Table 1. A tabulated summary of the studies.

Abbreviations: n = number of patients; S/V = Sacubitril/valsartan; HF = Heart failure; ADH = Acute decompensated heart failure; MR = Mitral regurgitation; PH =Pulmonary Hypertension; EF = Ejection fraction; LV = Left ventricle; IV = Intravenous; HFrEF = Heart failure with reduced ejection fraction; hs-TnT = High sensitivity troponin T; cTnT = Cardiac troponin T; NT-proBNP =  N-terminal pro b-type natriuretic peptide; PAPi = Pulmonary artery pulsatility index; TRANSITION trial = Study comparing pre‐discharge and post‐discharge treatment initiation with sacubitril/valsartan in heart failure patients with reduced ejectIon‐fraction hospItalised for an acute decompensation event; PIONEER-HF trial = Study comparing sacubitril/valsartan versus enalapril on effect on NT-proBNP in patients stabilized from an acute heart failure episode; ARB = Angiotensin receptor blockers; ACE = Angiotensin-converting enzyme; rhBNP = Recombinant human brain natriuretic peptide

Authors; trial name (if applicable)	Study design	Patients (n)	Intervention	Results of primary outcomes	Other results
Velazquez et al.; PIONEER-HF [7]	Double-blinded, multicentre, randomized controlled trial	n = 881	S/V (n = 440) vs enalapril (n = 441)	Time-averaged change NT-proBNP, from baseline to the mean of weeks four and eight was 47% in those taking S/V versus a 25% reduction in those taking enalapril.	S/V was safe in acute HF and new-onset HF patients. Significant reduction in HF hospitalizations.
DeVore AD et al.; PIONEER-HF [11]	Secondary analysis of the open-label extension of the PIONEER-HF trial	n = 831	Continuing S/V  (n = 417) vs enalapril switching to S/V (n = 415)	Time-averaged change of NT-proBNP in the period from eight weeks to 12 weeks: For patients who continued to take sacubitril/valsartan, NT-proBNP levels declined by 17.2%. For those switching from taking enalapril to S/V, it declined by 37.4%.	Patients on S/V since hospitalization had a lower hazard for rehospitalization or cardiovascular death than patients who initiated enalapril in the hospital and then initiated S/V eight weeks later.
Velazquez et al.; PIONEER-HF [12]	Secondary analysis of the PIONEER-HF trial	n=881	S/V vs enalapril in black patients (n=316) ; white patients (n=515); others (n=50)	Among black patients admitted for ADHF, S/V resulted in a significant reduction in NT-proBNP levels.	S/V was safe and well-tolerated among black patients and significantly improved clinical outcomes compared to enalapril.
Wachter et al.; TRANSITION [13]	Open-label, multicentre, randomized controlled trial	n = 1002	Predischarge (n = 500) vs postdischarge (n = 502) initiation of S/V	Percentage of patients achieving the target dose of S/V at 10 weeks: Predischarge, 45.4%; postdischarge, 50.7%.	S/V was safe and tolerated well in acute HF and new-onset HF patients.
Senni M et al.; TRANSITION [14]	Post-hoc analysis; a subgroup analysis of the TRANSITION study	n = 991	De novo HFrEF (n=286) vs prior diagnosis of HFrEF (n=705)	The percentage of patients achieving the target dose of S/V at 10 weeks was greater in De novo HFrEF; 56%, while in prior HFrEF it was 45%.	Initiation of S/V was associated with a significant reduction in both hs-TnT and NT-proBNP in both groups.
Pang, Zhihua, et al. [15]	Open-label, single-center, randomized controlled trial	n = 300	Basic HF treatment (n=100) vs basic treatment combined with rhBNP (n=100) vs basic HF treatment execluding ACE/ARB with rhBNP followed by S/V (n = 100)	The S/V treatment group had superior outcomes in terms of cardiac structure, pulmonary artery pressure, and cardiac biomarkers (NT-proBNP Levels and cTnT levels).	S/V significantly reduced the serum levels of inflammatory factors, oxidizing factors, and increased antioxidant factors.
