Abstract
Modifications of lean mass are a frequent critical determinant in the pathophysiology and progression of heart failure (HF). Sarcopenia may be considered one of the most important causes of low physical performance and reduced cardiorespiratory fitness in older patients with HF. Sarcopenia is frequently misdiagnosed as cachexia. However, muscle wasting in HF has different pathogenetic features in sarcopenic and cachectic conditions. HF may induce sarcopenia through common pathogenetic pathways such as hormonal changes, malnutrition, and physical inactivity; mechanisms that influence each other. In the opposite way, sarcopenia may favor HF development by different mechanisms, including pathological ergoreflex. Paradoxically, sarcopenia is not associated with a sarcopenic cardiac muscle, but the cardiac muscle shows a hypertrophy which seems to be “not-functional.” First-line agents for the treatment of HF, physical activity and nutritional interventions, may offer a therapeutic advantage in sarcopenic patients irrespective of HF. Thus, sarcopenia is highly prevalent in patients with HF, contributing to its poor prognosis, and both conditions could benefit from common treatment strategies based on pharmacological, physical activity, and nutritional approaches.
Highlights
Heart failure (HF) is defined by the European Society of Cardiology (ESC) guidelines as “a clinical syndrome characterized by typical symptoms that may be accompanied by signs caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intra-cardiac pressures at rest or during stress” [1]
An increase in inflammatory markers was found in patients with heart failure (HF), a condition characterized by chronic low-level inflammation, which may exert sustained effects on cardiovascular function and on skeletal muscle, representing a fundamental crossing point between HF and sarcopenia
In this scenario it is important to consider how sarcopenia-related abnormalities in peripheral blood flow and skeletal muscle can play a key role in producing both objective limitations to exercise and in explaining the generation of the exercise-limiting symptoms of Interestingly, in the analysis of SICA-HF by Emami et al while both peak VO2 and quadriceps strength were significantly reduced in sarcopenia and cachexia, the 6-min walking test (6MWT), hand grip strength, and quality of life were only reduced in patients with sarcopenia, suggesting that in HF sarcopenia may be responsible for a more severe impairment of functional capacity and muscle strength compared to cachexia [7]
Summary
Heart failure (HF) is defined by the European Society of Cardiology (ESC) guidelines as “a clinical syndrome characterized by typical symptoms (e.g., breathlessness, ankle swelling and fatigue) that may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles and peripheral edema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intra-cardiac pressures at rest or during stress” [1]. HF affects up to 2% of the population in developed countries It leads to morbidity, institutionalization, and death, and it poses a major challenge to healthcare institutions worldwide [1]. Much of this rise primarily stems from the implementation of more effective therapeutics that have augmented life expectancy in individuals with HF [2]. In addition to cardiac dysfunction and reduced cardiac output, which are obviously required for defining HF, age-related muscle decline overlapping with “cardiac skeletal myopathy” may be considered the most important cause of low physical performance and reduced cardiorespiratory fitness in older patients with HF [3]. Sarcopenia and HF appear to present several similar pathogenetic pathways, and they could benefit from a common therapeutic approach
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