scholarly journals Muscle Wasting and Sarcopenia in Heart Failure—The Current State of Science

2020 ◽  
Vol 21 (18) ◽  
pp. 6549
Author(s):  
Alessia Lena ◽  
Markus S. Anker ◽  
Jochen Springer
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Muscle Wasting ◽  
Current Knowledge ◽  
Strong Predictor ◽  
Ongoing Research ◽  
Cardiac Cachexia ◽  
Current State ◽  
Receptor Modulators

Sarcopenia is primarily characterized by skeletal muscle disturbances such as loss of muscle mass, quality, strength, and physical performance. It is commonly seen in elderly patients with chronic diseases. The prevalence of sarcopenia in chronic heart failure (HF) patients amounts to up to 20% and may progress into cardiac cachexia. Muscle wasting is a strong predictor of frailty and reduced survival in HF patients. Despite many different techniques and clinical tests, there is still no broadly available gold standard for the diagnosis of sarcopenia. Resistance exercise and nutritional supplementation represent the currently most used strategies against wasting disorders. Ongoing research is investigating skeletal muscle mitochondrial dysfunction as a new possible target for pharmacological compounds. Novel agents such as synthetic ghrelin and selective androgen receptor modulators (SARMs) seem promising in counteracting muscle abnormalities but their effectiveness in HF patients has not been assessed yet. In the last decades, many advances have been accomplished but sarcopenia remains an underdiagnosed pathology and more efforts are needed to find an efficacious therapeutic plan. The purpose of this review is to illustrate the current knowledge in terms of pathogenesis, diagnosis, and treatment of sarcopenia in order to provide a better understanding of wasting disorders occurring in chronic heart failure.

Exercise training leads to a reduction of elevated myostatin levels in patients with chronic heart failure

2011 ◽  
Vol 19 (3) ◽  
pp. 404-411 ◽  
Author(s):  
Karsten Lenk ◽  
Sandra Erbs ◽  
Robert Höllriegel ◽  
Ephraim Beck ◽  
Axel Linke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Serum Concentration ◽  
Late Stage ◽  
Healthy Subjects ◽  
Fold Increase ◽  
Control Group ◽  
Cardiac Cachexia

Background: In chronic heart failure (CHF), cardiac cachexia is often associated with the terminal stage of this disease. In animal studies it has been demonstrated that myostatin, a key regulator of skeletal muscle mass, is elevated in advanced stages of this syndrome. Design: The aim of the present study was to investigate the expression of myostatin in patients with late stage CHF (NYHA IIIb) in comparison to healthy subjects. Furthermore the effects of physical exercise on myostatin were analyzed. Methods: Twenty-four patients were either randomized to a sedentary control group (CHF-S) or exercise training (CHF-E). At baseline and after 12 weeks mRNA and myostatin protein in the peripheral skeletal muscle as well as myostatin serum concentration were measured. Furthermore 12 age-matched healthy men were compared to all patients at baseline (HC). Results: CHF patients showed a two-fold increase of myostatin mRNA ( p = 0.05) and a 1.7-fold ( p = 0.01) augmentation of protein content in skeletal muscle compared to healthy subjects. In late-stage CHF, exercise training led to a 36% reduction of the mRNA and a 23% decrease of the myostatin protein compared to baseline. The serum concentration of myostatin revealed no significant alteration between the groups. Conclusion: In the skeletal muscle, myostatin increases significantly in the course of CHF. The observed effects of a significant reduction of myostatin in skeletal muscle after 12 weeks of exercise training demonstrate the reversibility of molecular changes that might be able to halt the devastating process of muscle wasting in chronic heart failure.

scholarly journals A New Transgenic Mouse Model of Heart Failure and Cardiac Cachexia Raised by Sustained Activation of Met Tyrosine Kinase in the Heart

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Valentina Sala ◽  
Stefano Gatti ◽  
Simona Gallo ◽  
Enzo Medico ◽  
Daniela Cantarella ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Congestive Heart Failure ◽  
Body Weight ◽  
Transgenic Mouse ◽  
Muscle Wasting ◽  
Met Receptor ◽  
Cardiac Cachexia ◽  
New Model ◽  
Skeletal Muscle Wasting

Among other diseases characterized by the onset of cachexia, congestive heart failure takes a place of relevance, considering the high prevalence of this pathology in most European countries and in the United States, and is undergoing a rapid increase in developing countries. Actually, only few models of cardiac cachexia exist. Difficulties in the recruitment and follow-up of clinical trials implicate that new reproducible and well-characterized animal models are pivotal in developing therapeutic strategies for cachexia. We generated a new model of cardiac cachexia: a transgenic mouse expressing Tpr-Met receptor, the activated form of c-Met receptor of hepatocyte growth factor, specifically in the heart. We showed that the cardiac-specific induction of Tpr-Met raises a cardiac hypertrophic remodelling, which progresses into concentric hypertrophy with concomitant increase in Gdf15 mRNA levels. Hypertrophy progresses to congestive heart failure with preserved ejection fraction, characterized by reduced body weight gain and food intake and skeletal muscle wasting. Prevention trial by suppressing Tpr-Met showed that loss of body weight could be prevented. Skeletal muscle wasting was also associated with altered gene expression profiling. We propose transgenic Tpr-Met mice as a new model of cardiac cachexia, which will constitute a powerful tool to understand such complex pathology and test new drugs/approaches at the preclinical level.

