Heart Failure With Preserved Ejection Fraction

Abstract

Of the estimated 5 million patients in the US diagnosed with heart failure (HF), approximately 50% have HF with preserved ejection fraction (HFpEF), 1,2 and its prevalence is increasing by about 1% annually relative to that of heart failure with reduced ejection fraction (HFrEF). 3 The mortality associated with HF is substantial, and HF was estimated to account for more than 80 000 deaths annually in the US as of 2017. 4 In addition, because HF is projected to account for an estimated $69.8 billion in annual health care spending by 2030, HFpEF represents an important public health issue that will increase as the population ages, with a concurrent increasing prevalence of associated risk factors, including hypertension, obesity, and diabetes. 4 However, the science underpinning the management of HFrEF and HFpEF is quite different. Patients with HFrEF are

Changes in left ventricular size, geometry, pump function and left heart pressures during healthy aging

“…The cause of the symptoms and signs in heart failure with preserved EF (HFpEF) has generally been assumed to be diastolic dysfunction, but the nature of the changes in LV structure and function associated with the development of heart failure has been the source of considerable interest and debate [5][6][7][8]. Furthermore, the disappointing results from randomized trials of drug therapy in HFpEF [9][10][11][12] provides a compelling rationale for ongoing investigation into the pathophysiology of this condition.…”

Cardiovascular Endocrinology: Evolving Concepts and Updated Epidemiology of Relevant Diseases

“…Several studies estimate that as many as 40-60% of patients with heart failure (HF) have a normal (≥50%) LVEF ( 12 ). The proportion of patients with HF who have HFpEF is higher in older adults and appears to be increasing by about 1% annually relative to that of HF with reduced ejection fraction (HFrEF) ( 13 ).…”

Epigenetic Therapies for Heart Failure: Current Insights and Future Potential

“…Although novel drugs have successfully entered the clinical arena of heart failure with reduced ejection fraction (HFrEF), such as the PARADIGM-HF-derived angiotensin receptor neprilysin inhibitor (ARNI), disease-modifying therapies with a prognostic impact for patients affected by heart failure with preserved ejection fraction (HFpEF) are still lacking. [1][2][3][4][5] HF is a complex and highly prevalent syndrome for which the heart undergoes a substantial structural remodeling in patients at risk for major cardiovascular diseases (CVDs) (Figure 1). [1][2][3][4][5][6] Gene-environment interactions can be mediated by specific patterns of epigenetic-sensitive changes (mainly DNA methylation and histone modifications) which may modulate the individual responsiveness to HF development.…”

“…[1][2][3][4][5] HF is a complex and highly prevalent syndrome for which the heart undergoes a substantial structural remodeling in patients at risk for major cardiovascular diseases (CVDs) (Figure 1). [1][2][3][4][5][6] Gene-environment interactions can be mediated by specific patterns of epigenetic-sensitive changes (mainly DNA methylation and histone modifications) which may modulate the individual responsiveness to HF development. [6][7][8][9][10][11][12][13][14] This complex molecular circuit seems to trigger early cardiomyocyte loss, cardiac-remodeling, and micro-and macrovascular damage contributing to the development of major CVDs which may lead to differential HF clinical phenotypes.…”