Key result
Canagliflozin did not significantly reduce NT-proBNP levels compared to glimepiride overall (ratio of change 0.93), but showed a trend toward reduction in the subgroup with lower left ventricular diastolic function.
Why the study?
It was hypothesized that the beneficial effect of SGLT2 inhibitors on NT-proBNP levels might depend on baseline left ventricular diastolic function in patients with T2DM and chronic HF.
Does canagliflozin reduce NT-proBNP levels compared to glimepiride in patients with T2DM and chronic heart failure, stratified by baseline LV diastolic function?
RCT (n=233)
Open-label, blinded-endpoint
1:1 ratio
Yes
Does canagliflozin reduce NT-proBNP levels compared to glimepiride in patients with T2DM and chronic heart failure, stratified by baseline LV diastolic function?
Answers are grounded in this paper and cite their sources.
Canagliflozin showed a trend toward a greater reduction in NT-proBNP levels compared to glimepiride in patients with T2DM and chronic heart failure who had more severe baseline left ventricular diastolic dysfunction.
BACKGROUND: Identification of the effective subtypes of treatment for heart failure (HF) is an essential topic for optimizing treatment of the disorder. We hypothesized that the beneficial effect of SGLT2 inhibitors (SGLT2i) on the levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) might depend on baseline diastolic function. To elucidate the effects of SGLT2i in type 2 diabetes mellitus (T2DM) and chronic HF we investigated, as a post-hoc sub-study of the CANDLE trial, the effects of canagliflozin on NT-proBNP levels from baseline to 24 weeks, with the data stratified by left ventricular (LV) diastolic function at baseline. METHODS: Patients (n = 233) in the CANDLE trial were assigned randomly to either an add-on canagliflozin (n = 113) or glimepiride treatment groups (n = 120). The primary endpoint was a comparison between the two groups of the changes from baseline to 24 weeks in NT-pro BNP levels, stratified according to baseline ventricular diastolic function. RESULTS: The change in the geometric mean of NT-proBNP level from baseline to 24 weeks was 0.98 (95% CI 0.89-1.08) in the canagliflozin group and 1.07 (95% CI 0.97-1.18) in the glimepiride group. The ratio of change with canagliflozin/glimepiride was 0.93 (95% CI 0.82-1.05). Responder analyses were used to investigate the response of an improvement in NT-proBNP levels. Although the subgroup analyses for septal annular velocity (SEP-e') showed no marked heterogeneity in treatment effect, the subgroup with an SEP-e' < 4.7 cm/s indicated there was an association with lower NT-proBNP levels in the canagliflozin group compared with that in the glimepiride group (ratio of change with canagliflozin/glimepiride (0.83, 95% CI 0.66-1.04). CONCLUSIONS: In the subgroup with a lower LV diastolic function, canagliflozin showed a trend of reduced NT-pro BNP levels compared to that observed with glimepiride. This study suggests that the beneficial effects of canagliflozin treatment may be different in subgroups classified by the severity of LV diastolic dysfunction.
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Kusunose et al. (2021) conducted an RCT in Type 2 diabetes mellitus and chronic heart failure (n=233). Canagliflozin vs. Glimepiride was evaluated on Change in geometric mean of NT-proBNP level from baseline to 24 weeks (Ratio of change 0.93, 95% CI 0.82-1.05, p=0.244). Canagliflozin did not significantly reduce NT-proBNP levels compared to glimepiride overall (ratio of change 0.93), but showed a trend toward reduction in the subgroup with lower left ventricular diastolic function.
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