Key result
Neprilysin inhibitors show promise for HFpEF by boosting natriuretic peptide bioavailability and cGMP-PKG signaling.
Why the study?
Reduced cyclic guanosine-monophosphate-protein kinase G signaling contributes to worsening diastolic dysfunction in HFpEF, prompting evaluation of neprilysin inhibitors to restore natriuretic peptide bioavailability.
Does neprilysin inhibition improve outcomes in patients with heart failure with preserved ejection fraction?
Does neprilysin inhibition improve outcomes in patients with heart failure with preserved ejection fraction?
This review outlines the pathophysiological rationale and current evidence for using neprilysin inhibitors to target diastolic dysfunction in HFpEF.
May support trials of neprilysin inhibition in HFpEF; leaves open whether cGMP-PKG activation improves clinical outcomes.
Clinical and hemodynamic aggravation of heart failure with preserved ejection fraction (HFpEF) is largely due to progression of left ventricular (LV) diastolic dysfunction. The key role in the normal maintenance of diastolic function is played by a high level of activity of the intracellular signaling axis, cyclic guanosine-monophosphate-protein kinase G, the activity of which is significantly reduced in HFpEF. The activity of this axis can be increased by increasing the bioavailability of natriuretic peptides by blocking the enzyme neutral endopeptidase (neprilisin), which is responsible for the destruction of natriuretic peptides.This review presents experimental and clinical data on the use of neprilysin inhibitors in HFpEF and addresses prospects of this treatment.
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Овчинников et al. (2020) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Neprilysin inhibitors was evaluated. Neprilysin inhibitors increase natriuretic peptide bioavailability and activate the cGMP-PKG axis, representing a promising treatment for heart failure with preserved ejection fraction.
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