医学
心力衰竭
射血分数
失代偿
里奥西瓜特
环磷酸鸟苷
一氧化氮
内科学
心脏病学
内皮功能障碍
鸟苷酸环化酶
血管舒张
激活剂(遗传学)
药理学
受体
作者
Alberto Aimo,Vincenzo Castiglione,Giuseppe Vergaro,Giorgia Panichella,Michele Senni,Carlo Lombardi,Michele Emdin
标识
DOI:10.1007/s10741-021-10146-1
摘要
The significant morbidity and mortality associated with heart failure with reduced (HFrEF) or preserved ejection fraction (HFpEF) justify the search for novel therapeutic agents. The nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway plays an important role in the regulation of cardiovascular function. This pathway is disrupted in HF resulting in decreased protection against myocardial injury. 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 then reduced NO levels, but this comes at the expense of a greater risk of hypotension. Conversely, sGC stimulators (riociguat and vericiguat) enhance sGC sensitivity to endogenous NO, and then exert a more physiological action. The phase 3 VICTORIA trial found that vericiguat is safe and effective in patients with HFrEF and recent HF decompensation. Therefore, adding vericiguat may be considered in individual patients with HFrEF, particularly those at higher risk of HF hospitalization; the efficacy of the sacubitril/valsartan-vericiguat combination in HFrEF is currently unknown.
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