Hypothesis: Myostatin is a mediator of cardiac cachexia

AbstractCardiac cachexia (CC) is an unfavorable metabolic syndrome leading to exacerbation of chronic heart failure (CHF) and a higher risk of death. The main factor contributing to the development of cachexia is the ongoing inflammatory process mediated by genes (e.g. Integrin Subunit Alpha M—ITGAM). The study aimed to assess the relationship between a single nucleotide polymorphism (SNP) -323G > A of the ITGAM and the occurrence of nutritional disorders in patients with CHF. 157 CHF patients underwent clinical and nutritional screening. Body composition was evaluated by bioelectrical impedance analysis (BIA). Patients with cachexia were characterized by significantly lower weight, body mass index (BMI), lower fat mass (FM), albumin, and hemoglobin. Lower values of BIA parameters: capacitance of membrane (Cm), phase angle (PA), and impedance ratio (Z200/Z5) were noted in women. Those patients demonstrated significantly higher values of creatinine, c-reactive protein (CRP), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and pulmonary artery systolic pressure (PASP). A significantly higher risk of cachexia was reported in patients: aged ≥ 74 years (OR 3.55), with renal failure (OR 3.75), New York Heart Association classification (NYHA) III-IV (OR 2.83), with moderate or severe malnutrition according to the score of subjective global assessment (SGA) (OR 19.01) and AA genotype of ITGAM gene (OR 2.03). Determination of the -323G > A SNP in the ITGAM may prove to be a useful marker (after confirmation in further studies and appropriate validation) in the assessment of the risk of nutritional disorders in patients with CHF.

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The Cardiac Cachexia Syndrome and its Consequences Related to Nursing Interventions in Patients with Heart Failure

European Journal of Cardiovascular Nursing ◽

10.1177/147451510200100408 ◽

2002 ◽

Vol 1 (4) ◽

pp. 302-302

Author(s):

Bengt Fridlund

Keyword(s):

Heart Failure ◽

Nursing Interventions ◽

Cardiac Cachexia ◽

Patients With Heart Failure ◽

Cachexia Syndrome

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

International Journal of Molecular Sciences ◽

10.3390/ijms21186549 ◽

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.

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Transapical Valve-in-Valve-in-Ring for Stenotic Mitral Valve Repair

Innovations Technology and Techniques in Cardiothoracic and Vascular Surgery ◽

10.1097/imi.0b013e3182a6940b ◽

2013 ◽

Vol 8 (5) ◽

pp. 376-380 ◽

Cited By ~ 2

Author(s):

Gry Dahle ◽

Kjell-Arne Rein ◽

Anders L. Jönsson

Keyword(s):

Mitral Valve ◽

Mitral Valve Repair ◽

Pacemaker Implantation ◽

Coronary Bypass ◽

Valve Repair ◽

Cardiac Cachexia ◽

Edwards Sapien ◽

Valve In Valve ◽

Pleura Effusion ◽

Valve Implantation

A 53-year-old woman, previously treated with irradiation and chemotherapy for Hodgkin lymphoma, was referred for redovalve surgery. She had had a pacemaker implantation and undergone coronary bypass surgery, mitral valve repair with a Carpentier-Edwards 28-mm Physio-annuloplasty ring, as well as a mechanical tricuspid valve replacement and a transfemoral CoreValve 26-mm implantation. She had cardiac cachexia, pleura effusion, and a failed mitral valve repair with stenosis. She was judged inoperable for open surgery but suitable for a transapical valve-in-valve implantation on partial femorofemoral bypass. A 26-mm Edwards SAPIEN XT aortic valve inversely mounted on the Ascendra + delivery catheter was balloon expanded into the Physio ring. During expansion, the introducer sheath remained too deep into the left ventricle and rotated the SAPIEN valve upward to the left atrium, creating the onset of a new mitral regurgitation and retaining the stenosis. Another Edwards SAPIEN XT 26-mm valve was then positioned into the first valve in a “valve-in-valve-in-ring” tandem configuration. Both valves were supported by the Physio ring. The stenosis and the regurgitation were thereafter eliminated.

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