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Updated: Jun 11, 2025

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF
Published on: March 29, 2024
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.
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.
Abstract:
Heart failure (HF) is the predominant terminal stage and the leading cause of mortality in cardiac disease. Heart failure with preserved ejection fraction (HFpEF) affects roughly 50% of HF patients globally. Due to the global aging population, the prevalence, morbidity, and mortality of HFpEF have gradually increased. Epicardial adipose tissue (EAT), as a key visceral adipose tissue around the heart, affects cardiac diastolic function and exercise reserve capacity. EAT closely adheres to the myocardium and can produce inflammatory factors, neurotransmitters, and other factors through autocrine or paracrine mechanisms, affecting the heart function by inflammatory response, cardiac metabolism and energy supply, cardiomyocyte structure and electrical activity, and pericardial vascular function. Currently, research on the mechanism and treatment methods of HFpEF is constantly improving. EAT may play a multi-level impact on the occurrence and development of HFpEF. This review also summarizes the potential impact of EAT on the heart in HFpEF combined with other metabolism-related diseases such as obesity or diabetes over other obesity-related measures, such as body mass index (BMI) or other adipose tissue. Above all, this review comprehensively summarizes the potential mechanisms by which EAT may affect HFpEF. The objective is to enhance our comprehension and management of HFpEF. Future research should delve into the mechanistic relationship between EAT and HFpEF, and investigate interventions aimed at EAT to improve the prognosis of patients with HFpEF.
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