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Randomized Controlled Trial
. 2025 Jun;4(6):761-772.
doi: 10.1038/s44161-025-00657-7. Epub 2025 Jun 13.

Secondary analysis of the EMPACT-MI trial reveals cardiovascular-kidney efficacy and safety of empagliflozin after acute myocardial infarction

Affiliations
Randomized Controlled Trial

Secondary analysis of the EMPACT-MI trial reveals cardiovascular-kidney efficacy and safety of empagliflozin after acute myocardial infarction

Rahul Aggarwal et al. Nat Cardiovasc Res. 2025 Jun.

Abstract

Data on the cardiovascular-kidney effects and safety of empagliflozin among patients with acute myocardial infarction are limited. EMPACT-MI (Study to Evaluate the Effect of Empagliflozin on Hospitalization for Heart Failure and Mortality in Patients with Acute Myocardial Infarction) was a double-blind, multicenter clinical trial that randomized 6,522 patients with acute myocardial infarction and risk for heart failure to empagliflozin or placebo. Here we show in this secondary analysis that the mean estimated glomerular filtration rate at baseline was 76.1 ml min-1 1.73 m-2 (s.d. = 19.9 ml min-1 1.73 m-2), with longitudinal kidney function data available for 1,152 (17.7%) treated patients from select countries. By 24 months, compared with baseline, the estimated glomerular filtration rate was similar in the empagliflozin group but declined in the placebo group (P = 0.01). Empagliflozin reduced the total adverse events of heart failure or all-cause mortality irrespective of kidney function (Pinteraction = 0.30). Thirty-day adverse event rates were similar by treatment group and consistent across baseline kidney function. Empagliflozin had kidney-protective effects, reduced heart failure outcomes and was safe to initiate soon after acute myocardial infarction across baseline kidney function.

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Conflict of interest statement

