Key result
Switching to sacubitril/valsartan fails to alter cardiac or inflammatory biomarkers vs ACEI/ARB in acute HF.
Why the study?
Whether initiating sacubitril/valsartan after haemodynamic stabilization modifies cardiac injury/stress and systemic inflammatory biomarkers in acute heart failure was uncertain.
Does switching to sacubitril/valsartan versus continuing ACEI/ARB improve cardiac injury, stress, and systemic inflammatory biomarkers in stabilized acute heart failure patients?
RCT (n=365)
Open-label with blinded endpoint assessment
Randomized
Yes
Does switching to sacubitril/valsartan versus continuing ACEI/ARB improve cardiac injury, stress, and systemic inflammatory biomarkers in stabilized acute heart failure patients?
Initiating sacubitril/valsartan compared to continuing ACEI/ARB in hemodynamically stabilized acute heart failure patients does not significantly alter changes in systemic inflammatory and cardiac stress/injury biomarkers over 8 weeks.
Answers are grounded in this paper and cite their sources.
No support for switching to improve biomarkers in acute HF; challenges expectations of early ARNI anti-inflammatory effects.
AIMS: Acute heart failure (AHF) is accompanied by myocardial injury, wall stress, and systemic inflammatory activation. Whether initiating sacubitril/valsartan (Sac/Val) after haemodynamic stabilization modifies cardiac injury/stress and systemic inflammatory biomarkers is uncertain. METHODS AND RESULTS: The Program Angiotensin-Neprilysin Inhibition in Admitted Patients with Worsening Heart Failure (PREMIER) study was a multicentre, prospective, randomised, open-label trial with blinded endpoint assessment. Within 7 days of hospitalisation and after haemodynamic stabilisation, inpatients previously treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (ACEI/ARB) were randomised to switch to Sac/Val or continue ACEI/ARB. In this pre-specified secondary analysis, high-sensitivity cardiac troponin T (hs-cTnT), soluble ST2 (sST2), C-reactive protein (CRP), and growth differentiation factor-15 (GDF-15) were measured at baseline and week 8. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was also assessed. Among 365 patients with complete cardiac injury/stress and systemic inflammatory biomarker data, all biomarkers generally decreased over 8 weeks, but between-group differences in biomarker changes were not significant. In exploratory biomarker-stratified analyses, only baseline CRP showed a nominal treatment interaction for NT-proBNP (p for interaction=0.012). CONCLUSION: In haemodynamically stabilised patients hospitalised for AHF, no differential effects of Sac/Val versus continued ACEI/ARB therapy on cardiac injury/stress and systemic inflammatory biomarkers were demonstrated over 8 weeks. These findings do not support a broad biomarker-defined anti-inflammatory or cardioprotective effect of Sac/Val in this setting.
No takes yet. Share an insight, caveat, or question.
Doi et al. (2026) conducted an RCT in Acute heart failure (AHF) (n=365). Sacubitril/valsartan vs. Continued ACEI/ARB was evaluated on Changes in high-sensitivity cardiac troponin T (hs-cTnT), soluble ST2 (sST2), C-reactive protein (CRP), and growth differentiation factor-15 (GDF-15). Switching to sacubitril/valsartan did not modify cardiac or inflammatory biomarkers over 8 weeks vs continuing ACEI/ARB in acute heart failure.
Synapse has enriched 10 related papers. Consider them for comparative context: