Cardiorenal interactions in heart failure: insights from recent therapeutic advances

Figures

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  Figure 1. (A) Baseline risk and absolute risk reduction. Shown are absolute effect estimates in relation to absolute control arm event rate (on logarithmic scale) of pivotal randomized clinical trials in heart failure, chronic kidney disease and diabetes. (B) Baseline risk and absolute risk reduction relative to follow-up time. Shown are effect estimates per 100 patient-years follow-up in relation to control arm event rate per 100 patient-years follow-up (on logarithmic scale) of pivotal randomized clinical trials in heart failure, chronic kidney disease, and diabetes. ARR, absolute risk reduction; CKD, chronic kidney disease; DM, diabetes mellitus; GLP-1-RA, glucagon-like peptide 1 receptor agonist; HF, heart failure; MRA, mineralocorticoid receptor antagonist; RCT, randomized controlled trial; SGLT2i, sodium–glucose co-transporter 2 inhibitor.

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  Figure 2. Overview of hypothesized renal characteristics of SGLT2i, GLP-1-RA, and ns MRA therapy. ET1, endothelin 1; GFR, glomerular filtration rate; GLP-1-RA, glucagon-like peptide 1 receptor agonist; MR, mineralocorticoid receptor; (ns)MRA, (non-steroidal) mineralocorticoid receptor antagonist; NHE3, sodium–hydrogen anti-porter 3; NO, nitric oxide; SGLT2i, sodium–glucose co-transporter 2 inhibitor; TGF, tubuloglomerular feedback.

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  Figure 3. Overview of heart failure events, renal events, and safety across cardiovascular continuum and for different drug classes. ARR, absolute risk reduction; CV, cardiovascular; GFR, glomerular filtration rate; GLP-1-RA, glucagon-like peptide 1 receptor agonist; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HFpEF, heart failure with preserved ejection fraction; (ns)MRA, (non-steroidal) mineralocorticoid receptor antagonist; RRR, relative risk reduction; SGLT2i, sodium–glucose co-transporter 2 inhibitor.