Competing interests: R.A. is involved in research funded by the Bristol Myers Squibb-Pfizer alliance, Novartis, Lexicon, Cleerly and Amarin, and has previously served as a consultant for Lexicon. D.L.B. discloses the following relationships: advisory board membership for Angiowave, Bayer, Boehringer Ingelheim, CellProthera, Cereno Scientific, E-Star Biotech, High Enroll, Janssen, Level Ex, McKinsey, Medscape Cardiology, Merck, NirvaMed, Novo Nordisk, Stasys and Tourmaline Bio; board of directors membership and stock holding for the American Heart Association New York City, Angiowave (stock options), Bristol Myers Squibb (stock), DRS.LINQ (stock options) and High Enroll (stock). He has been a consultant for Broadview Ventures, Corcept Therapeutics, GlaxoSmithKline, Hims, SFJ, Summa Therapeutics and Youngene. He reports membership of the following data monitoring committees: Acesion Pharma, Assistance Publique-Hôpitaux de Paris, Baim Institute for Clinical Research (formerly Harvard Clinical Research Institute, for the PORTICO trial, funded by St. Jude Medical, now Abbott), Boston Scientific (Chair, PEITHO trial), Cleveland Clinic, Contego Medical (Chair, PERFORMANCE 2), Duke Clinical Research Institute, Mayo Clinic, Mount Sinai School of Medicine (for the ENVISAGE trial, funded by Daiichi Sankyo; for the ABILITY-DM trial, funded by Concept Medical; for ALLAY-HF, funded by Alleviant Medical), Novartis, Population Health Research Institute; and Rutgers University (for the National Institutes of Health (NIH)-funded MINT Trial). He reports honoraria from the American College of Cardiology (Senior Associate Editor, Clinical Trials and News, ACC.org; Chair, ACC Accreditation Oversight Committee), Arnold and Porter law firm (work related to Sanofi/Bristol Myers Squibb clopidogrel litigation), Baim Institute for Clinical Research (formerly Harvard Clinical Research Institute; AEGIS-II executive committee funded by CSL Behring), Belvoir Publications (Editor in Chief, Harvard Heart Letter), the Canadian Medical and Surgical Knowledge Translation Research Group (clinical trial steering committees), CSL Behring (AHA lecture), Cowen and Company, Duke Clinical Research Institute (clinical trial steering committees, including for the PRONOUNCE trial, funded by Ferring Pharmaceuticals), HMP Global (Editor in Chief, Journal of Invasive Cardiology), Journal of the American College of Cardiology (Guest Editor and Associate Editor), Level Ex, Medtelligence/ReachMD (CME steering committees), MJH Life Sciences, Oakstone CME (Course Director, Comprehensive Review of Interventional Cardiology), Piper Sandler, Population Health Research Institute (for the COMPASS operations committee, publications committee, steering committee and USA national co-leader, funded by Bayer), WebMD (CME steering committees), Wiley (steering committee), and Clinical Cardiology (Deputy Editor). He is named on a patent application (17/574,977) for sotagliflozin assigned to Brigham and Women’s Hospital, which was assigned to Lexicon. Neither D.L.B. nor Brigham and Women’s Hospital receive any income from this patent. The patent application is still pending. He has received research funding from Abbott, Acesion Pharma, Afimmune, Aker Biomarine, Alnylam, Amarin, Amgen, AstraZeneca, Bayer, Beren, Boehringer Ingelheim, Boston Scientific, Bristol Myers Squibb, Cardax, CellProthera, Cereno Scientific, Chiesi, CinCor, Cleerly, CSL Behring, Faraday Pharmaceuticals, Ferring Pharmaceuticals, Fractyl, Garmin, HLS Therapeutics, Idorsia, Ironwood, Ischemix, Janssen, Javelin, Lexicon, Lilly, Medtronic, Merck, Moderna, MyoKardia, NirvaMed, Novartis, Novo Nordisk, Otsuka, Owkin, Pfizer, PhaseBio, PLx Pharma, Recardio, Regeneron, Reid Hoffman Foundation, Roche, Sanofi, Stasys, Synaptic, The