Racial Differences in Quality of Life in Patients With Heart Failure Treated With Sodium–Glucose Cotransporter 2 Inhibitors: A Patient-Level Meta-Analysis of the CHIEF-HF, DEFINE-HF, and PRESERVED-HF Trials
Abstract
BACKGROUND:
Health status outcomes, including symptoms, function, and quality of life, are worse for Black compared with White patients with heart failure. Sodium–glucose cotransporter 2 inhibitors (SGLT2is) reduce cardiovascular mortality and improve health status in patients with heart failure, but whether the health status benefit of SGLT2is is similar across races is not established. The objective of this study was to compare the treatment effect of SGLT2is (versus placebo) on health status for Black compared with White patients with heart failure.
METHODS:
We combined patient-level data from 3 randomized clinical trials of SGLT2is: DEFINE-HF (Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure; n=263), PRESERVED-HF (Dapagliflozin in Preserved Ejection Fraction Heart Failure; n=324), and CHIEF-HF (A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure; n=448). These 3 United States–based trials enrolled a substantial proportion of Black patients, and each used the Kansas City Cardiomyopathy Questionnaire (KCCQ) to measure health status at baseline and after 12 weeks of treatment. Among 1035 total participants, selecting self-identified Black and White patients with complete information yielded a final analytic cohort of 935 patients. The primary endpoint was KCCQ Clinical Summary score. Twelve-week change in KCCQ with SGLT2is versus placebo was compared between Black and White patients by testing the interaction between race and treatment using multivariable linear regression models adjusted for trial, baseline KCCQ (as a restricted cubic spline), race, and treatment. The data that support the findings of this study are available from the corresponding author upon reasonable request.
RESULTS:
Among 935 participants, 236 (25%) self-identified as Black, and 469 (50.2%) were treated with an SGLT2i. Treatment with an SGLT2i, compared with placebo, resulted in KCCQ Clinical Summary score improvements at 12 weeks of +4.0 points (95% CI, 1.7–6.3; P=0.0007) in White patients and +4.7 points (95% CI, 0.7–8.7; P=0.02) in Black patients, with no significant interaction by race and treatment (P=0.76). Other KCCQ scales showed similar results.
CONCLUSIONS:
Treatment with an SGLT2i resulted in consistent and significant improvements in health status for both Black and White patients with heart failure.
Clinical Perspective
What Is New?
•
In a patient-level meta-analysis of 3 randomized clinical trials, we explicitly demonstrated that sodium–glucose cotransporter 2 inhibitors improve health status in both Black and White patients with heart failure to a similar degree, as early as 12 weeks after initiation, and irrespective of ejection fraction category.
What Are the Clinical Implications?
•
In Black patients with heart failure, who, on average, have more compromised health status, sodium–glucose cotransporter 2 inhibitor therapy can be prescribed with confidence to improve health status.
•
Additional efforts to ensure widened and equitable access to sodium–glucose cotransporter 2 inhibitors for patients with heart failure are justified.
