Vrachatis Dimitrios A, Papathanasiou Konstantinos A, Giotaki Sotiria G, Raisakis Konstantinos, Kaoukis Andreas, Kossyvakis Charalampos, Theodorakis Andreas, Pediotidis Stauros, Avramides Dimitrios, Siasos Gerasimos, Deftereos Spyridon
Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Second Department of Cardiology, National & Kapodistrian University of Athens, School of Medicine, University General Hospital ATTIKON, Athens, Greece.
Curr Pharm Des. 2023;29(7):509-518. doi: 10.2174/1381612829666230316142450.
Heart failure with reduced ejection fraction (HFrEF) has been associated with poor prognosis, reduced quality of life, and increased healthcare expenditure. Despite tremendous advances in HFrEF management, reduced survival and a high rate of hospitalization remain unsolved issues. Furthermore, HFrEF morbidity and economic burden are estimated to increase in the following years; hence, new therapies are constantly emerging. In the last few years, a series of landmark clinical trials have expanded our therapeutic armamentarium with a ground-breaking change in HFrEF-related outcomes. Sodium-glucose co-transporter 2 inhibitors (mainly dapagliflozin and empagliflozin) have already revolutionized the management of HFrEF patients via a significant reduction in cardiovascular mortality and heart failure hospitalizations. Furthermore, vericiguat and omecamtiv mecarbil have emerged as promising and novel disease-modifying therapies. The former restores the impaired cyclic guanosine monophosphate pathway, and the latter stimulates cardiac myosin without marked arrhythmogenesis. Both vericiguat and omecamtiv mecarbil have been shown to reduce heart failure admissions. Sacubitril/valsartan is an established and effective therapy in HFrEF patients and should be considered as a replacement for angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARBs). Lastly, inflammasome activity is implicated in HFrEF pathophysiology, and the role of anti-inflammatory agents in HFrEF trajectories is readily scrutinized, yet available therapies are ineffective. This mini-review summarizes the major and most recent studies in this field, thus covering the current advances in HFrEF therapeutics.
射血分数降低的心力衰竭（HFrEF）与预后不良、生活质量下降及医疗费用增加相关。尽管在HFrEF管理方面取得了巨大进展，但生存率降低和高住院率仍是未解决的问题。此外，预计未来几年HFrEF的发病率和经济负担将会增加；因此，新的治疗方法不断涌现。在过去几年中，一系列具有里程碑意义的临床试验扩展了我们的治疗手段，使HFrEF相关结局发生了突破性变化。钠-葡萄糖协同转运蛋白2抑制剂（主要是达格列净和恩格列净）已通过显著降低心血管死亡率和心力衰竭住院率，彻底改变了HFrEF患者的管理方式。此外，维立西呱和奥米卡替麦卡比已成为有前景的新型疾病改善疗法。前者恢复受损的环磷酸鸟苷途径，后者刺激心肌肌球蛋白而无明显致心律失常作用。维立西呱和奥米卡替麦卡比均已显示可减少心力衰竭住院。沙库巴曲/缬沙坦是HFrEF患者已确立的有效治疗方法，应被视为血管紧张素转换酶抑制剂（ACEi）或血管紧张素II受体阻滞剂（ARB）的替代药物。最后，炎性小体活性与HFrEF病理生理学有关，抗炎药物在HFrEF病程中的作用很容易受到审视，但现有治疗方法无效。本综述总结了该领域的主要和最新研究，从而涵盖了HFrEF治疗学的当前进展。
