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维立西呱在心力衰竭中的应用:从科学证据到临床实践。

Vericiguat in heart failure: From scientific evidence to clinical practice.

机构信息

Servicio de Cardiología, Hospital Clínico Universitario Santiago de Compostela, Centro de investigación Biomédica en Red Enfermedades Vasculares (CIBERCV), Santiago de Compostela, Spain.

Servicio de Cardiología, Hospital Reina Sofía, Córdoba, Spain.

出版信息

Rev Clin Esp (Barc). 2022 Jun-Jul;222(6):359-369. doi: 10.1016/j.rceng.2021.12.006. Epub 2022 Apr 23.

DOI:10.1016/j.rceng.2021.12.006
PMID:35473692
Abstract

Despite currently available treatments, risk of death and hospitalizations in patients with heart failure with reduced ejection fraction (HFrEF) remains high. The pathophysiology of HFrEF includes neurohormonal activation characterized by stimulation of deleterious pathways (i.e., sympathetic nervous and renin-angiotensin-aldosterone systems) and suppression of protective pathways such as nitric oxide-dependent pathways. Inhibition or stimulation of some, but not all, of these pathways is insufficient. In HFrEF, there is reduced nitric oxide, soluble guanylate cyclase, and cGMP activity, leading to deleterious effects in the myocardial, vascular, and renal systems. Vericiguat is able to stimulate the activity of this protective pathway. The VICTORIA study demonstrated that the addition of vericiguat to optimal medical treatment in patients with HFrEF and recent decompensation significantly reduced the incidence of the primary endpoint, a composite of cardiovascular death or HF hospitalization, with a number needed to treat of 24 patients and excellent tolerability.

摘要

尽管目前有治疗方法,但射血分数降低的心力衰竭(HFrEF)患者的死亡和住院风险仍然很高。HFrEF 的病理生理学包括神经激素激活,其特征是有害途径(即交感神经系统和肾素-血管紧张素-醛固酮系统)的刺激和保护途径(如依赖一氧化氮的途径)的抑制。这些途径中的一些被抑制或刺激,但不是全部,是不够的。在 HFrEF 中,一氧化氮、可溶性鸟苷酸环化酶和 cGMP 活性减少,导致心肌、血管和肾脏系统的有害作用。维立西呱能够刺激这种保护途径的活性。VICTORIA 研究表明,在 HFrEF 患者和近期失代偿的患者中,将维立西呱添加到最佳药物治疗中,显著降低了主要终点(心血管死亡或 HF 住院的复合终点)的发生率,需要治疗的患者数为 24 例,且耐受性良好。

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