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1. Effects of Sacubitril/Valsartan on left ventricular pressure-volume relationship in heart failure

Author

T Stegmann, L Parentin, S H Schirmer, A Hagendorff, U Laufs, and D Lavall

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Background In patients with heart failure (HF) and reduced ejection fraction, Sacubitril/Valsartan (S/V) reduces the risk for death and hospitalisations. However, the underlying mechanism for these beneficial effects of S/V, is still lacking. Methods Consecutive patients with symptomatic HF and LV ejection fraction (EF) ≤40% who were assigned to S/V were prospectively included in this study (n=117). Non-invasive pressure volume loops were obtained from echocardiography with simultaneous arm-cuff blood pressure measurement. By this method, LV end-systolic elastance (Ees), effective arterial elastance (Ea) and ventricular-arterial coupling (Ea/Ees) were calculated. LV end-diastolic pressure was derived from the E/e' ratio. This is a prespecified interim analysis of 50 patients with completed 6 months of follow-up. The study is registered with ClinicalTrials.gov, NCT04498780. Results Mean age was 61.8±18.6 years and 12 (24%) patients were females. Ischaemic heart failure was present in 22 (44%), non-ischaemic aetiology in 24 (48%), and myocarditis in 4 (8%) patients. 34 (68%) patients were on the target dose of S/V after 6 months of treatment. At 6 months, LV end-diastolic volume (110±28 ml/m2 vs. 87±31 ml/m2, p Conclusion After 6 months of treatment with Sacubitril/Valsartan, LV remodelling and reduced LV filling pressures were observed. These changes were associated with improvements in functional capacity, natriuretic peptide levels and NYHA functional class. Thus, the study provides important mechanistic insides into the hemodynamics of angiotensin–neprilysin inhibition in heart failure which might help to individualize therapy. Funding Acknowledgement Type of funding sources: None.

Published
2022
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2. Angiotensin receptor-neprilysin inhibition and improved ventricular-arterial coupling in heart failure with reduced ejection fraction.

Author

Stegmann T, Parentin L, Schirmer SH, Lavall P, Hagendorff A, Laufs U, and Lavall D

Subjects
Humans, Female, Male, Aged, Middle Aged, Prospective Studies, Treatment Outcome, Natriuretic Peptide, Brain blood, Peptide Fragments blood, Recovery of Function, Angiotensin II Type 1 Receptor Blockers therapeutic use, Heart Failure drug therapy, Heart Failure physiopathology, Valsartan therapeutic use, Aminobutyrates therapeutic use, Drug Combinations, Biphenyl Compounds, Neprilysin antagonists & inhibitors, Stroke Volume drug effects, Ventricular Function, Left drug effects, Angiotensin Receptor Antagonists therapeutic use, Tetrazoles therapeutic use
Abstract

Sacubitril/valsartan improves outcomes in chronic heart failure (HF) with reduced ejection fraction (EF). The underlying mechanisms on left ventricular (LV) myocardial function are incompletely understood. In this study, 117 patients with symptomatic HF and LVEF ≤ 40% were enrolled prospectively. Noninvasive pressure-volume analysis was calculated from transthoracic echocardiography with simultaneous arm-cuff blood pressure measurements. Primary outcome parameters were LV end-systolic elastance ( E es ; a measure of LV contractility), effective arterial elastance ( E a ; a measure of afterload), and the ventricular-arterial coupling ratio ( E a / E es ). The mean age was 65 ± 13 yr, 30% were female, and 54.7% had ischemic heart disease. During 6 mo of follow-up, eight patients died, three withdrew their consent, and four were lost to follow-up. About 102 patients were included in pressure-volume analyses. After 6 mo of sacubitril/valsartan treatment, E es increased (0.66 mmHg/mL [IQR 0.45-0.94] vs. 0.78 mmHg/mL [IQR 0.57-1.10], P = 0.001), E a decreased (1.76 mmHg/mL [IQR 1.48-2.13] vs. 1.62 mmHg/mL [IQR 1.36-1.96], P = 0.014), and the E a / E es ratio improved (2.52 [IQR 1.88-4.05] vs. 1.93 [IQR 1.50-2.63], P < 0.001). LV end-diastolic pressure and LV volumes were reduced, and LVEF increased from 33% to 43% (both P < 0.001). Clinical improvement occurred in NYHA functional class, NT-proBNP level, and 6-min walking distance. Change in LVEF correlated with change in E es ( r = 0.33, P = 0.0008), while change in NT-proBNP was associated with change in LV end-diastolic pressure (LVEDP) ( r = 0.42, P < 0.0001). In conclusion, sacubitril/valsartan is associated with improved ventricular-arterial coupling by enhancing LV contractility and reducing afterload. Beyond LV reverse remodeling, optimized ventricular-arterial interaction may contribute to the favorable outcome of sacubitril/valsartan treatment in HF with reduced EF. NEW & NOTEWORTHY The study demonstrates that 6-mo treatment with sacubitril/valsartan in patients with heart failure with reduced ejection fraction is associated with increased left ventricular contractility, reduced afterload, and improved ventricular-arterial coupling. Together with reverse remodeling, these changes indicate a leftward shift of the operating left ventricular pressure-volume relationship. These data provide new insights into the understanding of pharmacological mechanisms in the failing heart and may facilitate tailored medical therapy.

Published
2024
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