Medicines Company, Youngene, 89Bio. He has received royalties from Elsevier (Editor, Braunwald’s Heart Disease). He has been a site co-investigator for Cleerly. A.F.H. discloses research funding from American Regent, Amgen, AstraZeneca, Bayer, Beam, Boehringer Ingelheim, Crispr Therapeutics, Cytokinetics, Intellia, Merck, Novartis, Novo Nordisk, Pfizer and Verily. He has been a consultant to AstraZeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Bristol Myers Squibb, Novartis, Novo Nordisk and Pfizer. S.D.A. discloses receiving grants from Abbott Laboratories, and personal fees from Actimed Therapeutics, Alleviant, AstraZeneca, Bayer, Berlin Heals, BioVentrix, Boehringer Ingelheim, Brahms, Cardiac Dimensions, Cardior Pharmaceuticals, Cordio, CSL Vifor, CVRx, Cytokinetics, Edwards Lifesciences, Farraday Pharmaceuticals, GSK, HeartKinetics, Impulse Dynamics, Lilly, Mankind Pharma, Medtronic, Novartis, Novo Nordisk, Occlutech, Pfizer, Regeneron, Relaxera, Repairon, SCIRENT Clinical Research and Science, Sensible Medical, Servier, Vectorious Medical Technologies, Vivus and V-Wave. He was named co-inventor of two patent applications regarding MR-proANP (DE 102007010834 and DE 102007022367), but he does not benefit personally from the related issued patents. W.S.J. discloses research funding from Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Merck, the NIH, Novartis and the Patient-Centered Outcomes Research Institute. M.M. discloses employment from Boehringer Ingelheim. M.C.P. has received research funding from Boehringer Ingelheim, Roche, SQ Innovations, AstraZeneca, Novartis, Novo Nordisk, Medtronic, Boston Scientific and Pharmacosmos, and has served on committees or consulted for Abbott, Akero, Applied Therapeutics, Amgen, AnaCardio, Biosensors, Boehringer Ingelheim, Corteria, Novartis, AstraZeneca, Novo Nordisk, Abbvie, Bayer, Horizon Therapeutics, Foundry, Takeda, Cardiorentis, Pharmacosmos, Siemens, Eli Lilly, Vifor, New Amsterdam, Moderna, Teikoku, LIB Therapeutics, 3R Lifesciences, Reprieve, FIRE-1, Corvia and Regeneron. D.S., M.S. and V.T. disclose employment from Boehringer Ingelheim. J.A.U. discloses the following relationships: advisory board membership for Boehringer Ingelheim, Novavax, Novo Nordisk and Sanofi; speaker honoraria from Amgen, AstraZeneca, Boehringer Ingelheim and Eli Lilly and Company; and research funding to his institution from Amgen, Bayer, Boehringer Ingelheim and Novartis. J.B. discloses being a consultant to Abbott, American Regent, Amgen, Applied Therapeutic, AskBio, Astellas, AstraZeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Bristol Myers Squibb, Cardiac Dimension, Cardiocell, Cardior, CSL Bearing, CVRx, Cytokinetics, Daxor, Edwards, Element Science, Faraday, Foundry, G3P, Innolife, Impulse Dynamics, Imbria, Inventiva, Ionis, Levator, Lexicon, Lilly, LivaNova, Janssen, Medtronics, Merck, Occlutech, Owkin, Novartis, Novo Nordisk, Pfizer, Pharmacosmos, Pharmain, Prolaio, Pulnovo, Regeneron, Renibus, Roche, Salamandra, Salubris, Sanofi, SC Pharma, Secretome, Sequana, SQ Innovation, Tenex, Tricog, Ultromics, Vifor and Zoll. J.H. declares no competing interests. The study was supported and funded by the Boehringer Ingelheim and Eli Lilly and Company Alliance. The sponsor was involved in the study design, data collection and analysis. While the sponsor was allowed to comment or edit the paper, the authors were under no obligation to incorporate such changes or to submit the paper for publication. The authors meet the criteria for authorship as recommended by the ICMJE. The authors did not receive payment related to the development of the paper. Boehringer Ingelheim was given the opportunity to review the paper for medical and scientific accuracy and intellectual property considerations.

