Version 1
: Received: 1 July 2024 / Approved: 2 July 2024 / Online: 2 July 2024 (14:51:23 CEST)
How to cite:
Russo, P.; Vitiello, L.; Milani, F.; Volterrani, M.; Rosano, G. M.; Tomino, C.; Bonassi, S. New Therapeutics for Heart Failure Worsening: Focus on Vericiguat. Preprints2024, 2024070207. https://doi.org/10.20944/preprints202407.0207.v1
Russo, P.; Vitiello, L.; Milani, F.; Volterrani, M.; Rosano, G. M.; Tomino, C.; Bonassi, S. New Therapeutics for Heart Failure Worsening: Focus on Vericiguat. Preprints 2024, 2024070207. https://doi.org/10.20944/preprints202407.0207.v1
Russo, P.; Vitiello, L.; Milani, F.; Volterrani, M.; Rosano, G. M.; Tomino, C.; Bonassi, S. New Therapeutics for Heart Failure Worsening: Focus on Vericiguat. Preprints2024, 2024070207. https://doi.org/10.20944/preprints202407.0207.v1
APA Style
Russo, P., Vitiello, L., Milani, F., Volterrani, M., Rosano, G. M., Tomino, C., & Bonassi, S. (2024). New Therapeutics for Heart Failure Worsening: Focus on Vericiguat. Preprints. https://doi.org/10.20944/preprints202407.0207.v1
Chicago/Turabian Style
Russo, P., Carlo Tomino and Stefano Bonassi. 2024 "New Therapeutics for Heart Failure Worsening: Focus on Vericiguat" Preprints. https://doi.org/10.20944/preprints202407.0207.v1
Abstract
Heart failure (HF) is a syndrome characterized by signs and symptoms resulting from structural or functional cardiac abnormalities, confirmed by elevated natriuretic peptides or evidence of congestion. HF patients are classified according to left ventricular ejection fraction (LVEF). Worsening HF (WHF) is associated with increased short- and long-term mortality, re-hospitalization, and healthcare costs. Standard treatment of HF includes angioten-sin-converting enzyme inhibitors, angiotensin receptor-neprilysin inhibitors, mineralocorti-coid-receptor antagonists, beta-blockers, and sodium-glucose co-transporter 2 inhibitors. To manage systolic HF by reducing mortality and hospitalizations in patients experiencing WHF, treatment with vericiguat, a direct stimulator of soluble guanylate cyclase (sGC), is indicated. This drug acts by stimulating sGC enzymes, part of the nitric oxide (NO)-sGC-cyclic guanosine monophosphate (cGMP) signaling pathway, regulating the cardiovascular system by catalyzing cGMP synthesis in response to NO. cGMP acts as a second messenger, triggering various cellular effects. Deficiencies in cGMP production, often due to low NO availability, are implicated in cardiovascular diseases. Vericiguat stimulates sGC directly, bypassing the need for a functional NO-sGC-cGMP axis, thus preventing myocardial and vascular dysfunction associated with de-creased sGC activity in heart failure. Approved by the FDA in 2021, vericiguat administration should be considered, in addition to the four pillars of HFrEF therapy, in symptomatic patients with LVEF < 45% following a worsening event. Cardiac rehabilitation represents an ideal setting where there is more time to implement therapy with vericiguat and incorporate a greater num-ber of medications for the management of these patients. This review covers vericiguat's metab-olism, molecular mechanisms, and drug-drug interactions.
Medicine and Pharmacology, Cardiac and Cardiovascular Systems
Copyright:
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