The prevalence of heart failure (HF) is rising in the United States, and is projected to affect >8 million people by 2030.1–3 HF not only markedly shortens patients’ survival, but also impairs their health status due to severe symptoms, functional limitations, and impaired quality of life. Over the past decade, several new therapies for HF have dramatically changed the HF treatment landscape. In particular, sodium–glucose cotransporter 2 inhibitors (SGLT2is) have emerged as a treatment that improves patients’ health status across the spectrum of HF, including heart failure with reduced ejection fraction (HFrEF), heart failure with mildly reduced ejection fraction (HFmrEF), and heart failure with preserved ejection fraction (HFpEF).4–9 Thus, the clinical and health status benefits, coupled with a favorable tolerability profile of SGLT2is, represent a new opportunity to improve care for HF, as embraced by recent updates to clinical guidelines.10,11
Concordant with the growth of HF has been an increasing focus on the need to address and reduce racial disparities in care and outcomes.12–14 In the setting of HF, racial differences in the incidence of HF and response to some therapies are known, as are racial disparities in access to care and clinical outcomes.15–19 Black people have higher rates of HF risk factors (including hypertension and type 2 diabetes) compared with White people. Furthermore, data suggest that Black individuals develop HF at higher rates when similar risk factors are present, resulting in nearly twice the incidence of HF in Black people (4.6 versus 2.4 per 1000 person-years).20–23 Recent real-world data suggest that Black patients with HF have worse health status than their White counterparts, underscoring the need to address racial disparities in care and outcomes.24
Despite the disproportionate burden of HF among Black people, they are underrepresented in clinical trials due to a range of issues, including suboptimal engagement with the health care system, insufficient awareness of trials, impaired trust toward clinical trials, and others.25 In accordance, whether the health status benefits of SGLT2i use are undermined by these health disparities remains insufficiently clear because pivotal trials demonstrating the clinical and health status benefits of SGLT2is have enrolled few Black participants. Subgroup analyses of EMPEROR-Reduced (Empagliflozin Outcome Trial in Patients With Chronic Heart Failure and a Reduced Ejection Fraction; 257 [6.9%] Black patients of 3730 total) and DAPA-HF (Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure; 226 [4.8%] Black patients of 4744 total) showed similar effects among Black and White patients treated with an SGLT2i4,5; however, a meta-analysis of these 2 trials suggested a potential enhanced benefit among Black participants in reducing the primary combined end point of cardiovascular death and HF hospitalization.26,27 On the other hand, subgroup analysis of EMPEROR-Preserved (258 [4.3%] Black participants of 5988 total) suggested a similar effect across races.8 Neither of these studies has explicitly tested whether the health status benefits are similar in Black and White participants.
To address this gap in knowledge regarding the health status benefits of SGLT2i use in Black patients with HF, we conducted a patient-level analysis of data from 3 clinical trials conducted in the United States that enrolled a substantial proportion of Black patients with HF. To our knowledge, there is no clear physiological evidence to hypothesize that SGLT2i use would have differential effects in Black patients compared with White patients with HF, but given low enrollment rates of Black patients in the landmark clinical trials studying the benefit of SGLT2is in HF, this additional investigation was warranted. We specifically sought to quantify the treatment effect of SGLT2i on health status in Black patients compared with White patients across the full spectrum of ejection fractions (EFs). Quantification of the benefits of SGLT2i use in Black patients can aid discussions with patients regarding this treatment and better inform considerations of SGLT2is as means of potentially reducing disparities in health status outcomes.24
METHODS
Parent Studies and Patients
This study used data from 3 randomized clinical trials that have been reported previously and are summarized in Table S1, including DEFINE-HF (Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure; n=263), PRESERVED-HF (Dapagliflozin in Preserved Ejection Fraction Heart Failure; n=324), and CHIEF-HF (A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure; n=448), which enrolled individuals with reduced and preserved EF. All were randomized, blinded, parallel-group clinical trials recruiting patients with an established diagnosis of HF. The inclusion criteria of the studies were broadly similar, except for differences in EF; the inclusion criterion in DEFINE-HF was EF ≤40%, PRESERVED-HF required an EF ≥45%, and CHIEF-HF had no EF inclusion criterion (although randomization was stratified by EF >40% or ≤40%). Patients in DEFINE-HF and PRESERVED-HF were randomized to 10 mg of dapagliflozin versus placebo, whereas CHIEF-HF randomized patients to 100 mg of canagliflozin or placebo. All 3 trials treated patients for 12 weeks and assessed participants’ health status with the Kansas City Cardiomyopathy Questionnaire (KCCQ) at baseline and 12 weeks. For the current study, all patients who self-identified as either Black or White race were included. Patients with missing data (race or KCCQ) or who died before completing the 12-week follow-up were excluded. Due to insufficient data on people from other race groups, comparisons were made between participants who self-identified as Black or White races only. All studies were approved by their human studies committees and complied with the Declaration of Helsinki. All participants provided informed consent in the respective studies.
