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<p>Chronic heart failure with reduced ejection fraction (HFrEF) is a progressive syndrome associated with substantial residual morbidity and mortality despite contemporary guideline-directed medical therapy (GDMT) - angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs)/angiotensin receptor-neprilysin inhibitors (ARNIs), beta-blockers, mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is) [<CitationRef CitationID="CR1">1</CitationRef>]. Consequently, the need for novel therapeutic strategies has led to the exploration of new drug classes and pathways. In HF, impaired nitric-oxide (NO) signaling, reduced soluble guanylate cyclase (sGC) responsiveness/abundance, and downstream attenuation of cyclic guanosine monophosphate (cGMP) contribute to disease progression [<CitationRef CitationID="CR2">2</CitationRef>]. Vericiguat—an oral sGC stimulator—sensitizes sGC to endogenous NO and directly stimulates the enzyme, thereby restoring cGMP signaling in vascular smooth muscle and cardiomyocytes.</p>

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Victoria and Victor: event-driven lessons for integrating vericiguat into practice and reducing residual risk in HFrEF

  • 期刊论文

  • 发表日期：

    2025年12月11日

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  • Kalliopi Keramida,
  • Francesca Musella,
  • Magdy Abdelhamid,
  • Naoki Sato,
  • Stephen J. Greene,
  • Dimitrios Farmakis,
  • Josephine Harrrington,
  • Andrew P. Ambrosy

摘要

Chronic heart failure with reduced ejection fraction (HFrEF) is a progressive syndrome associated with substantial residual morbidity and mortality despite contemporary guideline-directed medical therapy (GDMT) - angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs)/angiotensin receptor-neprilysin inhibitors (ARNIs), beta-blockers, mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2is) [1]. Consequently, the need for novel therapeutic strategies has led to the exploration of new drug classes and pathways. In HF, impaired nitric-oxide (NO) signaling, reduced soluble guanylate cyclase (sGC) responsiveness/abundance, and downstream attenuation of cyclic guanosine monophosphate (cGMP) contribute to disease progression [2]. Vericiguat—an oral sGC stimulator—sensitizes sGC to endogenous NO and directly stimulates the enzyme, thereby restoring cGMP signaling in vascular smooth muscle and cardiomyocytes.