Department of Clinical Pharmacy, 15514University of Michigan College of Pharmacy, Ann Arbor, MI, USA.
Department of Pharmacy, 5228University of Wisconsin Hospitals and Clinics, Madison, WI, USA.
J Cardiovasc Pharmacol Ther. 2021 Nov;26(6):593-600. doi: 10.1177/10742484211042706. Epub 2021 Sep 6.
Over the past decade, soluble guanylate cyclase (sGC) activators and stimulators have been developed and studied to improve outcomes in patients with heart failure with reduced ejection fraction (HFrEF). The sGC enzyme plays an important role in the nitric oxide (NO)-sGC-cyclic guanosine monophosphate (cGMP) pathway, that has been largely untargeted by current guideline directed medical therapy (GDMT) for HFrEF. Disruption of the NO-sCG-cGMP pathway can be widely observed in patients with HFrEF leading to endothelial dysfunction. The disruption is caused by an oxidized state resulting in low bioavailability of NO and cGMP. The increase in reactive oxygen species can also result in an oxidized, and subsequently heme free, sGC enzyme that NO is unable to activate, furthering the endothelial dysfunction. The novel sGC stimulators enhance the sensitivity of sGC to NO, and independently stimulate sGC, while the sGC activators target the oxidized and heme free sGC to stimulate cGMP production. This review will discuss the pathophysiologic basis for sGC stimulator and activator use in HFrEF, review the pre-clinical and clinical data, and propose a place in the HFrEF armamentarium for this novel pharmacotherapeutic class.
在过去的十年中,已经开发和研究了可溶性鸟苷酸环化酶(sGC)激活剂和刺激剂,以改善射血分数降低的心力衰竭(HFrEF)患者的预后。sGC 酶在一氧化氮(NO)-sGC-环鸟苷酸(cGMP)途径中发挥重要作用,而当前针对 HFrEF 的指南指导的医学治疗(GDMT)在很大程度上未针对该途径。NO-sCG-cGMP 途径的破坏在 HFrEF 患者中广泛观察到,导致内皮功能障碍。这种破坏是由氧化状态引起的,导致 NO 和 cGMP 的生物利用度降低。活性氧的增加也会导致氧化,随后无血红素 sGC 酶,NO 无法激活,进一步导致内皮功能障碍。新型 sGC 刺激剂增强了 sGC 对 NO 的敏感性,并独立地刺激 sGC,而 sGC 激活剂针对氧化和无血红素 sGC 以刺激 cGMP 的产生。这篇综述将讨论 sGC 刺激剂和激活剂在 HFrEF 中的应用的病理生理基础,回顾临床前和临床数据,并为这一新的治疗类药物在 HFrEF 治疗中提出建议。