Health Status Outcomes Assessment
The KCCQ was used as the health status outcome for all 3 trials. The KCCQ is a self-administered, 23-item questionnaire designed to assess patients’ perceptions over the previous 2 weeks across 4 domains: total symptoms (KCCQ-TS scale), physical limitations (KCCQ-PL scale), social limitations (KCCQ-SL scale), and quality of life (KCCQ-QoL scale).28–30 Combining the KCCQ-TS and KCCQ-PL scales gives the clinical summary score (KCCQ-CS scale), which mirrors the New York Heart Association functional classification. Combining all 4 scales, the KCCQ-TS, KCCQ-PL, KCCQ-SL, and KCCQ-QoL give the overall summary score (KCCQ-OS scale), which provides a holistic summary of patients’ health status. Each domain of the KCCQ is scored from 0 to 100, where 0 represents the worst and 100 represents the best health status, with scores of 0 to 24 representing very poor to poor; 25 to 49, poor to fair; 50 to 74, fair to good; and 75 to 100, good to excellent health status.31 In addition, changes in the KCCQ score in increments of 5, 10, and 20 points are associated with clinically relevant small to moderate, moderate to large, or large to very large changes from patient and provider perspectives.31–33 KCCQ score and changes in scores are significantly and independently associated with mortality and hospitalization rates in patients with HF regardless of EF or pathogenesis.34
Statistical Analyses
A total of 1035 patients participated in the 3 trials, of whom we excluded those missing information for race or marked as “other” race (n=37), baseline clinical summary score (n=1), or 12-week clinical summary score (n=62, of which 11 were due to death), leaving a final sample of 935 participants (Figure 1). Continuous variables are described as mean and standard deviation and compared using the Student t test; categorical variables are described as proportions and compared with χ2 or Fisher exact tests, as appropriate. The primary analysis compared the change in clinical summary score (baseline to 12 weeks) by treatment arm (SGLT2i versus placebo) and tested the interaction of treatment by race using multivariable linear regression. Models included treatment, race, and the interaction effect of treatment and race, and were also adjusted for trial and baseline KCCQ score (as a restricted cubic spline term). In similar models, each domain of KCCQ (TS, PL, SL, and QoL) and total summary score were also tested. Responder analyses were conducted examining proportions of patients with deterioration (change less than −5 points), no improvement (change −5 to <5 points), small to moderate improvement (change 5 to <10 points), moderate to large improvement (change 10 to <20 points), or very large improvement (change ≥20 points) in KCCQ-CS and KCCQ-OS scales at the end of treatment period by race. Only those with a score ≤80 at baseline in the individual domains were included in the responder analyses, with 785 for the KCCQ-CS scale and 738 for the KCCQ-OS scale. Approximately one-quarter of those included in each scale were Black. A 2-sided α<0.05 was used to establish significance. All analyses were performed using SAS v9.4 (SAS Institute).

RESULTS
Among the 935 participants included in the analyses, 236 self-identified as Black (25%), and 469 (50.2%) were randomized to an SGLT2i. Table 1 describes the baseline characteristics, overall and stratified by race and treatment assignment. The mean age was 65.1±12.3 years, and 537 (56.4%) were male. The 2 treatment arms were well balanced in all baseline characteristics, overall and within race subgroups. Compared with White trial participants, Black participants tended to be younger (mean age 60.3±11.4 versus 66.7±12.2 years; P<0.001), were more often female (53% versus 41%; P=0.001), and more often had reduced EF (48.3% versus 40.8%; P=0.043), but had similar prevalence of type 2 diabetes (77.3% versus 74.6%; P=0.40).