Figures

Fig. 1
Fig. 1. Change in kidney function.
Patients randomized to empagliflozin or placebo with longitudinal eGFR data in EMPACT-MI. Longitudinal eGFR data were obtained only for a subset of patients, specifically those treated with the study drug, in Bulgaria, Germany, Hungary and Serbia, and with available data (n = 1,152, 17.7%). Patients were compared overall. The eGFR was determined using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Changes in eGFR over time on treatment were assessed using mixed models to account for repeated eGFR values. Models included age as a linear covariate and sex, geographical region, baseline LVEF, T2D status, persistent or permanent atrial fibrillation, previous MI, peripheral artery disease, smoking status, baseline eGFR according to visit, and visit according to treatment interactions as fixed effects. All significance testing was two-sided without adjustment for multiple testing. Estimates are shown with the 95% CI bars. The number of patients at the follow-up are presented for pooled treatment groups. The number of patients at the follow-up at 12 months excludes all patients counted at the 18-month and 24-month visits because only the latest of the 12–24-month measurements was expected. The number of patients at the follow-up at 18 months excludes all patients counted at the 24-month visits because only the latest of the 12–24-month measurements was expected. aUnadjusted baseline pooled over both treatment groups.
Fig. 2
Fig. 2. Change in kidney function according to baseline kidney function.
a,b, Patients randomized to empagliflozin or placebo with longitudinal eGFR data in EMPACT-MI. Longitudinal eGFR data were obtained only for a subset of patients, specifically those treated with the study drug, in Bulgaria, Germany, Hungary and Serbia, and with available data (n = 1,152, 17.7%). Patients were compared according to a baseline kidney function of <60 ml min−1 1.73 m2 (a) and ≥60 ml min−1 1.73 m2 (b). The eGFR was determined using the CKD-EPI equation. Changes in eGFR over time on treatment were assessed using mixed models to account for repeated eGFR values. Models included age as a linear covariate and sex, geographical region, baseline LVEF, T2D status, persistent or permanent atrial fibrillation, previous MI, peripheral artery disease, smoking status, baseline eGFR according to visit and visit according to treatment interactions as fixed effects. The model for the subgroup analyses included an additional factor for the subgroup according to visit and according to treatment interaction. All significance testing was two-sided without adjustment for multiple testing. Estimates are shown with the 95% CI bars. The number of patients at the follow-up are presented for the pooled treatment groups. The number of patients at the 12-month follow-up excludes all patients counted at the 18-month and 24-month visits because only the latest of the 12–24-month measurements was expected. The number of patients at the 18-month follow-up excludes all patients counted at the 24-month visits because only the latest of the 12–24-month measurements was expected. aUnadjusted baseline pooled over both treatment groups.
Fig. 3
Fig. 3. HF endpoints according to baseline kidney function.
Patients randomized to empagliflozin or placebo in EMPACT-MI. Patients were stratified according to baseline kidney function to the eGFR categories of −1 1.73 m2, ≥30 to <60 ml min−1 1.73 m2, ≥60 to <90 ml min−1 1.73 m2 and ≥90 ml min−1 1.73 m2. The absolute risk difference represents the adjusted rate difference per 100 patient years at risk. Endpoints included a composite of the total number of AEs of HF or all-cause mortality, the total number of AEs of HF and the total number of hospitalizations for HF. The AEs of HF were defined as investigator-reported AEs categorized as ‘cardiac failure’ according to the Medical Dictionary for Regulatory Activities (MedDRA), and included not only the events analyzed as the prespecified endpoint of HF hospitalization but a broader range of AEs of HF, including outpatient non-fatal AEs and those requiring or prolonging hospitalization or with a fatal outcome. Kidney function was determined as the eGFR using the CKD-EPI equation. Differences in HF outcomes between the empagliflozin and placebo groups were assessed using negative binomial regression models and included total events (first and recurrent). An interaction term for treatment and baseline eGFR category was included in the models. Models included adjustment for the baseline covariates of age, sex, geographical region, eGFR, LVEF (<35% or ≥35%), T2D status, persistent or permanent atrial fibrillation, previous MI, peripheral artery disease and smoking status. All significance testing was two-sided without adjustment for multiple testing. The figure shows the RR with the 95% CI error bars. N/A, not applicable.
Fig. 4
Fig. 4. Total AEs of HF or all-cause mortality according to kidney function (four categories).
