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Epidemiology and pathogenesis of heart failure with preserved ejection fraction
1Division of Cardiology, Department of Medicine, Texas Tech Health Sciences Center, Lubbock, 79430, TX, USA.
Insights
Heart failure with preserved ejection fraction (HFpEF) affects millions, with rising incidence and complex causes. Understanding its multifaceted pathophysiology is key to developing effective treatments for this challenging condition.
Area of Science:
- Cardiology
- Internal Medicine
Background:
- Heart failure (HF) impacts 6.5 million US adults, with heart failure with preserved ejection fraction (HFpEF) accounting for about half.
- HFpEF is a significant contributor to reduced quality of life, increased healthcare utilization, and premature mortality.
- The incidence of HFpEF has been increasing, while heart failure with reduced ejection fraction (HFrEF) incidence has declined.
Purpose of the Study:
- To review the epidemiology and pathophysiology of heart failure with preserved ejection fraction (HFpEF).
- To highlight the challenges in treating HFpEF due to its diverse etiologies.
- To explore recent findings in myocardial remodeling and potential therapeutic targets.
Main Methods:
- Review of epidemiological data on HF and HFpEF incidence trends.
- Analysis of the multifaceted pathophysiology of HFpEF, including inflammation, fibrosis, and ventricular-vascular coupling.
- Examination of novel insights into myocardial remodeling, fibroblast behavior, and reactive oxygen species (ROS) in HFpEF.
Main Results:
- HFpEF incidence increased from 48% to 57% between 2000 and 2007, stabilizing around 52% by 2010.
- HFpEF pathophysiology involves complex interactions including inflammation, endothelial dysfunction, cardiomyocyte hypertrophy, fibrosis, ventricular-vascular uncoupling, pulmonary hypertension, and chronotropic incompetence.
- Apoptosis-resistant fibroblasts and upregulated ROS are implicated in myocardial matrix abnormalities, driving HFpEF initiation and progression.
Conclusions:
- Identifying risk factors and etiologies is crucial for optimizing HFpEF management.
- Abnormal fibroblasts and ROS present potential therapeutic targets for halting HFpEF progression.
- Further research into HFpEF pathophysiology may uncover new avenues for targeted therapies.
Abstract:
Heart failure (HF) is a complex syndrome that affects approximately 6.5 million adults in the United States. About half of the 6.5 million adults with HF are estimated to be individuals with heart failure with preserved ejection fraction (HFpEF). It is a common cause for poor quality of life, increased health-care resource utilization, and early mortality. HF incidence has risen to epidemic proportions in the recent years. This review attempts to address the epidemiology and pathophysiology of HFpEF. The incidence of HFpEF increased from 48% to 57% from 2000 to 2007 with a slight decrease in 2010 to 52%. The temporal trends in heart failure show an overall stable incidence of HF over the last two decades with increasing incidence of HFpEF and decreasing HFrEF incidence. Many etiologies contribute to the development of HFpEF which makes the treatment very challenging. Pathophysiology of HFpEF is multifaceted stemming from several disease-specific aspects of inflammation and endothelial function, cardiomyocyte hypertrophy and fibrosis, ventricular-vascular uncoupling, pulmonary hypertension and chronotropic incompetence. Hence identifying the risk factors and etiologies is imperative to achieve optimal outcomes in this population. Newer insights into myocardial remodeling have led to an interesting finding of abnormal fibroblasts in HFpEF which are apoptosis resistant and initiate the development of an abnormal myocardial matrix resulting in initiation and progression of the disease. Upregulation of ROS has also been implicated in HFpEF. Further investigation could provide new avenues to target therapeutics specifically to stop initiation and progression of fibrosis.
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