1,721,000 research outputs found
Management of chronic heart failure: state of the art according to the 2021 guideline
No full textDie Therapie der Herzinsuffizienz mit reduzierter Ejektionsfraktion (HFrEF) umfasst mittlerweile vier Substanzgruppen, deren Gabe möglichst gleichzeitig begonnen und rasch aufdosiert werden soll. Alle vier verfügen über eine Klasse-I-Empfehlung. Sacubitril/Valsartan kann nun auch in der Initialtherapie ohne vorherige Angiotensin-converting-enzyme-Hemmer-Gabe eingesetzt werden. Der Einsatz von Dapagliflozin und Empagliflozin erfolgt unabhängig von einem Diabetes mellitus zur Verbesserung von Mortalität und herzinsuffizienzbedingten Krankenhausaufnahmen. Die meisten medikamentösen Therapieempfehlungen für die HFrEF lassen sich auf die Herzinsuffizienz mit mild reduzierter Ejektionsfraktion übertragen, obgleich die Evidenzlage hier weniger robust ist. Die Individualisierung der Therapie berücksichtigt Komorbiditäten wie Vorhofflimmern, Klappenerkrankungen und Eisenmangel sowie fortgeschrittene Herzinsuffizienz, wobei nach stattgehabter Dekompensation Vericiguat als neues Reservepräparat zur Verfügung steht.Treatment of heart failure with reduced ejection fraction (HFrEF) requires four drug classes that should be initiated simultaneously and up-titrated rapidly. All four have received class I recommendations. Sacubitril/valsartan can be considered in initial treatment, even for patients in whom no previous treatment with an angiotensin converting enzyme inhibitor has been given. Treatment with dapagliflozin and empagliflozin is started irrespective of diabetes mellitus to reduce mortality and hospitalization rates for heart failure. Most drug treatment recommendations for HFrEF can be extrapolated to heart failure with mildly-reduced ejection fraction, even though the evidence base is not as robust as in HFrEF. Treatment individualization considers co-morbidities such as atrial fibrillation, valvular disease and iron deficiency as well as advanced heart failure. Following cardiac decompensation, verciguat is now available as an additional treatment option
The role of microRNAs in critical illness—do miRs truly ‘miRror’ muscle wasting?
No full textOpen-Access-Publikationsfonds 202
The patient above all else: Introducing JCSM Clinical Reports A legitimate crown princess, daughter of the Journal of Cachexia, Sarcopenia and Muscle
No full textnot availabl
The fatter, the better in old age: the current understanding of a difficult relationship
No full textPurpose of review
Obesity has shown a protective effect on mortality in older adults, also known as the obesity paradox, but there are still controversies about this relationship.
Recent findings
Recent studies have shown a J or U-shaped relationship between BMI and mortality, wherein an optimal range is described between 22 and 37 kg/m2 depending on the condition. Many mechanisms can explain this protective effect of higher BMI, fat/muscle mass storage, more aggressive treatment in obese individuals, loss of bone mineral content and selection bias. However, BMI must be used with caution due to its limitations to determine body composition and fat distribution.
Summary
Although BMI is an easy tool to evaluate obesity, its protective effect may be present to certain extend, from normal range to class I obesity (BMI 30–34.9 kg/m2), but then it becomes detrimental. Skeletal muscle mass and muscle function associated with adipose tissue assessment can add valuable information in the risk stratification. Further studies should be performed prospectively, adjust BMI for cofounding variable and consider other elderly subpopulations. To promote healthy ageing, excessive fat mass should be avoided and maintenance or improvement of skeletal muscle mass and muscle function should be stimulated in older adults
The patient above all else: Introducing JCSM Clinical Reports A legitimate crown princess, daughter of the Journal of Cachexia, Sarcopenia and Muscle
No full textnot availabl
Recent developments in the field of cachexia, sarcopenia, and muscle wasting: highlights from the 11th Cachexia Conference
No full textAbstract This article highlights the updates from preclinical and clinical studies into the field of wasting disorders that were presented at the 11th Cachexia Conference held in Maastricht, the Netherlands, in December 2018. Herein, we summarize the biological and clinical significance of different markers and new diagnostic tools and cut‐offs for the detection of skeletal muscle wasting, including micro‐RNAs, siRNAs, epigenetic targets, the ubiquitin–proteasome system, mammalian target of rapamycin signalling, news in body composition analysis including the D3‐creatine dilution method, and electrocardiography that was modified to enable segmental impedance spectroscopy. Of particular interest were the beneficial effects of BIO101 on muscle cell differentiation, hypertrophy of myofibers associated with mammalian target of rapamycin pathways activation, and the effect of metal ion transporter ZIP14 loss that reduces cancer‐induced cachexia. The potential of anti‐ZIP14 antibodies and zinc chelation as anti‐cachexia therapy should be tested in patients with cancer cachexia. Big randomized studies were presented such as RePOWER (observational study of patients with primary mitochondrial myopathy), STRAMBO (influence of physical performance assessed as score and clinical testing), MMPOWER (treatment of elamipretide in subjects with primary mitochondrial myopathy), FORCE (examined differences in relative dose intensity and moderate and severe chemotherapy‐associated toxicities between a strength training intervention and a control group), and SPRINTT (effectiveness of exercise training in healthy aging). Effective treatments were urothelin A, rapamycin analogue treatment, epigenetic factor BRD 4 and epigenetic protein BET, and the gut pathobiont Klebsiella oxytoca. Clinical studies that investigated novel approaches, including urolithin A, the role of gut microbiota, metal ion transporter ZIP14, lysophosphatidylcholine and lysophosphatidylethanolamine, and BIO101, were described. It remains a fact, however, that effective treatments of cachexia and wasting disorders are urgently needed in order to improve patients' quality of life and their survival
Sarcopenia and Frailty in Heart Failure: Is There a Biomarker Signature?
No full textPURPOSE OF REVIEW: Sarcopenia and frailty are common in patients with heart failure (HF) and are strongly associated with prognosis. This review aims to examine promising biomarkers that can guide physicians in identifying sarcopenia and frailty in HF. RECENT FINDINGS: Traditional biomarkers including C-reactive protein, aminotransaminase, myostatin, and urinary creatinine as well as novel biomarkers including microRNAs, suppression of tumorigenicity 2 (ST2), galectin-3, and procollagen type III N-terminal peptide may help in predicting the development of sarcopenia and frailty in HF patients. Among those biomarkers, aminotransferase, urinary creatinine, and ST2 predicted the prognosis in HF patients with sarcopenia and frailty. SUMMARY: This review outlines the current knowledge of biomarkers that are considered promising for diagnosing sarcopenia and frailty in HF. The listed biomarkers might support the diagnosis, prognosis, and therapeutic decisions for sarcopenia and frailty in HF patients
Myostatin inhibitors as pharmacological treatment for muscle wasting and muscular dystrophy
No full textMyostatin, a member of the transforming growth factor beta (TGF‐β) superfamily that is highly expressed in skeletal muscle, was first described in 1997. It has been known that loss of myostatin function induces an increase in muscle mass in mice, cow, dogs and humans. Therefore, myostatin and its receptor have emerged as a therapeutic target for loss of skeletal muscle such as sarcopenia and cachexia, as well as muscular dystrophies. At the molecular level, myostatin binds to and activates the activin receptor IIB (ActRIIB)/Alk 4/5 complex. Therapeutic approaches therefore are being taken both pre‐clinically and clinically to inhibit the myostatin signaling pathway. Several myostatin inhibitors , including myostatin antibodies, anti‐myostatin peptibody, activin A antibody, soluble (decoy) forms of ActRIIB (ActRⅡB‐Fc), anti‐myostatin adnectin, ActRⅡB antibody have been tested in the last decade. The aim of this review is to present the current knowledge of several myostatin inhibitors as a therapeutic approach for patients with loss of skeletal muscle.Open-Access-Publikationsfonds 201
- …
