Epicardial Fat Expansion in Diabetic and Obese Patients With Heart Failure and Preserved Ejection Fraction—A Specific HFpEF Phenotype

Frontiers in Cardiovascular Medicine

Carsten Tschöpe²  Vivian Nelki²  Sebastian Kelle³  Sophie Van Linthout⁴  Ahmed Elsanhoury⁴ 

[1] Berlin Institute of Health at Charite (BIH), Universitätsmedizin Berlin, BIH Center for Regenerative Therapies (BCRT), Berlin, Germany;Department of Cardiology, Campus Virchow Klinikum (CVK), Charité Universitätsmedizin Berlin, Berlin, Germany;Department of Internal Medicine/Cardiology, German Heart Center Berlin, Berlin, Germany;German Center for Cardiovascular Research (DZHK), Partner Site Berlin, Berlin, Germany;

关键词: heart failure with a preserved ejection fraction;    epicardiac adipose tissue;    diabetes;    obesity;    SGLT2;    inhibitor;   

DOI  :  10.3389/fcvm.2021.720690

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown