Abstract

In terms of sacubitril/valsartan (S/V)-induced changes in heart failure with reduced ejection fraction (HFrEF) via three-dimensional (3D) transthoracic echocardiography (TTE) and S/V effects based on HF aetiology, data are lacking. We prospectively enrolled 51 HFrEF patients (24 ischaemic, 27 non-ischaemic). At baseline and at 6-month follow-up (6MFU) after S/V treatment optimisation, we assessed the N-terminal pro-B-type natriuretic peptide (NT-proBNP), and cardiac remodelling by two-dimensional (2D) and 3DTTE. In non-ischaemic patients, 2D and 3DTTE showed an improvement in left ventricular (LV) size and biventricular function at 6MFU vs. baseline: 3D-LV end-diastolic volume (EDV) 103 ± 30 vs. 125 ± 32 mL/m2 (p < 0.05), 3D-LV ejection fraction (EF) 40 ± 9 vs. 32 ± 5% (p < 0.05), right ventricular (RV) 3D-EF 48.4 ± 6.5 vs. 44.3 ± 7.5% (p < 0.05); only the 3D method detected RV size reduction: 3D-RVEDV 63 ± 27 vs. 71 ± 30 mL/m2 (p < 0.05). In ischaemic patients, only 3DTTE showed biventricular size and LV function improvement: 3D-LVEDV 112 ± 29 vs. 121 ± 27 mL/m2 (p < 0.05), 3D-LVEF 35 ± 6 vs. 32 ± 5% (p < 0.05), 3D-RVEDV 57 ± 11 vs. 63 ± 14 mL/m2 (p < 0.05); RV function did not ameliorate. In both ischaemic and non-ischaemic patients, diastolic function and NT-proBNP significantly improved. In HFrEF patients treated with S/V, 3DTTE helps to ascertain subtle changes in heart chambers’ size and function, which have a major impact on HFrEF prognosis. S/V has significantly different effects on LV function in non-ischaemic vs. ischaemic patients.

Highlights

  • Myocardial remodelling has a major pathogenetic role in the progression of heart failure with reduced ejection fraction (HFrEF), and it is strictly linked to neurohormonal upregulation, a recognized hallmark of HF worsening [1,2]

  • The diastolic function was assessable in a subset of patients (n = 40), since its evaluation was not feasible in nine cases due to atrial fibrillation, in one case for previous MitraClip implantation, and in one patient due to previous prosthetic mitral valve implantation (Figure 1)

  • No differences were noted in comorbidities between the IHD and non-IHD groups, nor was the pharmacological treatment significantly different, with the exception of antiplatelet therapy, which was more frequently prescribed in ischaemic patients

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Summary

Introduction

Myocardial remodelling has a major pathogenetic role in the progression of heart failure with reduced ejection fraction (HFrEF), and it is strictly linked to neurohormonal upregulation, a recognized hallmark of HF worsening [1,2]. It is well known that the inhibition of neurohormonal pathways (e.g., the renin–angiotensin–aldosterone and autonomic sympathetic systems) is the therapeutic cornerstone of HFrEF [1,2]. By inhibiting the renin-angiotensin-aldosterone system [2], sacubitril/valsartan (S/V) is proved to ameliorate left ventricular (LV) volumes, LV systolic [1,3,4,5,6,7] and diastolic function [5,6,8,9], and long-term prognosis in HFrEF [10,11,12,13]. A few studies, conducted on a limited number of cases, demonstrated an improvement in right ventricular (RV) function by two-dimensional (2D) transthoracic echocardiography (TTE) [5,8,9]. An extensive assessment of S/V-induced changes in all prognostically maneaexntienngsfiuvlepaasrsaemssemteernst[o1f4]S/byV-binodthuc2eDdacnhdantgherseei-ndaimll epnrosigonnoaslt(ic3aDll)yTmTEeahnainsgnfeuvleprabraemenaectecrosm[1p4li]shbeydbionthH2FDrEaFnpdattihernetes-.dimensional (3D) TTE has never been accomplished in HFrETFhpeaatimentosf. our study was to comprehensively assess echocardiographic indices of reverTsehereamimodoeflloinugr sbtyud2yDwaansdto3DcoTmTpErebheefonrseivaenlyda6s-smesosnethchsoacfaterdr ioopgtriampihsiactiionndiocfesS/oVf trheevrearpsey rienmHoFdreElFlinpgatbieyn2tsD, garnodup3DedTaTcEcobrdefionrgetaonHdF6-ametoionltohgsya(fitsecrhoapemtimicishaetaiortndoisfeSa/sVe, ItHheDra, pvys. innoHn-FisrcEhFapematicenhtesa,rgtrdoiuspeaesde,anccoonr-dIHinDg)t.o HF aetiology (ischaemic heart disease, IHD, vs. non-ischaemic heart disease, non-IHD)

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