New Study Reveals Link Between Obesity and Increased Risk of Heart Failure

Published On 2024-08-07 03:00 GMT   |   Update On 2024-08-07 03:00 GMT
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A recent study led by Johns Hopkins Medicine researchers and published in the journal Nature Cardiovascular Research revealed the impact of obesity on muscle structure in patients having a form of heart failure called heart failure with a preserved ejection fraction (HFpEF).
Over half of patients with heart failure have a preserved ejection fraction, a syndrome with substantial morbidity/mortality and few effective therapies. Its dominant comorbidity is now obesity, which worsens disease and prognosis.
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Myocardial data from patients with morbid obesity and heart failure with a preserved ejection fraction show depressed myocyte calcium-stimulated tension and disrupted gene expression of mitochondrial and lipid metabolic pathways abnormalities shared by human HF with a reduced EF but less so in heart failure with a preserved ejection fraction without severe obesity.
The impact of severe obesity on human heart failure with a preserved ejection fraction myocardial ultrastructure remains unexplored. Here the researchers assessed the myocardial ultrastructure in septal biopsies from patients with heart failure with a preserved ejection fraction using transmission electron microscopy.
They observed sarcomere disruption and sarcolysis, mitochondrial swelling with cristae separation and dissolution, and lipid droplet accumulation that was more prominent in the most obese patients with heart failure with a preserved ejection fraction and not dependent on comorbid diabetes.
Therefore, myocardial proteomics revealed associated reduction in fatty acid uptake, processing and oxidation and mitochondrial respiration proteins, particularly in very obese patients with heart failure with a preserved ejection fraction.
Ref: Meddeb, M., Koleini, N., Binek, A. et al. Myocardial ultrastructure of human heart failure with preserved ejection fraction. Nat Cardiovasc Res (2024). https://doi.org/10.1038/s44161-024-00516-x
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Article Source : Nature Cardiovascular Research

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