Key result
SGLT2i use during acute heart failure is linked to a ~38% NT-proBNP reduction versus no use.
Why the study?
While SGLT2 inhibitors are beneficial in chronic HF, emerging data suggest these benefits may extend to acute HF decompensation through enhanced decongestion.
Does SGLT2 inhibitor continuation or initiation reduce NT-proBNP levels in patients hospitalized for acute heart failure decompensation?
Cohort (n=159)
Does SGLT2 inhibitor continuation or initiation reduce NT-proBNP levels in patients hospitalized for acute heart failure decompensation?
Absolute Event Rate: -38.3% vs -2.1%
p-value: p=0.001
Continuation or initiation of SGLT2 inhibitors during hospitalization for acute heart failure decompensation is associated with significant reductions in NT-proBNP levels, suggesting enhanced decongestion.
Supports SGLT2i initiation or continuation in acute HF decompensation; hypothesis-generating given low-certainty observational data requiring RCT confirmation.**[[1]](https://www.mdpi.com/2075-1729/16/4/621)[[2]](https://www.mdpi.
Introduction: Sodium-glucose cotransporter-2 inhibitors (SGLT2is) have proven beneficial in chronic heart failure (HF) across a wide range of left ventricular ejection fractions (LVEFs). Emerging data suggests that these benefits may extend to acute HF decompensation through enhanced decongestion. Purpose: To investigate changes in N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels according to SGLT2i use among patients hospitalized for acute HF decompensation. Methods: In this prospective cohort study, consecutive patients hospitalized for HF decompensation were enrolled. Demographics, comorbidities, and cardiovascular risk factors were recorded. Participants were classified into three groups: Group 1—No SGLT2i use or discontinuation; Group 2—Prior SGLT2i use and continuation; Group 3—SGLT2i-naïve with initiation during hospitalization. NT-proBNP was measured on admission and discharge. Results: A total of 159 patients (median age 79 years, 64.8% male) were included. Group 1 patients exhibited negligible changes in NT-proBNP, whereas those continuing or newly initiating SGLT2i demonstrated significant reductions (absolute change: 506 [8792] pg/mL vs. −5610 [9461] pg/mL vs. −3602 [4409] pg/mL, p = 0.001, percentage change: −2.1 [63.4]% vs. −30.3 [39.0]% vs. −38.3 [41.5]%, p = 0.001). Multivariable regression confirmed that SGLT2i continuation or initiation independently predicted greater NT-proBNP reduction. Conclusions: NT-proBNP levels were significantly reduced among patients with decompensated HF treated with SGLT2i, with the greatest reduction in treatment-naïve patients. These findings highlight the potential role of SGLT2i even during acute HF hospitalization.
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Fountoulakis et al. (2026) conducted a cohort in Acute heart failure decompensation (n=159). SGLT2 inhibitors (continuation or initiation) vs. No SGLT2i use or discontinuation was evaluated on Percentage change in NT-proBNP levels (p=0.001). SGLT2i initiation or continuation during acute heart failure hospitalization significantly reduced NT-proBNP levels compared to no use (-38.3% and -30.3% vs -2.1%, p=0.001).
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