Evidence map›Paper›PMID 32743732›Full record

ReviewCurrent heart failure reports2020

Heart Failure-Induced Skeletal Muscle Wasting.

Anastassios Philippou, Dimitrios Xanthis, Costas Chryssanthopοulos, Maria Maridaki, Michael Koutsilieris

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current heart failure reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Anastassios PhilippouDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 75 Micras Asias, Goudi, 115 27, Athens, Greece.ORCID 0000-0003-0047-3003
Dimitrios XanthisIntensive Care Unit, Laiko General Hospital, Athens, Greece.
Costas ChryssanthopοulosDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 75 Micras Asias, Goudi, 115 27, Athens, Greece.
Maria MaridakiDepartment of Sports Medicine & Biology of Physical Activity, Faculty of Physical Education and Sport Science, National and Kapodistrian University of Athens, Athens, Greece.
Michael KoutsilierisDepartment of Physiology, Medical School, National and Kapodistrian University of Athens, 75 Micras Asias, Goudi, 115 27, Athens, Greece. mkoutsil@med.uoa.gr.
National and Kapodistrian University of Athens · GRLaiko General Hospital of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewHeart failure (HF) is a structural or functional cardiac abnormality which leads to failure of the heart to deliver oxygen commensurately with the requirements of the tissues and it may progress to a generalized wasting of skeletal muscle, fat tissue, and bone tissue (cardiac cachexia). Clinically, dyspnea, fatigue, and exercise intolerance are some typical signs and symptoms that characterize HF patients. This review focused on the phenotypic characteristics of HF-induced skeletal myopathy as well as the mechanisms of muscle wasting due to HF and highlighted possible therapeutic strategies for skeletal muscle wasting in HF. RECENT

findingsThe impaired exercise capacity of those patients is not attributed to the reduced blood flow in the exercising muscles, but rather to abnormal metabolic responses, myocyte apoptosis and atrophy of skeletal muscle. Specifically, the development of skeletal muscle wasting in chronic HF is characterized by structural, metabolic, and functional abnormalities in skeletal muscle and may be a result not only of reduced physical activity, but also of metabolic or hormonal derangements that favour catabolism over anabolism. In particular, abnormal energy metabolism, mitochondrial dysfunction, transition of myofibers from type I to type II, muscle atrophy, and reduction in muscular strength are included in skeletal muscle abnormalities which play a central role in the decreased exercise capacity of HF patients. Skeletal muscle alterations and exercise intolerance observed in HF are reversible by exercise training, since it is the only demonstrated intervention able to improve skeletal muscle metabolism, growth factor activity, and functional capacity and to reverse peripheral abnormalities.

Indexed as

Energy MetabolismExerciseHeart FailureHumansMuscle, SkeletalMuscular AtrophyHeart failureMuscle atrophyMuscle wastingMyopathySarcopenia

Identifiers

PMID32743732
OpenAlexW3046495891

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.