Characteristics | All (n=935) | All (n=935) | White (n=699 [74.8%]) | Black (n=236 [25.2%]) | ||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
SGLT2i (n=469) | Placebo (n=466) | P value | White (n=699) | Black (n=236) | P value | SGLT2i (n=346) | Placebo (n=353) | P value | SGLT2i (n=123) | Placebo (n=113) | P value | |
Age, y | 65.0±12.2 | 65.1±12.5 | 0.91 | 66.7±12.3 | 60.3±11.4 | <0.001 | 66.7±12.3 | 66.7±12.2 | 0.99 | 60.4±10.7 | 60.3±12.1 | 0.93 |
Sex | ||||||||||||
Male | 261 (55.7) | 266 (57.1) | 0.66 | 415 (59.4) | 112 (47.5) | 0.001 | 202 (58.4) | 213 (60.3) | 0.60 | 59 (48) | 53 (46.9) | 0.87 |
Female | 208 (44.3) | 200 (44.7) | 284 (40.6) | 124 (52.5) | 144 (41.6) | 140 (39.7) | 64 (52) | 60 (53.1) | ||||
Type 2 diabetes | ||||||||||||
Yes | 357 (76.1) | 359 (77) | 0.74 | 540 (77.3) | 176 (74.6) | 0.40 | 264 (76.3) | 276 (78.2) | 0.55 | 93 (75.6) | 83 (73.5) | 0.70 |
No | 112 (23.9) | 107 (23) | 159 (22.7) | 60 (25.4) | 82 (23.7) | 77 (21.8) | 30 (24.4) | 30 (26.5) | ||||
Ejection fraction | ||||||||||||
Reduced | 269 (57.4) | 267 (57.3) | 0.99 | 285 (40.8) | 114 (48.3) | 0.04 | 203 (58.7) | 211 (59.8) | 0.77 | 66 (53.7) | 56 (49.6) | 0.53 |
Preserved | 200 (42.6) | 199 (42.7) | 414 (59.2) | 122 (51.7) | 143 (41.3) | 142 (40.2) | 57 (46.3) | 57 (50.4) | ||||
Baseline KCCQ score | ||||||||||||
Clinical summary score | 61.6±20.9 | 61.2±20.7 | 0.77 | 61.9±20.3 | 59.9±22.0 | 0.19 | 62.9±20.5 | 61.0±20.1 | 0.20 | 57.9±21.6 | 62.0±22.4 | 0.15 |
Overall summary score | 59.4±20.9 | 59.1±20.7 | 0.79 | 59.6±20.6 | 58.3±21.6 | 0.42 | 60.6±20.6 | 58.6±20.5 | 0.18 | 56.1±21.5 | 60.7±21.5 | 0.10 |
Total symptom score | 64.3±22.3 | 63.5±22.6 | 0.59 | 63.9±21.9 | 63.9±24.0 | 0.99 | 65.3±21.6 | 62.5 + 22.1 | 0.09 | 61.4±23.9 | 66.7±23.9 | 0.10 |
Physical limitation score* | 58.9±23.4 | 58.7±22.8 | 0.93 | 59.8±22.2 | 55.8±25.3 | 0.02 | 60.5±22.6 | 59.1±21.8 | 0.43 | 54.3±24.9 | 57.4±25.7 | 0.36 |
Social limitation score† | 58.3±27.1 | 58.3±26.6 | 0.97 | 58.8±26.1 | 56.9±28.9 | 0.37 | 59.8±26.2 | 57.7±26.0 | 0.31 | 54.2±29.3 | 59.9±28.4 | 0.14 |
Quality of life score | 55.5±24.3 | 55.4±24.2 | 0.99 | 55.1±24.2 | 56.4±24.3 | 0.47 | 55.9±24.0 | 54.3±24.5 | 0.38 | 54.1±25.3 | 58.9±23.0 | 0.13 |
Continuous variables are expressed as mean±SD and compared using the Student t test. Categorical variables are expressed as n (%) and compared using χ2 or Fisher exact test. CHIEF-HF indicates A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure; DEFINE-HF, Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure; KCCQ, Kansas City Cardiomyopathy Questionnaire; PRESERVED-HF, Dapagliflozin in Preserved Ejection Fraction Heart Failure; and SGLT2i, sodium–glucose cotransporter 2 inhibitor.
*
Missing 9 observations for baseline KCCQ physical limitation score.
†
Missing 33 observations for baseline KCCQ social limitation score.
Baseline Health Status
The baseline and 12-week KCCQ scores by race, treatment, and by both race and treatment are shown in Table S2. Raw baseline KCCQ scores were similar when comparing Black and White participants across all domains except physical limitations, in which Black patients had worse baseline values (55.8±25.3 versus 59.8±22.2; P=0.02). However, when adjusted for age, sex, and trial, Black patients had significantly worse baseline KCCQ scores in OS, CS, PL, and SL domains compared with White patients (all P<0.015; Table S5). When considering treatment assignment in the overall study cohort, the KCCQ-CS score was similar in the SGLT2i and placebo arms (61.6±20.9 versus 61.2±20.7; P=0.77). When stratified by race and then comparing across treatment arms (SGLT2i versus placebo), there, again, was no significant difference in baseline KCCQ-CS scores within either race group.
Effect of SGLT2 Inhibition on Health Status in Black Compared With White Patients
The primary results of multivariable linear regression analysis of treatment effect and race are shown in Table 2. The effect of an SGLT2i (compared with placebo) on 12-week change in CS was not statistically different between White and Black participants. Among Black patients with HF (n=236; 123 SGLT2i versus 113 placebo), the change in CS score due to treatment with an SGLT2i was +4.7 points (95% CI, 0.7–8.7; P=0.02); among White patients (n=699; 346 SGLT2i versus 353 placebo), the treatment effect was +4.0 points (95% CI, 1.7–6.3; P=0.0007), with no significant race×treatment interaction (Pinteraction=0.76). Changes in the other domains of the KCCQ are also summarized in Table 2 and showed a similar pattern of health status benefit in both races without any significant interaction by race (all Pinteraction>0.44). We also tested 3-way interactions of race, EF category, and treatment, as well as race, diabetes status, and treatment, on the outcome of change in CS. Neither was statistically significant (both Pinteraction>0.3).
KCCQ domain* | Black patients | White patients | Race* treatment | |||
---|---|---|---|---|---|---|
Treatment effect difference (SGLT2i vs placebo) | P value | Treatment effect difference (SGLT2i vs placebo) | P value | Treatment effect difference (White compared with Black) | P value | |
Clinical summary score | 4.71 (0.74 to 8.68) | 0.02 | 3.99 (1.69 to 6.29) | 0.0007 | −0.7 (−5.3, 3.9) | 0.76 |
Overall summary score | 4.66 (0.65 to 8.66) | 0.02 | 3.01 (0.68 to 5.34) | 0.01 | −1.6 (−6.3, 3.0) | 0.49 |
Total symptom score | 4.92 (0.56 to 9.27) | 0.03 | 4.56 (2.04 to 7.09) | 0.0004 | −0.4 (−5.4, 4.7) | 0.89 |
Physical limitation score | 4.04 (−0.71 to 8.8) | 0.10 | 3.62 (0.85 to 6.38) | 0.01 | −0.4 (−5.9, 5.1) | 0.88 |
Social limitation score | 2.87 (−2.75 to 8.5) | 0.32 | 1.78 (−1.45 to 5.01) | 0.28 | −1.1 (−7.6, 5.4) | 0.74 |
Quality of life score | 4.98 (0.07 to 9.88) | 0.05 | 2.77 (−0.07 to 5.62) | 0.06 | −2.2 (−7.9, 3.5) | 0.45 |
CHIEF-HF indicates A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure; DEFINE-HF, Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure; KCCQ, Kansas City Cardiomyopathy Questionnaire; PRESERVED-HF, Dapagliflozin in Preserved Ejection Fraction Heart Failure; and SGLT2i, sodium–glucose cotransporter 2 inhibitors.
*
Models adjusted for trial, baseline KCCQ scores (as a restricted cubic spline), race, treatment category, and interaction effect of race and treatment.
In the responder analysis, similar patterns were seen regardless of race, with greater proportions of both White and Black participants treated with an SGLT2i (versus placebo) having small to moderate, moderate to large, or very large increases in KCCQ-CS and KCCQ-OS scores, and placebo-treated patients having relatively more frequent deterioration, as shown in Figure 2A and 2B.

