We thank the authors of the letter (DTY-D-21-00785R1) for their interest in our work [1]. As pointed out, the correct reference for the finding of a significant reduction in the incidence of stroke and myocardial infarction (MI) associated with the use of the SGLT1/2 inhibitor sotagliflozin is from the SCORED trial [2] rather than from the SOLOIST trial [3]. We agree that the significant reductions in MI and in stroke (as well as in heart failure) with sotagliflozin were proven in patients with type 2 diabetes mellitus and chronic kidney disease in SCORED and that the significant reduction in heart failure with sotagliflozin in SOLOIST was proven in patients with acute worsening heart failure, but we believe that these benefits may extend to other patients beyond those specifically studied in the trials. However, future trials will be necessary to evaluate sotagliflozin’s effect on cardiovascular outcomes in patients without diabetes—in those with or without chronic kidney disease and with or without heart failure.

We disagree with the authors’ suggestion that the addition of SGLT1 to SGLT2 inhibition in patients with worsening heart failure could be deleterious, since there were highly significant reductions in the primary endpoint of cardiovascular death, hospitalizations, and urgent visits for heart failure in patients randomized to sotagliflozin in both SCORED and SOLOIST, including in the patients who had evidence of heart failure—either with reduced or preserved ejection fraction. In fact, SCORED and SOLOIST were the first trials in any drug class to demonstrate significant benefit in patients with heart failure with preserved ejection fraction, with benefits across the full range of ejection fraction.