Adding SGLT2i to heart failure therapy in children with LVSD delayed time to death, MCS, transplant listing, or hospitalization by 5.1 months (p=0.03).
Does the addition of SGLT2 inhibitors to standard heart failure medical therapy delay the composite of death, mechanical circulatory support, heart transplant listing, or heart failure hospitalization in children with left ventricular systolic dysfunction?
The addition of SGLT2 inhibitors to standard medical therapy in pediatric patients with left ventricular systolic dysfunction is associated with a significantly delayed time to the composite of death, mechanical circulatory support, heart transplant listing, or heart failure hospitalization.
Absolute Event Rate: 0% vs 0%
Abstract Introduction Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are proven to reduce risk of cardiovascular death and hospitalization for heart failure (HHF) in adults across the range of left ventricular ejection fraction (LVEF). There are limited data on SGLT2i use in pediatric heart failure (HF). Purpose Assess if addition of SGLT2i to standard HF medical therapy (HFMT) in children with left ventricular systolic dysfunction (LVSD) is associated with improved outcomes. Methods Single-center, matched pair case-control analysis of 146 pediatric patients (≤ 21 years old) with LVSD. Cases (n=73) had SGLT2i added to HFMT between 2020-2024. Cases were matched 1:1 by age, cardiac diagnosis, LVEF, and HFMT received to historical controls (n=73) who did not receive SGLT2i from 2009 to 2019. Patients with single ventricular physiology, supported by mechanical circulatory support (MCS), or listed for heart transplant (HTX) were excluded. Results Median age was 11.3 years (range 1 day to 21 years); 73% (106/146) with dilated cardiomyopathy and remainder with repaired biventricular congenital heart disease. Baseline HFMT included sacubitril/valsartan (53%), ACE inhibitor (40%), or ARB (3%), beta-blocker (79%), and mineralocorticoid receptor antagonist (64%). Median initial daily SGLT2i dose (dapagliflozin 86%; empagliflozin 14%) received was 5 mg or 0.13 (IQR 0.10-0.17) mg/kg. Fifty-eight percent had a HHF within the prior year, 49% were started on HFMT during a HHF, 34% had new onset HF, and 70% had LVEF ≤ 40%. Median follow-up was 12.7 months (IQR 6.6-22.9). Among all 146 patients, median LVEF increased significantly from 34% (IQR 26-42) to 43% (IQR 31-53) and B-type natriuretic peptide (BNP) decreased from 295 pg/mL (IQR 64-826) to 73 pg/mL (IQR 15-399) (both p0.05). There was a significant difference in NYHA/Ross Class from baseline (I/II: 68%; III/IV: 32%) to latest follow-up (I/II: 83%; III/IV: 17%) (p0.01) with 36% improved, 54% unchanged, and 10% worsened. Changes in LVEF and NYHA/Ross Class were statistically significant from baseline to latest follow-up within each cohort (all p0.05 for intragroup comparison) but were not significantly different between cases and controls (all p0.05 for intergroup comparison). Fewer cases experienced composite event of death, MCS, or HTX listing (cases 10% vs controls 18%, p=0.15). Significantly fewer cases experienced HHF within 90 days of HFMT initiation (cases 1% vs controls 11%, p=0.03). Time to first composite event or HHF was significantly different (cases 8.7 months vs controls 3.6 months, p=0.03). Conclusion HFMT in children with LVSD is associated with improved clinical outcomes. Use of SGLT2i in addition to HFMT in children with LVSD is associated with significantly delayed time to composite of death, MCS, HTX listing, or HHF, and warrants further larger scale studies to determine efficacy.
Newland et al. (Sat,) reported a other. Adding SGLT2i to heart failure therapy in children with LVSD delayed time to death, MCS, transplant listing, or hospitalization by 5.1 months (p=0.03).