ad, Patients randomized to empagliflozin or placebo in EMPACT-MI. The endpoint was a composite of the total number of AEs of HF or all-cause mortality. Patients were stratified according to baseline kidney function to the eGFR categories of <30 ml min−1/1.73 m2 (a), ≥30 to <60 ml min−1 1.73 m2 (b), ≥60 to <90 ml min−1 1.73 m2 (c) and ≥90 ml min−1 1.73 m2 (d). Kidney function was determined according to the eGFR using the CKD-EPI equation. The AEs of HF were defined as investigator-reported AEs that were categorized as ‘cardiac failure’ according to MedDRA, and which included not only the events analyzed as the prespecified endpoint of HF hospitalization but also the broader range of AEs of HF, including outpatient non-fatal AEs and those requiring or prolonging hospitalization or with a fatal outcome. The x axis shows the time from randomization in days and the y axis shows the cumulative mean number of events per patient. Differences in endpoint between the empagliflozin and placebo group were assessed using a negative binomial regression model and included total events (first and recurrent). An interaction term for treatment and baseline eGFR category was included. The model included adjustment for the baseline covariates of age, sex, geographical region, eGFR, LVEF (<35% or ≥35%), T2D status, persistent or permanent atrial fibrillation, previous MI, peripheral artery disease and smoking status. All significance testing was two-sided without adjustment for multiple testing. No significant interaction was observed between treatment and baseline kidney function (Pinteraction = 0.30).
Extended Data Fig. 1
Extended Data Fig. 1. Change in Kidney Function by Baseline Use of Additional Medical Therapies.
Patients randomized to empagliflozin or placebo with longitudinal eGFR data were compared in EMPACT-MI from baseline to 24 months. Patients were stratified by baseline use or not use of key therapies, specifically ACEi/ARB/ARNi (panel a), MRA (panel b), and loop diuretics (panel c). Longitudinal eGFR data was obtained only for a subset of patients, specifically those treated in Bulgaria, Germany, Hungary, and Serbia. Changes in eGFR over time on-treatment was assessed using mixed models to account for repeated eGFR values. Models that age as a linear covariate and sex, geographic region, baseline left ventricular ejection fraction, type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, smoking status, baseline estimated GFR according to visit, visit according to treatment interactions as fixed effects and subgroup according to visit according to treatment interaction. Estimates are shown with 95% confidence intervals bars. Abbreviations: ACEi, angiotensin-converting enzyme; AE, adverse events; ARB, angiotensin II receptor blockers; ARNI, angiotensin receptor/neprilysin inhibitor; HF, eGFR, estimated glomerular filtration rate; heart failure; HHF, heart failure hospitalization, MRA, mineralocorticoid receptor antagonist.
Extended Data Fig. 2
Extended Data Fig. 2. Change in Kidney Function by Use of Additional Medical Therapies.
Patients randomized to empagliflozin or placebo with longitudinal eGFR data were compared in EMPACT-MI from baseline to 24 months. Patients were stratified by use key therapies, specifically ACEi/ARB/ARNi (panel a), MRA (panel b), and loop diuretics (panel c) at discharge with introduction prior to index hospitalization, at discharge with introduction during index hospitalization and not on medication at discharge. Longitudinal eGFR data was obtained only for a subset of patients, specifically those treated in Bulgaria, Germany, Hungary, and Serbia. Changes in eGFR over time on-treatment was assessed using mixed models to account for repeated eGFR values. Models that age as a linear covariate and sex, geographic region, baseline left ventricular ejection fraction, type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, smoking status, baseline estimated GFR according to visit, visit according to treatment interactions as fixed effects and subgroup according to visit according to treatment interaction. Estimates are shown with 95% confidence intervals bars. Abbreviations: ACEi, angiotensin-converting enzyme; AE, adverse events; ARB, angiotensin II receptor blockers; ARNI, angiotensin receptor/neprilysin inhibitor; HF, eGFR, estimated glomerular filtration rate; heart failure; HHF, heart failure hospitalization, MRA, mineralocorticoid receptor antagonist.
Extended Data Fig. 3
Extended Data Fig. 3. Cumulative Incidence of Kidney Outcomes.
Patients randomized to empagliflozin or placebo were compared in EMPACT-MI. The endpoints included the following time-to-first event endpoints: kidney disease progression (panel a); kidney disease progression or all-cause mortality (panel b); AKI (panel c); and AKI, chronic renal replacement therapy, renal transplantation, or death (panel d). The x-axis shows time from randomization in days and the y-axis shows estimated cumulative incidence function or respectively Kaplan-Meier estimates (panel b). First kidney disease progression was defined as time to first decline of eGFR ≥40% from baseline, estimated GFR < 15 ml min−1 1.73 m−2 for patients with baseline estimated GFR ≥ 30 ml min−1 1.73 m−2 or <10 ml min−1 1.73 m−2 for patients with baseline eGFR <30 ml min−1 1.73 m−2. Renal death was defined as a death event with primary adverse event leading to death in narrow Sandardized MedDRA queries (SMQ),’Acute Renal Failure’. Chronic renal replacement therapy was defined as renal replacement therapy lasting for at least 90 days. Differences between the empagliflozin and placebo group were assessed with Cox proportional hazard models. A HR less than 1 indicates reduction in risk for the endpoint with empagliflozin while a HR of greater than 1 indicating increase in risk for the endpoint with empagliflozin. Models included adjustment for the baseline covariates of age, sex, geographic region, eGFR, left ventricular ejection fraction ( < 35% or ≥35%), type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, and smoking status. All significance testing was two-sided without adjustment for multiple testing. Abbreviations: AKI, acute kidney injury; eGFR, estimated glomerular filtration rate; HR, hazard ratio.
Extended Data Fig. 4
