology setting emphasizes the clinical importance of cachexia. Despite reductions in overall lean mass, most previous work has focused on the loss of skeletal muscle. Few studies have assessed effects of cachexia on non-skeletal muscle types, such as the myocardium. Also, whereas pre-clinical models have been developed to elucidate the underlying effects of cancer cachexia on skeletal muscle, there remains a paucity of human data to inform the development of effective therapies.5

Although there is clear evidence that cancer therapy can negatively impact cardiac muscle function,6 it is less clear if tumour growth alone is sufficient to cause either cardiac atrophy (similar to skeletal muscle wasting) or cardiac dysfunction. Springer and colleagues now add to a growing body of literature suggesting that tumours can lead specifically to atrophy and dysfunction of cardiac tissue.7 Furthermore, they show that these effects …