DISCUSSION
A critical challenge confronting US health care is to address racial disparities in care and outcomes, underscoring the importance of examining racial differences in the benefits of novel therapies. Given the emerging evidence of the benefits of SGLT2i on the treatment of patients with HF, this study combined data from 3 randomized trials to create the largest reported cohort of Black patients, treated with an SGLT2i versus placebo, to explore potential racial differences in patient-reported health status outcomes. These data demonstrate a consistent health status benefit of SGLT2is in Black and White patients that were both statistically significant. To our knowledge, this is the first study to demonstrate a significant improvement in short-term quality of life in Black patients with HF (across the entire range of EF) treated with an SGLT2i. These data are critically important because much of the effect of HF lies in health status impairment (poor quality of life, severe symptoms, and functional limitations) and not simply survival.
The findings of this study support and extend the existing literature on SGLT2i use in HF. Data from EMPEROR-Reduced and DAPA-HF, summarized in a meta-analysis by Zannad et al,26 demonstrated a substantial reduction in the composite outcome of hospitalization due to HF or cardiovascular death in those treated with an SGLT2i compared with placebo and thereby suggested a potentially greater benefit in Black patients. However, data from EMPEROR-Preserved showed similar effects in clinical benefit across racial groups.8 Whereas the effect of SGLT2i use on reducing clinical events in HF is important, there are scarce data on the health status benefits of SGLT2is by race, which is a critically important outcome from patients’ perspectives.35,36 For example, the DELIVER trial showed that for patients with HFmrEF and HFpEF, the use of dapagliflozin versus placebo improved the KCCQ-TS score. However, the trial enrolled few Black patients (n=159/6263 [2.5%]).9,37 An important characteristic of the current study is that the health status benefits of an SGLT2i are apparent within 3 months, and these shorter-term improvements in symptoms and physical limitations are especially appreciable to patients.
These findings have important clinical implications; SGLT2i should be embraced for treatment of individuals with HF regardless of race, given the robust health status benefit from this class of treatment. However, implementing this could be challenging, particularly for Black patients with HF who have, on average, worse health status. One of the key barriers is likely cost. Recent studies reported favorable coverage decisions regarding SGLT2i use by most health insurance plans, including Medicaid.38,39 Despite this, the out-of-pocket costs for some patients are higher than other generically available guideline-directed medical therapies, which may represent an obstacle to their use. Additional barriers to implementing wider SGLT2i use among Black patients are likely to be encountered when considering the disproportionate burden of social determinants of health in Black individuals in the United States, with noted disparities in the availability of health insurance, financial resources, health literacy, and access to quality health care.14,40,41 Specific to HF, despite the availability of many treatments proven to reduce the progression of HF, uccesssful implementation of therapies among patients in need remains a major public health and societal challenge, and adverse social determinants of health are a known contributor to cardiometabolic disease among Black adults.12,42,43 In this context, simply waiting for prescription of an SGLT2i through the typical course of medical care may not be an effective strategy44 because it does not overcome the underlying critical barriers related to access, bias, or poor engagement with the health care system. These practical barriers can make conventional routes for medical care less effective, a dynamic clearly demonstrated regarding blood pressure control.12,42 Development and implementation of methods to overcome such barriers and ensure systematic application of these agents to those who are likely to benefit deserve further exploration and encouragement. These could include standardization or algorithm-based care, innovative, team-based coordinated delivery models that proactively engage vulnerable populations, or other novel interventions to enhance access to treatment.45
Our findings should be considered in the context of several potential limitations. First, we lacked extensive medical history and laboratory data in one trial (CHIEF-HF) due to its novel design (fully decentralized without in-person visits and with streamlined data collection), which, in turn, limited our ability to further adjust the racial differences in treatment effect for other comorbid conditions (other than diabetes) or laboratory markers. Previous studies, including DEFINE-HF and PRESERVED-HF, examined renal function and other medications and found no interaction with the effects of an SGLT2i. On the other hand, the potential modifiers of effects of an SGLT2i of highest interest are diabetes and EF category, which were previously noted not to affect SGLT2i benefit and we found to have no significant interaction with race and SGLT2i treatment in terms of health status benefit. Whereas all 3 trials used different KCCQ domains as their primary outcome, all collected the KCCQ prospectively and in the same rigorous manner so that this study could calculate all the scores directly from the collected data.
