Title:Advances in the Management of Heart Failure with Reduced Ejection Fraction;
The Role of SGLT2is, ARNI, Myotropes, Vericiguat, and Anti-inflammatory
Agents: A Mini-review
Volume: 29
Issue: 7
Author(s): Dimitrios A. Vrachatis*, Konstantinos A. Papathanasiou, Sotiria G. Giotaki, Konstantinos Raisakis, Andreas Kaoukis, Charalampos Kossyvakis, Andreas Theodorakis, Stauros Pediotidis, Dimitrios Avramides, Gerasimos Siasos and Spyridon Deftereos
Affiliation:
- Medical School, National and Kapodistrian University of Athens, Athens, Greece
Keywords:
HFrEF, HF, ARNIs, sacubitril/valsartan, SGLT2 inhibitors, vericiguat, omecamtiv mecarbil, anti-inflammatory agents, inflammation.
Abstract: 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.
