摘要
尽管有重要治疗学的进展，有长期的心失败(HF ) 的病人在病态和死亡的高风险留下。Sacubitril valsartan (以前作为 LCZ696 知道) 一个新口头的代理人与减少的喷射在成年人为征兆的长期的心失败的治疗被同意部分。自从它合并 neprilysin 禁止者， sacubitril 和血管收缩素 II，它在班血管收缩素受体 neprilysin 禁止者(ARNI ) 被描述为第一受体对手， valsartan。Neprilysin 是包括 natriuretic 毁坏几 vasoactive 肽的 endopeptidase 肽(NP ) ， bradykinin， endothelin 和血管收缩素 II (Ang-II ) 。因此，它的抑制的自然后果是两个， NP 和 Ang-II 的 plasmatic 层次的增加(随相反的生物行动) 。那么，这些的联合抑制两个系统(Sacubitril / valsartan ) 可以在 HF 提高 NP 效果的好处(natriuresis，多尿，等等) 当 Ang-II 受体被禁止时(减少的血管缩小和醛固酮版本) 。在大临床的试用(与 8442 个病人一起的 PARADIGM-HF ) ，这个新代理人被发现显著地减少心血管，所有由于 HF 象住院一样引起死亡(与 enalapril 相比) 。这张手稿为 sacubitril valsartan， dosing 和小心考察临床的证据，在有减少的喷射的 HF 的治疗的未来方向和它的考虑地方部分。
Despite significant therapeutic advances, patients with chronic heart failure （HF） remain at high risk of morbidity and mortality. Sacubitill valsartan （previously known as LCZ696） is a new oral agent approved for the treatment of symptomatic chronic heart failure in adults with reduced ejection fraction. It is described as the fast in class angiotensin receptor neprilysin inhibitor （ARNI） since it incorporates the neprilysin inhibitor, sacubitril and the angiotensin Ⅱ receptor antagonist, valsartan. Neprilysin is an endopeptidase that breaks down several vasoactive peptides including natriuretic peptides （NPs）, bradykinin, endothelin and angiotensin II （Ang-II）. Therefore, a natural consequence of its inhibition is an increase of plasmatic levels of both, NPs and Ang-Ⅱ （with opposite biological actions）. So, a combined inhibition of these both systems （Sacubitril / valsartan） may enhance the benefits of NPs effects in HF （natriuresis, diuresis, etc） while Ang-Ⅱ receptor is inhibited （reducing vasoconstriction and aldosterone release）. In a large clinical trial （PARADIGM-HF with 8442 patients）, this new agent was found to significantly reduce cardiovascular and all cause mortality as well as hospitalizations due to HF （compared to enalapril）. This manuscript reviews clinical evidence for sacubitril valsartan, dosing and cautions, future directions and its considered place in the therapy of HF with reduced ejection fraction.
