Lean Mass Abnormalities in Heart Failure: The Role of Sarcopenia, Sarcopenic Obesity, and Cachexia

Carbone, Salvatore; Billingsley, Hayley; Rodriguez‐Miguelez, Paula; Kirkman, Danielle L.; Garten, Ryan S.; Franco, R. Lee; Lee, Duck-chul; Lavie, Carl J.

doi:10.1016/j.cpcardiol.2019.03.006

Cited by 102 publications

(98 citation statements)

References 242 publications

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“…In only a few patients, dyspnoea is due to pulmonary congestion and elevation in pulmonary capillary wedge pressures, as well as fatigue linked to muscle underperfusion [64]. 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 HF [65].…”

Section: Sarcopenia Muscle Fatigue and Dyspnea In Hfmentioning

confidence: 99%

Sarcopenia and Heart Failure

et al. 2020

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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.

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Section: Sarcopenia Muscle Fatigue and Dyspnea In Hfmentioning

confidence: 99%

Sarcopenia and Heart Failure

et al. 2020

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“…There have been mixed reports regarding the effect of creatine supplementation combined with PR on muscle strength and endurance in patients with COPD [35,36]. Fat-free mass (FFM), a surrogate measure of SMM and a major determinant of CRF [27,53], was increased with creatinine supplementation and PR [35,36]. This may, however, be due to intramuscular fluid retention, which would be read as an increase in FFM, and not necessarily SMM [35,36].…”

Section: Creatine Supplementation In Copdmentioning

confidence: 99%

“…Cardiac cachexia, or the concomitant loss of lean mass (LM) and FM, in advanced HF patients is linked to poor prognosis [27,107]. Gaps in understanding continue to exist, but multiple mechanisms are likely at play, including high levels of inflammation, alterations in hunger/satiety signaling, changes in energy metabolism, as well as poor perfusion leading to malabsorption in the gut [107].…”

Section: Nutrition Support Supplementation In Hfrefmentioning

confidence: 99%

“…When low physical performance accompanies these characteristics, sarcopenia is considered severe [132]. Sarcopenia affects 5-20% of the population above 60 and up to 50% of individuals over 80 years of age [27]. Individuals with sarcopenia have a reduced CRF compared to their non-sarcopenic peers, especially in the presence of high FM, a condition known as sarcopenic obesity [133][134][135][136].…”

Section: Sarcopenia and Frailtymentioning

confidence: 99%

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Lifestyle Interventions with a Focus on Nutritional Strategies to Increase Cardiorespiratory Fitness in Chronic Obstructive Pulmonary Disease, Heart Failure, Obesity, Sarcopenia, and Frailty

et al. 2019

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Cardiorespiratory fitness (CRF) is an independent predictor for all-cause and disease-specific morbidity and mortality. CRF is a modifiable risk factor, and exercise training and increased physical activity, as well as targeted medical therapies, can improve CRF. Although nutrition is a modifiable risk factor for chronic noncommunicable diseases, little is known about the effect of dietary patterns and specific nutrients on modifying CRF. This review focuses specifically on trials that implemented dietary supplementation, modified dietary pattern, or enacted caloric restriction, with and without exercise training interventions, and subsequently measured the effect on peak oxygen consumption (VO 2 ) or surrogate measures of CRF and functional capacity. Populations selected for this review are those recognized to have a reduced CRF, such as chronic obstructive pulmonary disease, heart failure, obesity, sarcopenia, and frailty. We then summarize the state of existing knowledge and explore future directions of study in disease states recently recognized to have an abnormal CRF.

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“…15,18 However, a major component of frailty is muscular strength, which is a very important predictor of CVD survival and overall survival. 19,20 At least in HF, there is evidence that increased body fat, besides providing higher metabolic reserves and having the opposite effect as cachexia, 20,21 also is associated with greater muscular strength, 21,22 which could provide benefit in patients recovering from TAVR. Thus, other potential benefits of relatively higher BMI in patients with AS might include resistance to HF, relatively efficient maintenance of blood pressure resisting presyncope or syncope, and improved healing of valve seating site after TAVR, minimizing risk of perivalvular AR, which is known to be an important risk factor for poor late survival.…”

Section: Discussionmentioning

confidence: 99%