Effect of sodium-glucose cotransporter 2 inhibitors on ventricular function in systemic right ventricular failure

Figures

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  Figure 1. Changes in sRV GLS and FAC after starting SGLT2i. (A) Predicted longitudinal change in sRV GLS with 95% CIs. There is a significant improvement in the first 50 days after starting SGLT2i (−1.4%-point per month, p<0.001) and subsequent stabilisation (p=0.520). There was a significant negative effect of age (−0.1%-point per year of age, p=0.049), but age did not influence the temporal changes after starting SGLT2i. (B) Predicted longitudinal change in sRV FAC. There is a similar initial improvement in the first 50 days (3.2%-point per month, p=0.002), followed by a significant deterioration in patients with single-site spLV pacing (−0.9%-point per month, p=0.012). In contrast, patients without spLV pacing remained stable (p=0.573). FAC, fractional area change; FU, follow-up; GLS, global longitudinal strain; SGLT2i, sodium-glucose cotransporter 2 inhibitor; spLV, subpulmonary left ventricle; sRV, systemic right ventricle.

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  Figure 2. Changes in TAPSE and S’ after starting SGLT2i. (A) Predicted longitudinal change in TAPSE with 95% CIs. A significant improvement can be appreciated in the first 50 days (1.2 mm per month, p=0.006). After 50 days, this was no longer significant (p=0.721). No covariates contributed significantly to the model. (B) Predicted change in S’ over time. Patients with ccTGA had a significant decrease in S’ in the first 50 days (−1.4 cm/s per month, p=0.014), followed by a significant improvement (0.5 cm/s per month, p<0.001). TGA atrial switch patients remained stable. (cc)TGA, (congenitally corrected) transposition of the great arteries; FU, follow-up; SGLT2i, sodium-glucose cotransporter 2 inhibitor; sRV, systemic right ventricle; TAPSE, tricuspid annular plane systolic excursion.

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  Figure 3. Changes in spLV FWS and FAC after starting SGLT2i. (A) Predicted longitudinal change in spLV FWS (%) with 95% CIs, faceted for sRV anatomical subgroups. There was a significant improvement in the first 50 days for patients without spLV pacing (−1.5%-point per month, p=0.048). This improvement was more pronounced in patients with spLV pacing (−3.9%-point per month, interaction p=0.046). After the first 50 days, there were no significant changes in both groups (p=0.368). Overall, ccTGA patients had a significantly better spLV FWS than TGA atrial switch patients (intercept 6.5%-point, p<0.001). (B) Predicted change in spLV FAC (%) over time. Patients with an escalation in HF pharmacotherapy during follow-up had a significantly higher spLV FAC at baseline (intercept 12.0%-point, p=0.003) and showed a significant deterioration (−2.3%-point per month, p<0.001) compared with patients without an escalation in pharmacotherapy (0.2%-point per month, p=0.237). (cc)TGA, (congenitally corrected) transposition of the great arteries; FAC, fractional area change; FU, follow-up; FWS, free-wall strain; HF, heart failure; SGLT2i, sodium-glucose cotransporter 2 inhibitor; spLV, subpulmonary left…

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  Figure 4. Effect of SGLT2i on ventricular function in sRV failure. This real-world evaluation of data from the ACHIEVE-SGLT2i registry demonstrated that SGLT2i are associated with improvements in systolic function in sRV failure patients. sRV GLS improved significantly in the first 50 days and stabilised afterwards. Age at start SGLT2i significantly influenced overall sRV GLS, as indicated by the separate lines for the first quartile (Q1), median and third quartile (Q3) of age. sRV FAC also improved significantly in the first 50 days. After 50 days, patients without spLV pacing remained stable, while patients with spLV pacing deteriorated. (cc)TGA, (congenitally corrected) transposition of the great arteries; FAC, fractional area change; FU, follow-up; GLS, global longitudinal strain; HF, heart failure; SGLT2i, sodium-glucose cotransporter 2 inhibitor; spLV, subpulmonary left ventricle; sRV, systemic right ventricle; TTE, transthoracic echocardiography.