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Review
. 2024 Jul 31;120(9):982-998.
doi: 10.1093/cvr/cvae073.

Biological basis and treatment of frailty and sarcopenia

Ryosuke Sato  1   2 , Mirela Vatic  1   2 , Guilherme Wesley Peixoto da Fonseca  3   4 , Stefan D Anker  5   6 , Stephan von Haehling  1   2
Affiliations
Review

Biological basis and treatment of frailty and sarcopenia

Ryosuke Sato et al. Cardiovasc Res. .

Abstract

In an ageing society, the importance of maintaining healthy life expectancy has been emphasized. As a result of age-related decline in functional reserve, frailty is a state of increased vulnerability and susceptibility to adverse health outcomes with a serious impact on healthy life expectancy. The decline in skeletal muscle mass and function, also known as sarcopenia, is key in the development of physical frailty. Both frailty and sarcopenia are highly prevalent in patients not only with advanced age but also in patients with illnesses that exacerbate their progression like heart failure (HF), cancer, or dementia, with the prevalence of frailty and sarcopenia in HF patients reaching up to 50-75% and 19.5-47.3%, respectively, resulting in 1.5-3 times higher 1-year mortality. The biological mechanisms of frailty and sarcopenia are multifactorial, complex, and not yet fully elucidated, ranging from DNA damage, proteostasis impairment, and epigenetic changes to mitochondrial dysfunction, cellular senescence, and environmental factors, many of which are further linked to cardiac disease. Currently, there is no gold standard for the treatment of frailty and sarcopenia, however, growing evidence supports that a combination of exercise training and nutritional supplement improves skeletal muscle function and frailty, with a variety of other therapies being devised based on the underlying pathophysiology. In this review, we address the involvement of frailty and sarcopenia in cardiac disease and describe the latest insights into their biological mechanisms as well as the potential for intervention through exercise, diet, and specific therapies.

Keywords: Biological mechanism; Frailty; Heart failure; Sarcopenia; Treatment.

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Conflict of interest statement

Conflict of interest: R.S. reports grants from Japan Heart Foundation/Bayer Yakuhin Research Grant Abroad, during the conduct of the study. S.D.A. reports grants and personal fees from Vifor Int, personal fees from Bayer, personal fees from Boehringer Ingelheim, personal fees from Servier, grants and personal fees from Abbott Vascular, personal fees from Cardiac Dimensions, personal fees from Actimed, personal fees from Astra Zeneca, personal fees from Amgen, personal fees from Bioventrix, personal fees from Janssen, personal fees from Respicardia, personal fees from V-Wave, personal fees from Brahms, personal fees from Cordio, personal fees from Occlutech, outside the submitted work. S.v.H. has been a paid consultant for and/or received honoraria payments from AstraZeneca, Bayer, Boehringer Ingelheim, BRAHMS, Chugai, Grünenthal, Helsinn, Hexal, Novartis, Pharmacosmos, Respicardia, Roche, Servier, Sorin, and Vifor. S.v.H. reports research support from Amgen, Boehringer Ingelheim, IMI, and the German Center for Cardiovascular Research (DZHK).

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