Loss of muscle mass: Current developments in cachexia and sarcopenia focused on biomarkers and treatment

Drescher, Cathleen; Konishi, Masaaki; Ebner, Nicole; Springer, Jochen

doi:10.1016/j.ijcard.2015.10.033

Cited by 43 publications

(54 citation statements)

References 122 publications

(95 reference statements)

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“…39 Therefore, patients are in dire needs for a specialized sarcopenia therapy. [41][42][43] As a result, the definition of sarcopenia (two standard deviations of normal muscle mass) has been modified to contain measurements of impaired physical function, such as slow walking speed and low grip strength. 35,40 This fact is exacerbated by the fact that no clinically validated biomarkers have been identified despite enormous research efforts both by academia and industry.…”

Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 99%

Skeletal muscle wasting in chronic heart failure

2018

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Patients suffering from chronic heart failure (CHF) show an increased prevalence (~20% in elderly CHF patients) of loss of muscle mass and muscle function (i.e. sarcopenia) compared with healthy elderly people. Sarcopenia, which can also occur in obese patients, is considered a strong predictor of frailty, disability, and mortality in older persons and is present in 5–13% of elderly persons aged 60–70 years and up to 50% of all octogenarians. In a CHF study, sarcopenia was associated with lower strength, reduced peak oxygen consumption (peak VO2, 1173 ± 433 vs. 1622 ± 456 mL/min), and lower exercise time (7.7 ± 3.8 vs. 10.22 ± 3.0 min, both P < 0.001). Unfortunately, there are only very limited therapy options. Currently, the main intervention remains resistance exercise. Specialized nutritional support may aid the effects of resistance training. Testosterone has significant positive effects on muscle mass and function, and low endogenous testosterone has been described as an independent risk factor in CHF in a study with 618 men (hazard ratio 0.929, P = 0.042). However, the use of testosterone is controversial because of possible side effects. Selective androgen receptor modulators have been developed to overcome these side effects but are not yet available on the market. Further investigational drugs include growth hormone, insulin‐like growth factor 1, and several compounds that target the myostatin pathway. The continuing development of new treatment strategies and compounds for sarcopenia, muscle wasting regardless of CHF, and cardiac cachexia makes this a stimulating research area.

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Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 99%

Skeletal muscle wasting in chronic heart failure

2018

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“…Such problems may be particularly important in patients admitted to the intensive care unit with sarcopenia being already present. [46][47][48][49] An interesting candidate biomarker Cterminal agrin fragment has been used in patients with HF 50 and in patients after acute stroke. Therefore, androgen deprivation appears to cause selective deficits in the biochemical leg muscle function, which may also play a role in patients with HF in whom the deficiency of anabolic hormones has been reported to play a major role and to have prognostic significance.…”

Section: Screening and Diagnosing Sarcopeniamentioning

confidence: 99%

Muscle wasting and sarcopenia in heart failure: a brief overview of the current literature

Haehling

2018

ESC Heart Failure

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“…1 Cachexia is characterized by an involuntary weight loss due to the atrophy of skeletal muscle with or without loss of adipose tissue 2 affecting~50-80% of patients with cancer and is the direct cause of 30% of cancer deaths. [4][5][6][7] Although several inflammatory, hormonal, and oxidative stress molecules have been suggested as markers of prognosis in cachexia, 8 there are no universally accepted specific biomarkers for this condition. Although impaired cardiac function in cancer patients is usually attributed to cardiotoxicity of anti-neoplastic therapies, the effects of cancer cachexia (CC) on cardiac atrophy and function have given rise to the hypothesis that CC itself results in cardiac atrophy and cardiac dysfunction, which lead to heart failure (HF), which is well supported by several pre-clinical studies.…”

Section: Introductionmentioning

confidence: 99%

Cardiac expression of neutrophil gelatinase‐associated lipocalin in a model of cancer cachexia‐induced cardiomyopathy

et al. 2018

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AimsCachexia is a severe consequence of cancer. Although cancer‐induced heart atrophy leads to cardiac dysfunction and heart failure (HF), biomarkers for their diagnosis have not been identified. Neutrophil gelatinase‐associated lipocalin (NGAL) is an aldosterone‐responsive gene increased in HF. We studied NGAL and its association with aldosterone levels in a model of cancer cachexia‐induced cardiomyopathy.Methods and resultsRats were injected with Yoshida 108 AH‐130 hepatoma cells to induce tumour. Cachectic rats were treated daily, for 16 days, with placebo or with 5 or 50 mg/kg/day of spironolactone. Cardiac function was analysed by echocardiography at baseline and at Day 11. Weight loss and atrophy of lean body and fat mass of cachectic rats were significantly attenuated by spironolactone. Cardiac dysfunction of tumour‐bearing rats was improved by spironolactone. Plasma aldosterone was up‐regulated from 337 ± 7 pg/mL in sham animals to 591 ± 31 pg/mL in the cachectic rats (P < 0.001 vs. sham). Treatment with 50 or 5 mg/kg/day of spironolactone reduced plasma aldosterone to 396 ± 22 and 391 ± 25 pg/mL (P < 0.01 vs. placebo). Plasma levels of NGAL were also increased in cachectic rats (1.462 ± 0.3603 μg/mL) than in controls (0.0936 ± 6 μg/mL, P < 0.001). Spironolactone treatment (50 mg/kg/day) significantly reduced cardiac mRNA and protein NGAL levels (P < 0.05 and P < 0.001 vs. placebo, respectively). NGAL mRNA and protein levels were overexpressed in cachectic animal hearts treated with placebo, compared with control (P < 0.05 and P < 0.01 vs. sham). Spironolactone treatment at 50 mg/kg/day reduced significantly cardiac NGAL (P < 0.05 and P < 0.001 vs. placebo).ConclusionsCancer cachexia induced increased levels of aldosterone and NGAL, contributing to worsening cardiac damage in cancer cachexia‐induced cardiomyopathy. Spironolactone treatment may greatly attenuate cardiac dysfunction and lean mass atrophy associated with cancer cachexia.

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Loss of muscle mass: Current developments in cachexia and sarcopenia focused on biomarkers and treatment

Cited by 43 publications

References 122 publications

Skeletal muscle wasting in chronic heart failure

Skeletal muscle wasting in chronic heart failure

Muscle wasting and sarcopenia in heart failure: a brief overview of the current literature

Cardiac expression of neutrophil gelatinase‐associated lipocalin in a model of cancer cachexia‐induced cardiomyopathy

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