Extended Data Fig. 4. Change in Kidney Function Over Time During the Study.
Patients randomized to empagliflozin or placebo with longitudinal eGFR data in EMPACT-MI. Longitudinal eGFR data was obtained only for a subset of patients, specifically those randomised in Bulgaria, Germany, Hungary, and Serbia. Analysis is through end of study and not restricted to time on study drug. Changes in eGFR over time was assessed using mixed models to account for repeated eGFR values. Changes in eGFR over time was assessed using mixed models to account for repeated eGFR values. Models included age as a linear covariate and sex, geographic region, baseline left ventricular ejection fraction, type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, smoking status, baseline estimated GFR according to visit, and visit according to treatment interactions as fixed effects. Estimates are shown with 95% confidence interval bars.
Extended Data Fig. 5
Extended Data Fig. 5. Kaplan Meier Estimates of Heart Failure Hospitalization or All-Cause Mortality by Kidney Function.
Patients randomized to empagliflozin or placebo were compared in EMPACT-MI. The endpoint was a composite of time to first HHF or all-cause mortality. Patients were stratified by baseline kidney function, to categories eGFR of −1 1.73 m−2 (panel a), 30- < 60 ml min−1 1.73 m−2 (panel b), 60- < 90 ml min−1 1.73 m−2 (panel c), ≥90 ml min−1 1.73 m−2 (panel d). Kidney function was determined by eGFR with the CKD-EPI equation. The x-axis shows time from randomization in days and the y-axis shows probability of event based on Kaplan Meier estimates. Differences between the empagliflozin and placebo group were assessed with a Cox proportional hazard model. A HR less than 1 indicates reduction in risk for the endpoint with empagliflozin while a HR of greater than 1 indicates an increase in risk for the endpoint with empagliflozin. An interaction term for treatment and baseline eGFR category was included. The models included adjustment for the baseline covariates of age, sex, geographic region, eGFR, left ventricular ejection fraction ( < 35% or ≥35%), type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, and smoking status. All significance testing was two-sided without adjustment for multiple testing. No significant interaction was observed between treatment effect and baseline kidney function (Pinteraction = 0.81). Abbreviations: CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio; HHF, heart failure hospitalization.
Extended Data Fig. 6
Extended Data Fig. 6. Total Adverse Events of HF or All-Cause Mortality by Continuous Kidney Function.
Patients randomized to empagliflozin or placebo in EMPACT-MI. The endpoint was a composite of total number of AEs of HF or all-cause mortality. Baseline kidney function was evaluated continuously by eGFR. Kidney function was determined by eGFR with the CKD-EPI equation. The adverse events of Heart Failure were defined as investigator-reported adverse events that were categorized as “cardiac failure” per MedDRA,21 and included not only the events analyzed as prespecified endpoint of heart failure hospitalization but broader range of adverse events of heart failure including outpatient non-fatal adverse events as well as those requiring or prolonging hospitalization or with a fatal outcome. The x-axis shows baseline eGFR and the y-axis shows event rate ratio for empagliflozin compared with placebo. The shaded area shows the 95% Confidence interval. A rate ratio less than 1 indicates reduction in the risk of outcome with empagliflozin while a rate ratio of greater than 1 indicates an increase in the risk of outcome with empagliflozin. Differences between the empagliflozin and placebo group were assessed across the baseline eGFR range using cubic splines. The negative binomial regression model included adjustment for the baseline covariates of age, sex, geographic region, eGFR, left ventricular ejection fraction ( 
Extended Data Fig. 7
Extended Data Fig. 7. Kaplan Meier Estimates of All-Cause Mortality by Kidney Function.
Patients randomized to empagliflozin or placebo were compared in EMPACT-MI. The endpoint was all-cause mortality. Patients were stratified by baseline kidney function, to categories eGFR of −1 1.73 m−2 (panel a), 30- < 60 ml min−1 1.73 m−2 (panel b), 60- < 90 ml min−1 1.73 m−2 (panel c), ≥90 ml min−1 1.73 m−2 (panel d). Kidney function was determined by eGFR with the CKD-EPI equation. The x-axis shows time from randomization in days and the y-axis shows probability of event based on Kaplan Meier estimates. Differences between the empagliflozin and placebo group were assessed with Cox proportional hazard models. A HR less than 1 indicates reduction in risk for the endpoint with empagliflozin while a HR of greater than 1 indicates increased risk in endpoint with empagliflozin. An interaction term for treatment and baseline eGFR category was included. The model included adjustment for the baseline covariates of age, sex, geographic region, eGFR, left ventricular ejection fraction ( < 35% or ≥35%), type 2 diabetes status, persistent or permanent atrial fibrillation, previous myocardial infarction, peripheral artery disease, and smoking status. HR was not reported for the eGFR of <30 ml min−1 1.73 m−2 group due to less than 14 patients with events. All significance testing was two-sided without adjustment for multiple testing. No significant interaction was observed between treatment effect and baseline kidney function (Pinteraction = 0.89). Abbreviations: CI, confidence interval; eGFR, estimated glomerular filtration rate; HR, hazard ratio.

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