Abstract
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with diverse etiologies and pathophysiological factors. Obesity and type 2 diabetes mellitus (T2DM), conditions that coexist frequently, induce a cluster of metabolic and non-metabolic signaling derangements which are in favor to induce inflammation, fibrosis, myocyte stiffness, all hallmarks of HFpEF. In contrast to other HFpEF risk factors, obesity and T2DM are often associated with the generation of enlarged epicardial adipose tissue (EAT). EAT acts as an endocrine tissue that may exacerbate myocardial inflammation and fibrosis via various paracrine and vasocrine signals. In addition, an abnormally large EAT poses mechanical stress on the heart via pericardial restrain. HFpEF patients with enlarged EAT may belong to a unique phenotype that can benefit from specific EAT-targeted interventions, including life-style modifications and pharmacologically via statins and fat modifying anti-diabetics drugs; like metformin, sodium-glucose cotransporter 2 inhibitors, or glucagon-like peptide-1 receptor agonists, respectively.
Highlights
One-half of heart failure (HF) patients have a preserved ejection fraction (HFpEF), with rising prevalence in the United States of America and Western populations [1, 2]
Stratifying Heart failure with preserved ejection fraction (HFpEF) patients based on phenotypic data results in novel classifications including obese and diabetic HFpEF phenotypes
There is a close association between epicardial adipose tissue (EAT) volume and HFpEF
Summary
One-half of heart failure (HF) patients have a preserved ejection fraction (HFpEF), with rising prevalence in the United States of America and Western populations [1, 2]. The pathophysiology of HFpEF is complex, exacerbated by a variety of comorbidities including age, hypertension, renal dysfunction, diabetes mellitus (DM), and obesity [4, 5], and may reflect different phenotypes and differences in pathology [6]. This could be especially important for the obese and DM subgroup of HFpEF. In dispersion through large outcome studies and registries, around 80% of HFpEF patients are obese and 20–45% have type 2 DM (T2DM) [7,8,9,10]. Thirty-percent of HFpEF patients have both obesity and T2DM [11]. HFpEF is perceived as an inflammatory cardiometabolic disease, which includes all major mechanisms discussed in
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