Abstract
Heart failure with preserved ejection fraction (HFpEF) is a multi-organ disorder that represents about 50% of total heart failure (HF) cases and is the most common form of HF in the elderly. Because of its increasing prevalence caused by the aging population, high mortality and morbidity, and very limited therapeutic options, HFpEF is considered as one of the greatest unmet medical needs in cardiovascular medicine. Despite its complex pathophysiology, numerous preclinical models have been established in rodents and in large animals to study HFpEF pathophysiology. Although age and sex differences are well described in HFpEF population, there are knowledge gaps in sex- and age-specific differences in established preclinical models. In this review, we summarize various strategies that have been used to develop HFpEF models and discuss the knowledge gaps in sex and age differences in HFpEF.
Highlights
Heart failure (HF) is a leading cause of death worldwide and its prevalence is estimated to be 1%–2% of the adult population in developed countries, rising to ≥10% among people over 70 years of age (McDonagh et al, 2021)
The myocardium of patient with HF with preserved ejection fraction (HFpEF) is characterized by structural remodeling and cellular abnormalities such as cardiomyocyte hypertrophy, fibrosis, and inflammation that eventually lead to diastolic dysfunction of left ventricle (Mishra and Kass, 2021)
Most of the pharmacological and device therapies for HFpEF investigated in completed clinical trials have been shown to be ineffective
Summary
Heart failure (HF) is a leading cause of death worldwide and its prevalence is estimated to be 1%–2% of the adult population in developed countries, rising to ≥10% among people over 70 years of age (McDonagh et al, 2021). Young male mice infused with angiotensin II develop hypertension and display preserved systolic function, cardiac fibrosis, increased LV hypertrophy, and diastolic dysfunction (Becher et al, 2012; Inoue et al, 2012; Westermann et al, 2012; Regan et al, 2015), which all are features of human HFpEF. Exercise intolerance and pulmonary congestion are observed in this model (Broderick et al, 2012; Ostler et al, 2014) These models of metabolic stress have marked obesity with (ob/ob and db/db mice) or without diabetes (Zucker rats) and develop cardiac features of HFpEF in both sexes. Sex differences in cardiac HFpEF features have been observed, but age differences have not been determined in these models
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