Key result
Epicardial adipose tissue and the pericardium link to HFpEF and emerge as potential therapeutic targets.
Why the study?
HFpEF incidence and prevalence are increasing, with the obesity-associated phenotype being the most frequent, and both epicardial adipose tissue and pericardial restriction are linked to HFpEF.
This review highlights the pathophysiological role of epicardial adipose tissue and the pericardium in HFpEF, particularly the obesity phenotype, and explores their potential as therapeutic targets.
May inform future HFpEF trials targeting epicardial fat; leaves open clinical efficacy pending interventional data.
Heart failure is an important cause of mortality and morbidity worldwide. Heart failure with preserved ejection fraction (HFpEF) incidence and prevalence is increasing, and the phenotype associated with obesity is the most frequent. Epicardial adipose tissue (EAT) is directly associated with systemic obesity and several previous studies have shown a clear link between EAT and HFpEF. Moreover, the restriction induced by the pericardium is also linked to HFpEF. In this review we will describe the epidemiological association between the pericardium, EAT and HFpEF, how to quantify EAT, what are the pathophysiological mechanism to explain theses association and how can the pericardium and EAT be a treatment target in patients with HFpEF.
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Timóteo et al. (2024) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Pericardium and epicardial adipose tissue targeting was evaluated. Epicardial adipose tissue and the pericardium are pathophysiologically linked to heart failure with preserved ejection fraction and represent potential therapeutic targets.
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