Conclusions
Treatment with an SGLT2i improves health status in Black patients with HF as soon as 12 weeks. This benefit was similar to that found among White patients and extended across a variety of health status domains including symptom burden, physical and social limitations, and quality of life. These agents should be used with confidence among Black patients with HF; and efforts to ensure equitable access to these treatments have the potential to improve the health status of Black and White patients with HF.
ARTICLE INFORMATION
Supplemental Material
Tables S1–S5
Footnote
Nonstandard Abbreviations and Acronyms
- CHIEF-HF
- A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure
- DAPA-HF
- Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure
- DEFINE-HF
- Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure
- EF
- ejection fraction
- EMPEROR-
- Empagliflozin Outcome Trial Preserved in Patients with Chronic Heart Failure and a Preserved Ejection Fraction
- EMPEROR-
- Empagliflozin Outcome Trial Reduced in Patients with Chronic Heart Failure and a Reduced Ejection Fraction
- HF
- heart failure
- HFmrEF
- heart failure with mildly reduced ejection fraction
- HFpEF
- heart failure with preserved ejection fraction
- HFrEF
- heart failure with reduced ejection fraction
- KCCQ
- Kansas City Cardiomyopathy Questionnaire
- PRESERVED-HF
- Dapagliflozin in Preserved Ejection Fraction Heart Failure
- SGLT2i
- sodium–glucose cotransporter 2 inhibitor
Supplemental Material
File (circ_circulationaha-2022-063263_supp1.pdf)
- Download
- 84.47 KB
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© 2023 American Heart Association, Inc.
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Received: 16 November 2022
Accepted: 28 March 2023
Published online: 16 May 2023
Published in print: 18 July 2023
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Disclosures Dr Spertus is a principal investigator on grants from the National Institutes of Health (NIH), Abbott Vascular, and the American College of Cardiology Foundation; is a consultant to Janssen, Novartis, Amgen, MyoKardia, AstraZeneca, Bayer, and Merck; serves on the scientific advisory board of United Healthcare and the board of directors for Blue Cross Blue Shield of Kansas City; owns the copyright to the Kansas City Cardiomyopathy Questionnaire, Seattle Angina Questionnaire, and Peripheral Artery Questionnaire; and has an equity interest in Health Outcomes Sciences. Dr Birmingham is an employee of Janssen Scientific Affairs, LLC. Dr Husain has received research grants from AstraZeneca, Merck, and Novo Nordisk and advisory/consultancy fees from AstraZeneca, Boehringer Ingelheim, Eli Lilly, Janssen, Merck, Novo Nordisk, and Roche. Dr Kitzman has served as a consultant for Pfizer, Rivus, Corvia Medical, Boehringer-Ingelheim, Novo Nordisk, AstraZeneca, and Novartis; received grant funding from NIH, Pfizer, Novartis, Bayer, Novo Nordisk, and AstraZeneca; and has stock ownership in Gilead Sciences. Dr Pitt consults with AstraZeneca, Bayer, Sanofi Aventis, Vifor, Sarfez, KBP Pharmaceuticals, scPharmaceuticals, and Cereno; has a company relationship with Vifor, Sarfez, KBP Pharmaceuticals, scPharmaceuticals, and Cereno; and holds US patent 9931412 (site-specific delivery of eplerenone to the myocardium). Dr Shah consults with Actelion Clinical Research Inc, Amgen, Aria CV Inc, AstraZeneca, Axon Therapies, Bayer HealthCare Pharmaceuticals Inc, Boehringer Ingelheim, Boston Scientific Corporation, Bristol Myers Squibb, Cyclerion, Cytokinetics, Edwards Lifesciences, Eidos, GlaxoSmithKline, Intellia Therapeutics, Ionis, Merck Sharp & Dohme