Heart Failure with Preserved Ejection Fraction: Mechanisms and Treatment Strategies

Abstract

Approximately half of all patients with heart failure (HF) have a preserved ejection fraction, and the prevalence is growing rapidly given the aging population in many countries and the rising prevalence of obesity, diabetes, and hypertension. Functional capacity and quality of life are severely impaired in heart failure with preserved ejection fraction (HFpEF), and morbidity and mortality are high. In striking contrast to HF with reduced ejection fraction, there are few effective treatments currently identified for HFpEF, and these are limited to decongestion by diuretics, promotion of a healthy active lifestyle, and management of comorbidities. Improved phenotyping of subgroups within the overall HFpEF population might enhance individualization of treatment. This review focuses on the current understanding of the pathophysiologic mechanisms underlying HFpEF and treatment strategies for this complex syndrome.

Keywords: heart failure; heart failure with preserved ejection fraction; pathophysiology; treatment.

Figure 1:

The pathophysiology of heart failure with preserved ejection fraction. Arrows show causal inter-relationships between components. Abbreviations: CVP, central venous pressure; DVI, diastolic ventricular interaction; LA, left atrial; LV, left ventricular. *Since it is uncertain whether autonomic dysfunction can connect to chronotropic, it is titled as “Abnormal Autonomic Regulation*”.

Figure 2:

Potential Treatment according to HFpEF phenogroups. Abbreviations: AF, atrial fibrillation; ERAs, endothelin receptor antagonists; GSN, greater splanchnic nerve; HFpEF, heart failure with preserved ejection fraction; MPO, myeloperoxidase; MRA, mineralocorticoid receptor antagonists; PCAs, prostacyclin analogues; PDEi, phosphodiesterase inhibitor; SGLT-2i, sodium-glucose transporter-2 inhibitor; Other abbreviations are as in Figure 1.