scholarly journals Cardiac Cachexia Associated With Valvular Heart Failure

Cureus ◽  
2021 ◽  
Author(s):  
Miguel A Rodriguez-Guerra ◽  
Neelanjana Pandey ◽  
Timothy J Vittorio
Circulation ◽  
1997 ◽  
Vol 96 (2) ◽  
pp. 526-534 ◽  
Author(s):  
Stefan D. Anker ◽  
Tuan Peng Chua ◽  
Piotr Ponikowski ◽  
Derek Harrington ◽  
Jon W. Swan ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Grzegorz Sobieszek ◽  
Radosław Mlak ◽  
Tomasz Powrózek ◽  
Marcin Mazurek ◽  
Aneta Skwarek-Dziekanowska ◽  
...  

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.


2020 ◽  
Vol 21 (18) ◽  
pp. 6549
Author(s):  
Alessia Lena ◽  
Markus S. Anker ◽  
Jochen Springer

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.


Global Heart ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e91
Author(s):  
R. Sánchez-Santillán ◽  
A. Orea-Tejeda ◽  
E. Arámbula-Garza ◽  
D. González-Islas ◽  
B. Santellano-Suárez ◽  
...  

2011 ◽  
Vol 19 (3) ◽  
pp. 404-411 ◽  
Author(s):  
Karsten Lenk ◽  
Sandra Erbs ◽  
Robert Höllriegel ◽  
Ephraim Beck ◽  
Axel Linke ◽  
...  

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.


2011 ◽  
Vol 141 (11) ◽  
pp. 1954-1960 ◽  
Author(s):  
André P. Lourenço ◽  
Francisco Vasques-Nóvoa ◽  
Dulce Fontoura ◽  
Carmen Brás-Silva ◽  
Roberto Roncon-Albuquerque ◽  
...  

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