Left ventricular stiffening plays a pivotal role in the development of heart failure with preserved ejection fraction, highlighting the need for noninvasive assessment and targeted therapeutic strategies.
Left ventricular passive stiffness is a key contributor to the development of HFpEF and represents a critical therapeutic target.
The high prevalence of patients with heart failure (HF) with preserved ejection fraction (HFpEF) has highlighted the pivotal role of diastolic function in the development of HF. Abnormalities of diastolic function induce elevated left ventricular (LV) end-diastolic pressure, which leads to pulmonary edema and the symptoms of HF because the LV, left atrium and the pulmonary veins form 1 chamber while the mitral valve is opening. Thus, LV diastolic dysfunction results in the development of HF, in particular, HFpEF. LV stiffness mainly contributes to the transition to HFpEF, but noninvasive assessment and the therapeutic strategy for LV stiffness have not been fully established. This review will focus on the contribution of LV passive stiffness to the development of HFpEF and on the evaluation and treatment of LV stiffening based on insights gained from a hypertensive HFpEF animal model we have developed.
Sakata et al. (Tue,) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Left ventricular stiffening plays a pivotal role in the development of heart failure with preserved ejection fraction, highlighting the need for noninvasive assessment and targeted therapeutic strategies.