Multivariate biomarker study for sarcopenia in heart failure

  • Research type

    Research Study

  • Full title

    Towards diagnosis of secondary sarcopenia as comorbidity in heart failure: a multivariate biomarker approach

  • IRAS ID

    324573

  • Contact name

    Masoud Isanejad

  • Contact email

    masoudi@liverpool.ac.uk

  • Sponsor organisation

    University of Liverpool

  • Clinicaltrials.gov Identifier

    UoL001725, University of Liverpool Sponsor Refrence

  • Duration of Study in the UK

    2 years, 0 months, 1 days

  • Research summary

    BACKGROUND

    Sarcopenia is the loss of muscle mass and strength. In comparison to primary sarcopenia (age-related sarcopenia), secondary sarcopenia occurs if other factors, including malignancy or organ failure, are evident in addition to aging. Secondary sarcopenia is highly common in patients with heart failure (Sarc-HF) (prevalence is 35%-69%), and has a significant negative impact on exercise capacity, weight-adjusted peak maximal oxygen consumption, left ventricular function and re-hospitalization rates and mortality. Altered appetite leading to reduced food intake, especially via mediators such as ghrelin, adiponectin and leptin that are involved in lipid and glucose metabolism, alongside the reduced capacity of exercise due to cardiac cachexia and changes in cardiac energy metabolism, lead to weight loss and an incremental rate of muscle tissue losses.

    AIM
    In this integrated study of NHS patients with heart failure (HF), our aim is to identify and test by a multivariate/multidimensional modelling of a panel of complementary biomarkers including body composition, circulating metabolites (metabolic profile), and functional tests for
    (1) early detection of otherwise subclinical HF
    (2) diagnostic assessment of clinically manifest HF-sarcopenia
    (3) the risk stratification of subjects with suspected or confirmed diagnosis
    (4) selection of an appropriate therapeutic intervention.
    CLINICAL PERSPECTIVE
    To investigate the hypothesis that muscle strength loss (sarcopenia) is the result of impaired energy metabolism and comorbidity-induced systemic inflammation, we developed a comprehensive analysis on circulating metabolites (metabolic profile) and circulating proteins via proteomics in the current study and to validate our results externally. Previous studies on HF comorbidities a) did not account for body composition and sarcopenia as a burden, b) they focused on single HF population mainly with not control group.

    Lay summary of study results:

    Heart failure is a condition where the heart can't pump blood as well as it should. Doctors have noticed that people with heart failure often have changes in the way their bodies process energy and fuel at a chemical level.

    This study looked at whether those chemical changes are worse in heart failure patients who are also physically weaker and less active, meaning they have less strength and stamina in everyday tasks like gripping, standing up from a chair, or walking. The researchers compared three groups: heart failure patients with poorer physical fitness, heart failure patients who were still physically capable, and healthy older adults without heart failure.

    They studied 25 people with heart failure and 29 healthy adults, all around 68 years old. Each person had their body composition, muscle strength, and activity levels measured, and the researchers analyzed chemical markers in their blood.

    The main findings were that heart failure patients with reduced physical fitness showed signs their bodies were struggling to produce and use energy properly, were breaking down muscle protein, and had higher levels of inflammation. One marker of stress and inflammation in the body was several times higher in the weaker patients than in healthy adults. They also found that a simple measure, hand-grip strength adjusted for body size, lined up well with how far and how fast people could walk, suggesting it could be a useful, easy way to gauge a heart failure patient's physical condition.

    In short, heart failure patients who are weaker and less active have a distinct chemical "fingerprint" tied to energy problems, muscle breakdown, and inflammation. These markers might one day become targets for treatments to help slow physical decline. The researchers are careful to note this was a snapshot study, so it can't prove cause and effect, and the promising grip-strength measure needs to be confirmed in larger studies.

  • REC name

    London - Queen Square Research Ethics Committee

  • REC reference

    23/PR/0050

  • Date of REC Opinion

    3 Apr 2023

  • REC opinion

    Further Information Favourable Opinion