Biomarkers and mechanisms associated with cancer-induced cardiac cachexia: A systematic review

Abstract

Cancer cachexia is a severe multifactorial syndrome¹ that affects up to 80% of patients with advanced cancer, causing death in 20–80% with no effective treatments.^{2, 3} It causes multi-organ alteration and loss of skeletal and cardiac (myocardium) muscle mass.^{4, 5} Cardiac muscle wasting may result from cardiac protein loss associated with increased oxygen consumption and energy expenditure, resulting in cardiac insufficiency.⁵ It is hypothesized that significant tissue inflammation and oxidative stress during cancer progression cause cardiac wasting-associated cardiomyopathy, such as a thinned ventricular wall, local tissue hypoxia and arrhythmias.⁶ This review provided available evidence of cancer-induced cardiac cachexia in human and non-human models by examining biomarkers and the contributing factors to the development and progression of cardiac cachexia. Investigation of the potential biomarkers affecting cardiac muscle wasting is essential for improving patient outcomes.

Our knowledge about the causes of cardiac cachexia in cancer remains limited and the possible mechanisms have only been explored in animal studies to date. A better understanding of the pathophysiology of cardiac cachexia may help to determine if targeted therapies can effectively block the upregulation of various genes and cytokines that initiate and facilitate cancer-induced cardiac cachexia. Understanding the distinct nature of cancer-related cardiac cachexia and what distinguishes it from other causes may also lead to finding targeted, effective treatments. Treating cardiac cachexia early and before clinical changes are noted may improve overall cardiac function and lead to better patient outcomes.

The authors have no conflicts of interest.