Potential Mechanisms of Epicardial Adipose Tissue Influencing Heart Failure with Preserved Ejection Fraction

Qiuxuan Li1, Ur Rehman Muhib1, Xiaoteng Ma1

  • 1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing Key Laboratory of Precision Medicine of Coronary Atherosclerotic Disease, Clinical Center for Coronary Heart Disease, 100029 Beijing, China.

PubMed

Insights

Epicardial adipose tissue (EAT) significantly impacts heart failure with preserved ejection fraction (HFpEF). Understanding EAT

Area of Science:

  • Cardiology
  • Metabolic Diseases
  • Physiology

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is a growing global health concern, affecting approximately 50% of heart failure patients.
  • The aging population contributes to the increasing prevalence, morbidity, and mortality associated with HFpEF.
  • Epicardial adipose tissue (EAT), a visceral fat depot surrounding the heart, influences cardiac function, particularly diastolic function and exercise capacity.

Purpose of the Study:

  • To comprehensively review the potential mechanisms by which EAT influences the development and progression of HFpEF.
  • To explore the role of EAT in HFpEF, especially when co-occurring with metabolic diseases like obesity and diabetes.
  • To enhance the understanding and management strategies for HFpEF.

Main Methods:

  • This review synthesizes current research on the multifaceted roles of EAT in cardiac health.
  • It examines EAT's paracrine and autocrine functions, including the production of inflammatory factors and neurotransmitters.
  • The review considers EAT's impact on cardiac metabolism, cardiomyocyte structure, electrical activity, and pericardial vascular function.

Main Results:

  • EAT exerts multi-level effects on the heart, influencing inflammatory responses, energy metabolism, and cardiomyocyte integrity.
  • EAT's contribution to HFpEF is potentially exacerbated by co-existing metabolic conditions such as obesity and diabetes.
  • The review highlights the complex interplay between EAT and HFpEF pathophysiology.

Conclusions:

  • EAT is implicated as a significant factor in the pathogenesis of HFpEF.
  • Further research into the mechanistic links between EAT and HFpEF is crucial.
  • Targeting EAT presents a potential therapeutic avenue for improving HFpEF patient outcomes.

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