Vericiguat for Heart Failure with Reduced Ejection Fraction
Authors:
- Carlo Mario LombardiCLCarlo Mario Lombardi
- Giuliana CiminoGCGiuliana Cimino
- Matteo PagnesiMPMatteo Pagnesi
- Andrea Dell’aQuilaAndrea Dell’aQuila
- Daniela TomasoniDTDaniela Tomasoni
- Alice RaveraARAlice Ravera
- Riccardo InciardiRiccardo Inciardi
- Valentina CarubelliVCValentina Carubelli
- Enrico VizzardiEVEnrico Vizzardi
- Savina NodariSavina Nodari
- Michele EmdinMEMichele Emdin
- Alberto AimoAAAlberto Aimo
Open Access
- 19 August 2021
- journal article
- review article
- Published by Springer Nature in Current Cardiology Reports
- Vol. 23 (10) , 1-7
Abstract
Purpose of Review: The nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway plays an important role in the regulation of cardiovascular function, and it is disrupted in heart failure (HF), resulting in decreased protection against myocardial injury. Impaired NO-sGC-cGMP signaling in HF is secondary to reduced NO bioavailability and altered redox state of sGC, which becomes less responsive to NO. The sGC activator cinaciguat increases cGMP levels by direct NO-independent activation of sGC and may be particularly effective in conditions of increased oxidative stress and endothelial dysfunction, and therefore reduced NO levels, at the expense of a greater risk of hypotension. Conversely, sGC stimulators (riociguat and vericiguat) enhance sGC sensitivity to endogenous NO, thus exerting a more physiological action.Recent Findings: Clinical trials have suggested the benefit of vericiguat in patients with high-risk HF; in particular, a lower incidence of death from cardiovascular causes or HF hospitalization.Summary: Adding vericiguat may be considered in individual patients with HF, and reduced left ventricular ejection fraction (HFrEF) particularly those at higher risk of HF hospitalization.Keywords
Funding Information
- Università degli Studi di Brescia
This publication has 42 references indexed in Scilit:
- The cGMP Signaling Pathway as a Therapeutic Target in Heart Failure With Preserved Ejection FractionJournal of the American Heart Association, 2013
- Dual Angiotensin Receptor and Neprilysin Inhibition as an Alternative to Angiotensin-Converting Enzyme Inhibition in Patients with Chronic Systolic Heart Failure: Rationale for and Design of the Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and morbidity in Heart Failure Trial (PARADIGM-HF)European Journal of Heart Failure, 2013
- Effect of Phosphodiesterase-5 Inhibition on Exercise Capacity and Clinical Status in Heart Failure With Preserved Ejection FractionJAMA, 2013
- Endothelial Dysfunction, Arterial Stiffness, and Heart FailureJACC, 2012
- The pathophysiology of heart failureCardiovascular Pathology, 2012
- Soluble guanylate cyclase: a potential therapeutic target for heart failureHeart Failure Reviews, 2012
- Impaired Natriuretic and Renal Endocrine Response to Acute Volume Expansion in Pre-Clinical Systolic and Diastolic DysfunctionJACC, 2011
- Neurohormonal Activation in Acute Heart Failure: Results from VERITASCardiology, 2011
- Cyclic GMP signaling in cardiovascular pathophysiology and therapeuticsPharmacology & Therapeutics, 2009
- The pathophysiology of acute heart failure—It is a lot about fluid accumulationAmerican Heart Journal, 2008