Key result
Cancer and cancer therapies, particularly anthracyclines, induce cardiac atrophy and dysfunction through complex mechanisms including altered protein metabolism, apoptosis, and mitochondrial damage.
Emphasizes the need for a multidisciplinary approach by cardiologists and oncologists to optimize care and limit cancer-associated cardiac atrophy and heart failure.
Warrants cardiac monitoring in anthracycline recipients; leaves open mechanism-specific cardioprotection for prospective trials.
Functional changes in the heart in patients with cancer can be a result of both the disease itself and various cancer therapies, and limiting cardiac damage has become an increasingly important issue as survival rates in patients with cancer have improved. Processes involved in cancer-induced cardiac atrophy may include cardiomyocyte atrophy and apoptosis, decreased protein synthesis, increased autophagy and proteolysis via the ubiquitin-proteosome system. Further to direct effects of malignancy on the heart, several chemotherapeutic agents are known to affect the myocardium, in particular the anthracyclines. The aim of this report is to review the effects of cancer and cancer treatment on the heart and what is known about the underlying mechanisms. Furthermore, clinical strategies to limit and treat cancer-associated cardiac atrophy are discussed, emphasising the benefit of a multidisciplinary approach by cardiologists and oncologists to optimise models of care to improve outcomes for patients with cancer.
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Sweeney et al. (2017) conducted a review in Cancer-associated cardiac atrophy. Cancer and cancer therapies was evaluated. Cancer and cancer therapies, particularly anthracyclines, induce cardiac atrophy and dysfunction through complex mechanisms including altered protein metabolism, apoptosis, and mitochondrial damage.
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