Abstract
Heart failure with preserved ejection fraction (HFpEF) is a multifaceted disease resulting from a wide range of comorbidities. Obesity and diabetes are the main factors in the formation of HFpEF due to increased epicardial adipose tissue (EAT) volume. Stratification of HFpEF patients based on phenotypes leads to new classifications, including HFpEF phenotypes with obesity and DM. There is a close relationship between EAT volume and HFpEF. Patients with HFpEF can be further classified according to EAT volume using advanced imaging techniques, including сardiovascular magnetic resonance and computed tomography. EAT functions as an endocrine tissue that promotes myocardial inflammation. In addition, EAT dilatation acts as a spaceoccupying lesion, resulting in decreased functional pericardial volume, increased ventricular filling pressure, and increased ventricular coupling (interaction). Nonpharmacological lifestyle interventions, lipid-lowering therapy, and fat-modulating antidiabetic agents such as metformin, sodium-glucose cotransporter-2 inhibitors, or glucagon-like peptide 1 agonists are capable of inducing EAT regression may be particularly effective for this subgroup of patients. The direct effects of sodiumglucose
cotransporter-2 inhibitor, and glucagon-like peptide-1 agonist on HFpEF are currently under clinical investigation. Clinical trial data indicate that morbidity and long-term mortality rates in type 2 diabetes patients with HFpEF are higher than in patients without diabetes. One of the major obstacles to the clinical therapy for HFpEF is the poorly understood pathophysiology of HFpEF, making drug development a challenging task. Several potential therapeutic targets have currently been identified. Thus, upcoming drug development requires a more comprehensive approach not only for the comorbidities of HFpEF, but also for its classification and phenotypic identification.
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