Sacubitril/Valsartan Effects on Right Ventricular-Pulmonary Coupling and Albumin-bilirubin Score in Heart Failure with Reduced Ejection Fraction in China

Background Impaired right ventricular (RV) function coupled with progressive uncoupling of the pulmonary circulation (PA) represents a turning point in clinical deterioration with profound consequences for prognosis. Several studies have proposed that RV-PA coupling, calculated by measuring the tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP), can be used as an early indicator of right ventricular dysfunction(RVD) in patients with heart failure with a reduced ejection fraction (HFrEF). Patients with HFrEF benefit from sacubitril/valsartan therapy in terms of left ventricular (LV) function as well as functional and symptomatic improvement. The objective of this study was to evaluate the effect of sacubitril/valsartan treatment on TAPSE/PASP in patients with HFrEF. Methods A retrospective observational study was conducted on 305 patients with HFrEF and RVD who were hospitalized between June 2020 and December 2021.One year after treatment, we reevaluated laboratory tests, transthoracic echocardiography (TTE), NYHA(New York Heart Association) classification, Minnesota Living with Heart Failure Questionnaire (MLWHFQ) scores and changes in relevant variables. Results A significant improvement was demonstrated in the following echocardiography parameters assessing RV function after 1 year of treatment with sacubitril/valsartan:TAPSE (15 ± 1 vs. 18 ± 2 mm,p < 0.001), PASP (45 ± 8 vs. 40 ± 9mmHg,p < 0.001), Pulmonary artery diastolic pressure(PADP)(22 ± 4 vs. 19 ± 4mmHg, p < 0.001),RV-PA coupling (0.35 ± 0.08 vs. 0.48 ± 0.12,p < 0.001),and RV s’(8.7 ± 2.2 vs. 9.5 ± 2.6 cm/s, p < 0.001). Multivariable analysis showed that RV-PA coupling improved with baseline PASP (r-0.45, p < 0.001) and PADP (r-0.45, p < 0.001). Conclusions Sacubitril/valsartan improves RV-PA conjugation in patients with RVD and HFrEF, however, this effect may not be a result of left ventricular remodeling, but rather a result of reduced left atrial pressure.