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The aging heart in focus: The advanced understanding of heart failure with preserved ejection fraction
Zhewei Zhang1, Yu Wang2, Xiangqi Chen3
1Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, National Health Commission Key Laboratory of Chronobiology, Development and Related Diseases of Women and Children Key Laboratory of Sichuan Province, Children's Medicine Key Laboratory of Sichuan Province, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, No.2222 Xinchuan Road, Chengdu 610041, China; Department of Cardiology and Laboratory of Cardiovascular Diseases, Institute of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, China; West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu 610041, China.
Insights
Heart failure with preserved ejection fraction (HFpEF) is the most common heart failure type. Advances in animal models and treatments like SGLT2 inhibitors are improving understanding and outcomes for this complex syndrome.
Area of Science:
- Cardiology
- Systemic Syndromes
- Geriatric Medicine
Background:
- Heart failure with preserved ejection fraction (HFpEF) is the most prevalent form of heart failure, affecting 50% of patients.
- Its incidence is rising in aging populations, presenting as a heterogeneous systemic syndrome influenced by factors like metabolic syndrome and hypertension.
- HFpEF involves multi-organ dysfunction, including the heart, lungs, muscles, and vasculature, with cellular abnormalities in cardiomyocytes, endothelial cells, fibroblasts, adipocytes, and immune cells.
Purpose of the Study:
- To provide a comprehensive review of the etiology, pathobiology, and molecular mechanisms of HFpEF.
- To discuss the utility and limitations of preclinical animal models in HFpEF research.
- To summarize recent therapeutic trials in both animal models and human patients, focusing on agents like SGLT2 inhibitors.
Main Methods:
- Literature review of recent advances in HFpEF research.
- Analysis of studies on systemic pathology and clinically relevant animal models.
- Examination of data from clinical trials investigating novel therapeutic interventions.
Main Results:
- Recent progress in animal models and systemic pathology has enhanced the understanding of HFpEF.
- Clinical trials with sodium-glucose cotransporter 2 inhibitors show promise for HFpEF treatment.
- The complex nature of HFpEF necessitates a multi-faceted approach involving cellular and organ-level investigations.
Conclusions:
- Improved understanding of HFpEF's complex etiology and pathobiology is crucial for developing effective treatments.
- Advances in preclinical models and targeted therapies offer new hope for improving clinical outcomes in HFpEF patients.
- Continued research into molecular mechanisms and therapeutic strategies is essential to combat the growing burden of HFpEF.
Abstract:
Heart failure with preserved ejection fraction (HFpEF) accounts for 50 % of heart failure (HF) cases, making it the most common type of HF, and its prevalence continues to increase in the aging society. HFpEF is a systemic syndrome resulting from many risk factors, such as aging, metabolic syndrome, and hypertension, and its clinical features are highly heterogeneous in different populations. HFpEF syndrome involves the dysfunction of multiple organs, including the heart, lung, muscle, and vascular system. The heart shows dysfunction of various cells, including cardiomyocytes, endothelial cells, fibroblasts, adipocytes, and immune cells. The complex etiology and pathobiology limit experimental research on HFpEF in animal models, delaying a comprehensive understanding of the mechanisms and making treatment difficult. Recently, many scientists and cardiologists have attempted to improve the clinical outcomes of HFpEF. Recent advances in clinically related animal models and systemic pathology studies have improved our understanding of HFpEF, and clinical trials involving sodium-glucose cotransporter 2 inhibitors have significantly enhanced our confidence in treating HFpEF. This review provides an updated comprehensive discussion of the etiology and pathobiology, molecular and cellular mechanisms, preclinical animal models, and therapeutic trials in animals and patients to enhance our understanding of HFpEF and improve clinical outcomes.
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