What is the primary principle underlying heart failure preserved ejection fraction (HFpEF)?

The primary principle underlying heart failure preserved ejection fraction (HFpEF) is related to the complex interplay of various pathophysiological mechanisms, with inflammation being a significant contributing factor. In HFpEF, the heart maintains a relatively normal ejection fraction, which indicates that the pumping ability of the heart is preserved. However, the diastolic function—how well the heart fills with blood—can be impaired.

In HFpEF, inflammation can lead to changes in the myocardial tissue, resulting in stiffness and impaired relaxation of the heart muscle. This local inflammation often contributes to the pathogenesis of HFpEF by promoting fibrosis, which reduces the heart's ability to fill properly during diastole. Consequently, individuals may experience symptoms of heart failure even with normal ejection fraction levels.

Fluid overload, although relevant in managing heart failure, relates more to the overall heart failure clinical picture rather than being a primary principle specifically for HFpEF. Ventilation-perfusion mismatch primarily is associated with respiratory conditions and does not directly define the mechanisms behind HFpEF. Similarly, while coronary artery obstruction can cause heart failure, it is more characteristic of heart failure with reduced ejection fraction (HFrEF) rather than HFpEF, where other factors such