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. 2021 Jun 15;143(24):2329-2331.
doi: 10.1161/CIRCULATIONAHA.120.052821. Epub 2021 Jun 14.

Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure: Racial Differences and a Potential for Reducing Disparities

Alanna A Morris  1 , Jeffrey M Testani  2 , Javed Butler  3
Affiliations

Sodium-Glucose Cotransporter-2 Inhibitors in Heart Failure: Racial Differences and a Potential for Reducing Disparities

Alanna A Morris et al. Circulation. .
No abstract available

Keywords: ethnic groups; healthcare disparities; heart failure; race; salt tolerance; sodium-glucose transporter 2 inhibitors.

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Figures

Figure 1.
Figure 1.
Effect of SGLT2 inhibitors on primary composite outcome according to pre-specified subgroup analyses by race-ethnicity (A); and potential mechanisms for racial differences that could explain overwhelming benefit of SGLT2-inhibitors in Black patients with HFrEF, as well as racial disparities that could impact real-world access to SGLT2-inhibitors for Black patients (B). A meta-analysis of the pooled treatment effects of empagliflozin and dapagliflozin on the composite endpoint of cardiovascular death or first hospitalization for HF in subgroups by race-ethnicity demonstrates a greater effect in Black patients (Panel A, modified with permission from Zannad et al. Lancet 2020; 396: 819–29). Numerous mechanisms have been suggested that may contribute to higher renal reabsorption of sodium in subjects of African ancestry, with biomarkers or receptors with known racial differences depicted in orange (Panel B). The putative decongestive properties induced through use of SGLT2 inhibitors are outlined, and may help overcome this pathophysiology, translating to improved clinical outcomes for Black patients enrolled in these clinical trials. However, various mechanisms could reduce access to SGLT2 inhibitors for Black patients, serving to actually worsen pre-existing healthcare disparities. ANP, atrial natriuretic peptide; BNP, B-type natriuretic peptide; ENaC, epithelial sodium channel; GDMT, guideline directed medical therapy; GLUT2, glucose transporter 2; GRK-4, G protein--coupled receptor kinase 4; NEDD4, neural precursor cell expressed, developmentally downregulated 4; NHE3, sodium-hydrogen exchanger 3; RAAS, renin angiotensin aldosterone system; SNS, sympathetic nervous system; SCNN1B, sodium channel epithelial 1 beta subunit.
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