The pathophysiology of heart failure with preserved ejection fraction

Abstract

Approximately half of all patients with heart failure have preserved ejection fraction (HFpEF) and, as life expectancies continue to increase in western societies, the prevalence of HFpEF will continue to grow. In contrast to heart failure with reduced ejection fraction (HFrEF), no treatment has been proven in pivotal clinical trials to be effective for HFpEF, largely because of the pathophysiological heterogeneity that exists within the broad spectrum of HFpEF. This syndrome was historically considered to be caused exclusively by left ventricular diastolic dysfunction, but research has identified several other contributory factors, including limitations in left ventricular systolic reserve, systemic and pulmonary vascular function, nitric oxide bioavailability, chronotropic reserve, right heart function, autonomic tone, left atrial function, and peripheral impairments. Multiple individual mechanisms frequently coexist within the same patient to cause symptomatic heart failure, but between patients with HFpEF the extent to which each component is operative can differ widely, confounding treatment approaches. This Review focuses on our current understanding of the pathophysiological mechanisms underlying HFpEF, and how they might be mechanistically related to typical risk factors for HFpEF, including ageing, obesity, and hypertension.

Impairment of Coronary Flow Reserve Evaluated by Phase Contrast Cine‐Magnetic Resonance Imaging in Patients With Heart Failure With Preserved Ejection Fraction

“…Furthermore, a significant correlation between serum BNP level and CFR was also observed in this study. A previous study showed that BNP level is a prognostic marker for HFpEF 7. Our finding suggests that impairment of CFR might predict future cardiovascular events in HFpEF patients.…”

“…Outcomes for patients with HFpEF are poor and are similar to those of heart failure (HF) patients with reduced ejection fraction (EF) 1, 4. However, an effective treatment of HFpEF has not been identified because the precise pathophysiological mechanisms of HFpEF have not been fully elucidated 7. The pathophysiology of HFpEF is complex and multifactorial and includes diastolic dysfunction,8 myocardial ischemia, cardiomyocyte hypertrophy, cardiac inflammation,9 and endothelial dysfunction 10, 11…”

Hjertesvikt med bevart ejeksjonsfraksjon

“…This is independent of the use of negative chronotropic medication (such as betablockers). The phenomenon is probably an expression of either local desensitisation of beta-adrenergic receptors in the sinus node or global autonomic dysfunction (7,19).…”

“…Peripheral vascular function is compromised in HFpEF patients (7). Microvascular dysfunction affects the small vessels both in the coronary circulatory system and in peripheral organs.…”

“…In particular, long-axis myocardial shortening measured using strain-based techniques is reduced (7,16,18).…”