Heart failure

Ejection fraction preserved heart failure as a model disease for cardiopulmonary-renal syndrome: Importance of visceral fat expansion as a central pathological mechanism


This article was originally published here

Internist (Berl). October 6, 2021. doi: 10.1007 / s00108-021-01182-y. Online ahead of print.

ABSTRACT

Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with various underlying etiologies and pathophysiological factors. Obesity and type 2 diabetes mellitus (T2DM), diseases which frequently coexist, induce a set of metabolic and non-metabolic signaling disorders, which promote the induction of inflammation, fibrosis and myocytic stiffness, all representing characteristics of HFpEF. Unlike other risk factors for HFpEF, obesity and T2DM are often associated with the formation of enlarged visceral adipose tissue (VAT), which is a very active endocrine organ that can exacerbate inflammation and remodeling over time. fibrotic myocardial, renal and vascular tissue. via various paracrine and vasocrine signals. Abnormally large epicardial fat tissue (EAT) therefore not only causes mechanical constriction of the diastolic filling procedure of the heart, but is also associated with increased release of pro-inflammatory adipokines which trigger atrial fibrillation and altered blood parameters. left ventricular contraction. Obese patients with HFpEF therefore belong to a unique HFpEF phenotype with a particularly poor prognosis which could benefit from a phenotype-specific intervention oriented towards EAT. In addition to statins and anti-diabetic drugs such as metformin, glucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose transporter 2 (SGLT-2) inhibitors may also play an important role.

PMID: 34613426 | DOI: 10.1007 / s00108-021-01182-y


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