Current treatment of acute decompensated heart failure (ADHF) has not reduced the significant morbidity or mortality associated with this disease, and has promoted drug development aimed at neurohormonal targets. Hypervolemic hyponatremia, which is linked to the nonosmotic release of arginine vasopressin, is associated with a poor prognosis in patients with heart failure (HF). Vasopressin acts on V(2) and V(1a) receptors to cause water retention and vasoconstriction, respectively. Clinical trials have demonstrated that vasopressin receptor antagonists (VRAs) are effective in treating hypervolemic hyponatremia in ADHF without a negative impact on renal function. The small hemodynamic benefit seen with VRA use appeared to result from V(2)-receptor antagonist-induced increase in urine output rather than from a vasodilatory drug effect. VRA use in ADHF trials was associated with minimal symptomatic improvement and no impact on morbidity or mortality. At present, clinical trial evidence does not support the routine use of VRAs in ADHF. Given the favorable renal profile of VRAs, studies on the possible benefit of VRAs in ADHF patients with renal insufficiency and diuretic resistance appear warranted.

Background Most clinical data regarding the use of sacubitril-valsartan (SV) in patients with heart failure with reduce EF (HFrEF) come from clinical trials, while observational studies in real life are scarce. Purpose To analyse the efficacy, safety and tolerability of SV in patients with HFrEF in real life. Methods An analysis of the SAVE-RLife (SV Evidence in Real Life) study was performed. This is an observational and ambispective study that included all patients with HFrEF who started SV between SEP2016 and DEC2018. Results A total of 291 patients were included in the study with a median follow-up of 326 (169; 523). Mean age 66.16±11.8, 71 were women (24.4%), 209 patients started treatment at office (71.8%) and 82 during the admission (28.2%). The main aetiologies were ischemic heart disease (51.5%) and idiopathic dilated cardiomyopathy (35.4%). Comorbidities included: 71.5% hypertensive, 55.3% dyslipidemic, 37.1% AF and 44% T2DM. Baseline treatment included 85.9% beta-blockers, 87.2% ACEI or ARA-II, 65.6% MRA and 17.5% iSGLT2. After treatment start with SV, baseline and follow-up analytical parameters such as GFR, K+ levels and NT-BNP, and echo parameters of LV reverse remodeling were evaluated (Table 1). Improvement of the functional NYHA class (Figure 1) and reduction in the incidence of hospital admission or visits to emergency room (ER) were observed. Side effects were 16.2% acute renal failure, 9.3% symptomatic hypotension, 9.7% asymptomatic hypotension and 15.9% hyperkalemia. In 31 patients (11%) the drug was discontinued, one patient due to angioedema. 7.9% of patients died during follow-up, 7 of them due to HF (2.4%). Table 1 Before SV After SV P value Analytical data GFR (ml/min) 70.25±24.95 68.27±24.62 0.008 Serum K+(mEq/L) 4.53±0.50 4.71±0.456 <0.001 NT-proBNP (pg/ml) 2201 (846; 4664) 1146 (436; 2564) <0.001 Echocardiographic data LVEF (%) (n=84) 30.60±7.16 38.30±12.22 <0.001 LVED (mm) (n=72) 65.22±7.82 60.81±8.37 <0.001 PAPs (mmHg) (n=48) 44.48±13.03 37.52±12.25 0.002 MR (grade 1–4) (n=71) 1.83±0.91 1.38±0.90 <0.001 Clinical outcomes HF Hospital/ER Admission the year before (mean± SD) 0.79±1.09 0.41±0.963 <0.001 Predictors of clinical improvement Conclusions SV has shown to improve morbidity and mortality in patients with HFrEF by improving functional class, decreasing NT-proBNP levels and reducing admissions due to HF, without significant side effects. In our study SV improved LVEF and reverse remodeling echocardiographic parameters too.

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