The dangerous liaison between epicardial adipose tissue and heart failure with preserved ejection fraction

Biase, Nicolò De; Punta, Lavinia Del; Pugliese, Nicola Riccardo

doi:10.1002/ejhf.2733

Cited by 2 publications

(3 citation statements)

References 15 publications

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“…The role of EAT appears to be related to inflammation, mechanical effects, and its proximity to the heart and major blood vessels. In the study of De Biase et al ., 1 greater EAT thickness showed an inverse correlation with peak VO 2 at cardiopulmonary exercise testing in both HFpEF and AS. When analysing the AS cohort, EAT thickness was directly related to indices of valve disease severity, including peak transvalvular velocity, mean transvalvular pressure gradient (at rest and peak exercise), and aortic valve calcium score and volume.…”

Section: Figurementioning

confidence: 82%

See 1 more Smart Citation

Aortic stenosis and heart failure with preserved ejection fraction: A shared phenotypic puzzle

Scotti,

Slipczuk,

Latib

2023

European J of Heart Fail

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Section: Figurementioning

confidence: 82%

“…In this issue of the Journal, De Biase et al 1 . compare the haemodynamic and metabolic characteristics of patients with degenerative severe AS versus patients with HFpEF.…”

Section: Figurementioning

confidence: 99%

Aortic stenosis and heart failure with preserved ejection fraction: A shared phenotypic puzzle

Scotti,

Slipczuk,

Latib

2023

European J of Heart Fail

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“…In particular, the interplay of cytokines such as TNF-α, IL-1β, IL-10, IL-4, and IL-13 seems to play a crucial role in modulating LV remodeling and myocardial fibrosis and repair in HFpEF [ 46 , 47 ]. EAT may represent the local mediator and promote proinflammatory adverse effects by expressing changes in the inflammasome and developing a proatherogenic transcriptional profile with increased synthesis of biologically active adipokines with proinflammatory properties [ 48 , 49 ]. This may be the case independently of the level of inflammation in other fat depots, supporting the hypothesis of a local, paracrine effect of EAT [ 17 , 50 ].…”

Section: Epicardial Adipose Tissue In Heart Failure With Preserved Ej...mentioning

confidence: 99%

The Different Pathways of Epicardial Adipose Tissue across the Heart Failure Phenotypes: From Pathophysiology to Therapeutic Target

Rossi

Gruebler

Monzo

et al. 2023

IJMS

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Epicardial adipose tissue (EAT) is an endocrine and paracrine organ constituted by a layer of adipose tissue directly located between the myocardium and visceral pericardium. Under physiological conditions, EAT exerts protective effects of brown-like fat characteristics, metabolizing excess fatty acids, and secreting anti-inflammatory and anti-fibrotic cytokines. In certain pathological conditions, EAT acquires a proatherogenic transcriptional profile resulting in increased synthesis of biologically active adipocytokines with proinflammatory properties, promoting oxidative stress, and finally causing endothelial damage. The role of EAT in heart failure (HF) has been mainly limited to HF with preserved ejection fraction (HFpEF) and related to the HFpEF obese phenotype. In HFpEF, EAT seems to acquire a proinflammatory profile and higher EAT values have been related to worse outcomes. Less data are available about the role of EAT in HF with reduced ejection fraction (HFrEF). Conversely, in HFrEF, EAT seems to play a nutritive role and lower values may correspond to the expression of a catabolic, adverse phenotype. As of now, there is evidence that the beneficial systemic cardiovascular effects of sodium-glucose cotransporter-2 receptors-inhibitors (SGLT2-i) might be partially mediated by inducing favorable modifications on EAT. As such, EAT may represent a promising target organ for the development of new drugs to improve cardiovascular prognosis. Thus, an approach based on detailed phenotyping of cardiac structural alterations and distinctive biomolecular pathways may change the current scenario, leading towards a precision medicine model with specific therapeutic targets considering different individual profiles. The aim of this review is to summarize the current knowledge about the biomolecular pathway of EAT in HF across the whole spectrum of ejection fraction, and to describe the potential of EAT as a therapeutic target in HF.

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The dangerous liaison between epicardial adipose tissue and heart failure with preserved ejection fraction

Cited by 2 publications

References 15 publications

Aortic stenosis and heart failure with preserved ejection fraction: A shared phenotypic puzzle

Aortic stenosis and heart failure with preserved ejection fraction: A shared phenotypic puzzle

The Different Pathways of Epicardial Adipose Tissue across the Heart Failure Phenotypes: From Pathophysiology to Therapeutic Target

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