Corp, Novartis, Novo Nordisk, Pfizer, Prothena Biosciences Limited, Regeneron Pharmaceuticals, Shifamed LLC/Adona, Tenax Therapeutics, Third Rock Ventures, RIVUS, and Gordian Biotechnology; and has a grant and contract with AstraZeneca, Corvia, Novartis, and Pfizer. Dr Januzzi is a trustee of the American College of Cardiology; is a board member of Imbria Pharmaceuticals; has received research support from Abbott, Applied Therapeutics, Innolife, Novartis Pharmaceuticals, and Roche Diagnostics; has received consulting income from Abbott, Beckman, Bristol Myers, Boehringer Ingelheim, Janssen, Novartis, Pfizer, Merck, Roche Diagnostics, and Siemens; and participates in clinical end point committees/data safety monitoring boards for Abbott, AbbVie, Bayer, CVRx, Intercept, Janssen, and Takeda. Dr Lingvay received research funding (paid to the institution) from Novo Nordisk, Sanofi, Merck, Pfizer, Mylan, and Boehringer-Ingelheim; and advisory/consulting fees or other support from Novo Nordisk, Eli Lilly, Sanofi, AstraZeneca, Boehringer-Ingelheim, Janssen, Intercept, Intarcia, TARGETPharma, Merck, Pfizer, Novartis, GI Dynamics, Mylan, Mannkind, Valeritas, Zealand Pharma, Shionogi, and Bayer. Dr Butler consults with Abbott, Adrenomed, Amgen, Array, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, CVRx, G3 Pharmaceutical, Impulse Dynamics, Innolife, Janssen, LivaNova, Luitpold, Medtronic, Merck, Novartis, Novo Nordisk, Roche, and Vifor. Dr Kosiborod has received research grants from AstraZeneca and Boehringer Ingelheim; consults for and is on the advisory board of Alnylam, Amgen, Applied Therapeutics, AstraZeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Eli Lilly, Esperion Therapeutics, Janssen, Lexicon, Merck (Diabetes and Cardiovascular), Novo Nordisk, Pharmacosmos, Sanofi, and Vifor Pharma; and has received other research support from AstraZeneca. Dr Lanfear is supported in part by grants from NIH (P50MD017351 and R01HL132154); has received research funding or support from Amgen, AstraZeneca, Eli Lilly, and SomaLogic; and has acted as consultant to ACI Clinical (Abbott Laboratories), AstraZeneca, Cytokinetics, Duke Clinical Research Institute (CONNECT-HF [Care Optimization Through Patient and Hospital Engagement Clinical Trial for Heart Failure]), Illumina, Janssen, Martin Pharmaceuticals, Ortho Clinical Diagnostics, Otsuka, and Vicardia. The other authors report no conflicts.
Sources of Funding
CHIEF-HF (A Study on Impact of Canagliflozin on Health Status, Quality of Life, and Functional Status in Heart Failure) was funded and sponsored by Janssen Scientific Affairs, and the current work was supported in part by Janssen Scientific Affairs, LLC. DEFINE-HF (Dapagliflozin Effect on Symptoms and Biomarkers in Patients With Heart Failure) and PRESERVED-HF (Dapagliflozin in Preserved Ejection Fraction Heart Failure) were both investigator-initiated trials funded by AstraZeneca and conducted by Saint Luke’s Mid America Heart Institute independent of the funding source.
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- Racial and Ethnic Disparities in Perceived Health Status Among Patients With Cardiovascular Disease, Preventing Chronic Disease, 21, (2024).https://doi.org/10.5888/pcd21.240264
- Nature and Magnitude of the Benefits of Dapagliflozin and Empagliflozin for Heart Failure, Circulation, 149, 11, (839-842), (2024)./doi/10.1161/CIRCULATIONAHA.123.068089
- Early Longitudinal Change in Heart Failure Health Status Following Initiation of Canagliflozin, JACC: Heart Failure, 12, 4, (711-718), (2024).https://doi.org/10.1016/j.jchf.2024.01.005
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