IMR Press / RCM / Volume 21 / Issue 4 / DOI: 10.31083/j.rcm.2020.04.154
Open Access Review
Epidemiology and pathogenesis of heart failure with preserved ejection fraction
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1 Division of Cardiology, Department of Medicine, Texas Tech Health Sciences Center, Lubbock, 79430, TX, USA
Rev. Cardiovasc. Med. 2020 , 21(4), 531–540;
Submitted: 28 July 2020 | Revised: 25 October 2020 | Accepted: 27 October 2020 | Published: 30 December 2020

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.

diastolic dysfunction
oxidative stress
myocardial remodeling
Fig. 1.
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