TERAPI NUTRISI PADA PASIEN CARDIAC CACHEXIA ET CAUSA CHRONIC HEART FAILURE NYHA III DENGAN PENYULIT EDEMA PARU KARDIOGENIK AKUT

2020 ◽  
Vol 3 (1) ◽  
pp. 38-45
Author(s):  
Layle Rahmiyanti ◽  
Suryani As’ad ◽  
Nurbaya Syam
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Chronic Heart Failure ◽  
Muscle Wasting ◽  
Handgrip Strength ◽  
Cardiac Cachexia ◽  
Food Recall

Pendahuluan Cardiac cachexia (CC) adalah penurunan berat badan dengan/ tanpa muscle wasting pada pasien gagal jantung. Terapi nutrisi merupakan salah satu upaya untuk mencegah perburukan klinis CC. Laporan Kasus Ny.R, 54 tahun dikonsultasikan dengan diagnosa edema paru kardiogenik akut dan congestive heart failure NYHA III. Keluhan utama berupa masukan makan berkurang sejak 1 tahun dan memberat dalam 8 hari terakhir karena sesak  napas. Ada riwayat penurunan berat badan, namun tidak diketahui besar penurunannya. Tampak lemah dan sesak napas. Antropometri: TB 154 cm, LLA 19.5 cm. Terdapat kehilangan jaringan lemak subkutan dan muscle wasting tanpa edema. Handgrip strength 5.2 kg. Food recall 24 hour 343 kkal. Status gizi buruk berdasarkan SGA. Terapi nutrisi: kalori 1600 kkal diberikan bertahap, dengan komposisi makronutrien: karbohidrat 45-50%, protein 1.5 gr/kgBBI/hari dan lemak 32-37%. Diberikan nutrient spesifik berupa EPA dan BCAA. Suplementasi mikronutrien: zink, curcuma, vitamin Bkompleks, thiamin dan ekstrak ikan gabus. Setelah Pasien dipulangkan, kami lakukan pemantauan selama 8 bulan untuk menilai asupan kalori, berat badan dan kapasitas fungsional serta kepatuhan pasien terhadap program terapi nutrisi yang diberikan. Terdapat perbaikan klinis peningkatan asupan energi, berat badan yang stabil, dan peningkatan kapasitas fungsional. Kesimpulan Terapi nutrisi yang adekuat dan pemberian nutrient spesifik dapat mencegah perburukan CC.

scholarly journals Myostatin from the heart: local and systemic actions in cardiac failure and muscle wasting

2011 ◽  
Vol 300 (6) ◽  
pp. H1973-H1982 ◽  
Author(s):  
Astrid Breitbart ◽  
Mannix Auger-Messier ◽  
Jeffery D. Molkentin ◽  
Joerg Heineke
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Wasting ◽  
Muscle Growth ◽  
Skeletal Muscle Atrophy ◽  
Cardiac Cachexia ◽  
Heart Failure Patients ◽  
Skeletal Muscle Growth ◽  
Skeletal Muscle Wasting

A significant proportion of heart failure patients develop skeletal muscle wasting and cardiac cachexia, which is associated with a very poor prognosis. Recently, myostatin, a cytokine from the transforming growth factor-β (TGF-β) family and a known strong inhibitor of skeletal muscle growth, has been identified as a direct mediator of skeletal muscle atrophy in mice with heart failure. Myostatin is mainly expressed in skeletal muscle, although basal expression is also detectable in heart and adipose tissue. During pathological loading of the heart, the myocardium produces and secretes myostatin into the circulation where it inhibits skeletal muscle growth. Thus, genetic elimination of myostatin from the heart reduces skeletal muscle atrophy in mice with heart failure, whereas transgenic overexpression of myostatin in the heart is capable of inducing muscle wasting. In addition to its endocrine action on skeletal muscle, cardiac myostatin production also modestly inhibits cardiomyocyte growth under certain circumstances, as well as induces cardiac fibrosis and alterations in ventricular function. Interestingly, heart failure patients show elevated myostatin levels in their serum. To therapeutically influence skeletal muscle wasting, direct inhibition of myostatin was shown to positively impact skeletal muscle mass in heart failure, suggesting a promising strategy for the treatment of cardiac cachexia in the future.

Hormonal Changes and Catabolic/Anabolic Imbalance in Chronic Heart Failure and Their Importance for Cardiac Cachexia

Circulation ◽  
1997 ◽  
Vol 96 (2) ◽  
pp. 526-534 ◽  
Author(s):  
Stefan D. Anker ◽  
Tuan Peng Chua ◽  
Piotr Ponikowski ◽  
Derek Harrington ◽  
Jon W. Swan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Hormonal Changes ◽  
Cardiac Cachexia

Physical deconditioning may be a mechanism for the skeletal muscle energy phosphate metabolism abnormalities in chronic heart failure

1996 ◽  
Vol 131 (3) ◽  
pp. 560-566 ◽  
Author(s):  
Zukaï Chati ◽  
Faïez Zannad ◽  
Claude Jeandel ◽  
Brigitte Lherbier ◽  
Jean-Marie Escanye ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Phosphate Metabolism ◽  
Muscle Energy ◽  
Physical Deconditioning
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