International journal of cardiology · 2026
SGLT2 inhibitors and risk of new-onset left bundle branch block in heart failure with preserved ejection fraction.
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Zuin Marco, Vitali Francesco, Canovi Luca, Serenelli Matteo, Fucili Alessandro, Bertini Matteo
Аннотация
BACKGROUND: Whether sodium-glucose cotransporter 2 inhibitors (SGLT2i) may reduce the risk of developing new-onset left bundle branch block (LBBB) in patients with heart failure with preserved ejection fraction (HFpEF) remains unknown. We investigate the association between SGLT2i use and incident LBBB in patients with HFpEF.
METHODS: We conducted a cohort study using a prospectively database of patients with HFpEF. Patients receiving SGLT2i were propensity score-matched 1:1 with historical controls not receiving SGLT2i. The primary endpoint was new-onset LBBB, over a median 24-month follow-up. Cox proportional hazards models and Fine-Gray competing risk analyses were used to assess the association. Pre-specified subgroup analyses evaluated potential effect modification.
RESULTS: A total of 254 patients were included after matching (mean age 73 years, 62% female; 127 SGLT2i, 127 controls). Over a median follow-up of 24 month [interquartile range 22-26 months], new-onset LBBB occurred in 6 of 127 patients (4.7%) treated with SGLT2i versus 15 of 127 patients (11.8%) in the control group, corresponding to a hazard ratio (HR) of 0.41 (95% CI: 0.18-0.61, p < 0.001), which remained significant in competing risk analysis for all-cause of death (sHR 0.40; 95% CI 0.18-0.92; p = 0.01). The association was consistent across most subgroups, with no significant interactions. In patients with baseline QRS ≥110 ms and in those without diabetes, the effect did not reach statistical significance, although point estimates were directionally similar.
CONCLUSIONS: In HFpEF, SGLT2i use reduced incident LBBB risk over two years, consistent across subgroups, suggesting a role in preserving conduction integrity and preventing electrical dyssynchrony progression.
METHODS: We conducted a cohort study using a prospectively database of patients with HFpEF. Patients receiving SGLT2i were propensity score-matched 1:1 with historical controls not receiving SGLT2i. The primary endpoint was new-onset LBBB, over a median 24-month follow-up. Cox proportional hazards models and Fine-Gray competing risk analyses were used to assess the association. Pre-specified subgroup analyses evaluated potential effect modification.
RESULTS: A total of 254 patients were included after matching (mean age 73 years, 62% female; 127 SGLT2i, 127 controls). Over a median follow-up of 24 month [interquartile range 22-26 months], new-onset LBBB occurred in 6 of 127 patients (4.7%) treated with SGLT2i versus 15 of 127 patients (11.8%) in the control group, corresponding to a hazard ratio (HR) of 0.41 (95% CI: 0.18-0.61, p < 0.001), which remained significant in competing risk analysis for all-cause of death (sHR 0.40; 95% CI 0.18-0.92; p = 0.01). The association was consistent across most subgroups, with no significant interactions. In patients with baseline QRS ≥110 ms and in those without diabetes, the effect did not reach statistical significance, although point estimates were directionally similar.
CONCLUSIONS: In HFpEF, SGLT2i use reduced incident LBBB risk over two years, consistent across subgroups, suggesting a role in preserving conduction integrity and preventing electrical dyssynchrony progression.