M Fudim et al. [16]	A retrospective observational study	n = 99767	Patients eligible for S/V using PIONEER criteria (n=20 704) vs  patients eligible for S/V using actionable criteria (n = 68739)	There is a slight difference in patients' characteristics and clinical outcomes eligible for PIONEER-HF compared to those encountered in routine practice.	All-cause mortality and readmission rate were similar in both groups.
Carballo D et al. [17]	A prospective cohort study	n = 799	Patients eligible for S/V (n = 123) vs Patients non-eligible for S/V with EF<40% (n = 138) and patients non-eligible for S/V with EF>40% (n = 538)	Similar clinical outcomes (including all-cause mortality and readmission) in both eligible and non-eligible groups were noted.
Liang HW et al. [18]	A retrospective cohort study	n = 1278	S/V	Lower risk of all-cause mortality, cardiovascular death, and HF rehospitalizations within one year.	The intervention was associated with more significant medical expenses.
Martyn et al. [19]	Retrospective observational study	n = 22	S/V	Hemodynamic improvement in ICU patients switched from vasoactive IV therapy to oral S/V therapy.	Improvement in PAPi with S/V compared to both admission and vasoactive therapy.
Martyn T et al. [20]	Retrospective observational study	n = 22	S/V	Favorable hemodynamic impact and tolerability in cardiogenic shock patients using S/V	Hypotension was the most common cause of intolerance.
Yaranov D et al. [21]	Prospective observational study	n = 10	S/V	Patients with cardiogenic shock tolerated initiation of S/V subsequent successful weaning of IV vasodilator or inotropic therapy.
Chng BLK et al. [22]	Retrospective observational study	n = 840	Inpatient S/V (n = 89) vs Outpatient S/V (n = 551)	Initiation of S/V in the inpatient group was associated with higher ADRs and discontinuation rates than in the outpatient group.	The inpatient population tolerated S/V.
Akerman CC et al. [23]	Retrospective observational study	n = 143	S/V	Most patients were tolerant of S/V, with hypotension being the most common cause of intolerance.	Patients with newly diagnosed HF were more likely to tolerate the initiation of S/V.
Peppin et al. [24]	Retrospective observational study	n = 61	S/V	The most common cause of intolerance to S/V was hypotension.	There was an improvement in EF from baseline to ≥ 30 days post-initiation of S/V.
Acanfora D et al. [25]	Case series	n = 40	S/V	S/V was found to be effective in terms of functional capacity and cardiac biomarkers (e.g., NT-proBNP)	S/V was found to be safe.
Taghavi S et al. [26]	Case series	n = 4	S/V in inotrope-dependent HF patients.	S/V use led to discontinuation of inotrope and reducing the need for inotrope in the follow-up period.
Gerges F et al. [27]	Case report	n = 1	S/V	Improvement of symptoms and LV function following the use of S/V	After S/V was used, a significant reduction of secondary MR severity, PH, and normalization of right ventricular function was noted.
Lo SH et al. [28]	Case report	n = 1	S/V in a child.	S/V was found to be effective in a pediatric ADH in the setting of chemotherapy-induced cardiomyopathy.
Bell TD et al. [29]	Case report	n = 1	S/V	S/V was found to be effective and led to the discontinuation of inotropes.
Rawal HA et al. [30]	Case report	n = 1	S/V	S/V led to cardiogenic shock in advanced HF patients.
Almazroa L et al. [31]	Case report	n = 1	S/V	S/V was unsafe in cardiogenic shock as it led to vasoplegic shock.
Ntalianis A et al. [32]	Editorial: Expert consensus		S/V	S/V is safe and well-tolerated and results in a more significant reduction of NT-proBNP and reduction for HF rehospitalizations.	Clinical practical strategies and action plans were recommended.