Cardiometabolic Crossroads: Obesity, Sleep-Disordered Breathing, and Epicardial Adipose Tissue in Heart Failure with Preserved Ejection Fraction – A Mini-Review

Abstract

Abstarct Obesity, a multifaceted metabolic disorder, stands out as a significant risk factor in the development of heart failure with preserved ejection fraction (HFpEF). Its involvement in HFpEF pathogenesis encompasses a complex interplay with adipose tissue, particularly epicardial adipose tissue (EAT), and the effects of sleep-disordered breathing (SDB). Understanding these intricate relationships is pivotal for devising targeted therapeutic approaches to alleviate the burden of HFpEF in individuals with obesity. EAT assumes a central role in linking obesity to HFpEF. As it expands in the context of obesity, EAT contributes to systemic inflammation and insulin resistance, fostering an environment conducive to cardiac remodeling and dysfunction. Furthermore, SDB, prevalent comorbidity in the obese population, emerges as a significant mediator in HFpEF pathogenesis through various mechanisms. The convergence of obesity, EAT expansion, and SDB creates a synergistic effect, heightening the risk of HFpEF development. On the pharmaceutical front, ongoing investigations explore novel strategies targeting inflammation, oxidative stress, and metabolic pathways associated with obesity. These include the potential roles of sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, offering innovative therapeutic avenues for managing HFpEF in individuals with obesity. In addition, lifestyle modifications such as weight management and interventions addressing SDB and EAT reduction emerge as promising approaches for preventing and managing HFpEF in the obese population. These interventions hold the potential to mitigate obesity-related cardiac risks and improve HFpEF outcomes.