Author + information
- Received January 30, 2018
- Revision received April 12, 2018
- Accepted April 17, 2018
- Published online September 24, 2018.
- Kavita Sharma, MDa,∗ (, )
- Joban Vaishnav, MDa,
- Rohan Kalathiya, MDa,
- Jiun-Ruey Hu, MD, MPHa,
- John Miller, MDa,
- Nishant Shah, MDa,
- Terence Hill, MDa,
- Michelle Sharp, MDa,
- Allison Tsao, MDa,
- Kevin M. Alexander, MDa,
- Richa Gupta, MDa,
- Kristina Montemayor, MDa,
- Lara Kovell, MDa,
- Jessica E. Chasler, PharmDa,
- Yizhen J. Lee, MDa,
- Derek M. Fine, MDb,
- David A. Kass, MDa,
- Robert G. Weiss, MDa,
- David R. Thiemann, MDa,
- Chiadi E. Ndumele, MD, PhDa,
- Steven P. Schulman, MDa,
- Stuart D. Russell, MDa,
- on behalf of the Osler Medical Housestaff
- aDepartment of Medicine, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland
- bDivision of Nephrology, Johns Hopkins University School of Medicine, Baltimore, Maryland
- ↵∗Address for correspondence:
Dr. Kavita Sharma, Advanced Heart Failure/Transplant Cardiology, The Johns Hopkins Hospital, 600 North Wolfe Street, Carnegie 568C, Baltimore, Maryland 21287.
Objectives This study sought to compare a continuous infusion diuretic strategy versus an intermittent bolus diuretic strategy, with the addition of low-dose dopamine (3 μg/kg/min) in the treatment of hospitalized patients with heart failure with preserved ejection fraction (HFpEF).
Background HFpEF patients are susceptible to development of worsening renal function (WRF) when hospitalized with acute heart failure; however, inpatient treatment strategies to achieve safe and effective diuresis in HFpEF patients have not been studied to date.
Methods In a prospective, randomized, clinical trial, 90 HFpEF patients hospitalized with acute heart failure were randomized within 24 h of admission to 1 of 4 treatments: 1) intravenous bolus furosemide administered every 12 h; 2) continuous infusion furosemide; 3) intermittent bolus furosemide with low-dose dopamine; and 4) continuous infusion furosemide with low-dose dopamine. The primary endpoint was percent change in creatinine from baseline to 72 h. Linear and logistic regression analyses with tests for interactions between diuretic and dopamine strategies were performed.
Results Compared to intermittent bolus strategy, the continuous infusion strategy was associated with higher percent increase in creatinine (continuous infusion: 16.01%; 95% confidence interval [CI]: 8.58% to 23.45% vs. intermittent bolus: 4.62%; 95% CI: −1.15% to 10.39%; p = 0.02). Low-dose dopamine had no significant effect on percent change in creatinine (low-dose dopamine: 12.79%; 95% CI: 5.66% to 19.92%, vs. no-dopamine: 8.03%; 95% CI: 1.44% to 14.62%; p = 0.33). Continuous infusion was also associated with greater risk of WRF than intermittent bolus (odds ratio [OR]: 4.32; 95% CI: 1.26 to 14.74; p = 0.02); no differences in WRF risk were seen with low-dose dopamine. No significant interaction was seen between diuretic strategy and low-dose dopamine (p > 0.10).
Conclusions In HFpEF patients hospitalized with acute heart failure, low-dose dopamine had no significant impact on renal function, and a continuous infusion diuretic strategy was associated with renal impairment. (Diuretics and Dopamine in Heart Failure With Preserved Ejection Fraction [ROPA-DOP]; NCT01901809)
- acute decompensated heart failure
- heart failure with preserved ejection fraction
- worsening renal function
Heart failure with preserved ejection fraction (HFpEF) constitutes nearly one-half of more than 1 million hospital patients discharged for heart failure per year and is projected to be the predominant form of hospitalized heart failure by 2020 (1–4) There is an unmet need for effective HFpEF treatment, which has no proven therapies to date and no evidence-based strategies to guide the management of acute HF in HFpEF. HFpEF outcomes are comparable to HF with reduced ejection fraction (HFrEF), and studies of hospitalized HFpEF patients have shown a 12% to 40% rate of development of worsening renal function (WRF) (5–8). WRF in hospitalized HF is associated with prolonged length of stay, more readmissions, and increased short-term mortality (9–12). Achieving effective and safe diuresis without compromising renal function is a primary goal of acute HF management; however, optimal methods to achieve this in HFpEF patients have not been prospectively studied.
Diuretic therapy is a mainstay of treatment for acute HF regardless of ejection fraction (13). Some studies have suggested a possible benefit with continuous infusion diuretic therapy compared to intermittent bolus dosage therapy in HFrEF; however, these findings were not corroborated in a large clinical trial, and there have been no prospective trials evaluating diuretic strategy in HFpEF (14–17).
Dopamine is a catecholamine that exhibits dose-dependent effects on the systemic and renal vasculature. At low doses (≤3 μg/kg/min), dopamine acts on the A1 receptors, causing vasodilation of the renal arteries and mesenteric, coronary, and cerebral vascular beds. The use of low-dose or “renal-dose” dopamine in acute HF has been proposed as a renal protective strategy, and smaller studies in HFrEF patients have shown improvement in urine output and renal blood flow, but a recent study of low-dose dopamine in a predominantly HFrEF population showed no benefit in urinary volume or cystatin C in the treatment of acute HF (18–21).
The ROPA-DOP (Randomized Evaluation of Heart Failure with Preserved Ejection Fraction Patients with Acute Heart Failure and Dopamine) trial was designed to address 2 questions: first, does a continuous infusion versus the standard intermittent bolus furosemide diuretic strategy enhance diuresis while limiting renal injury, and second, does the addition of low-dose dopamine facilitate diuresis while preserving renal function in HFpEF patients hospitalized with acute HF?
The ROPA-DOP study was a prospective, randomized, single-blinded trial conducted by the Osler Medical Housestaff of the Johns Hopkins Hospital. HFpEF patients (n = 90) hospitalized for treatment of acute HF were enrolled within 24 h of admission. The diagnosis of acute HF was based on the presence of at least 1 symptom (dyspnea, orthopnea, or edema) and 1 sign of HF (rales, jugular venous distension, positive hepatojugular reflex, peripheral edema, ascites, or pulmonary vascular congestion on chest radiography) (Online Table 1). Patients were included if they had an established left ventricular EF ≥50% within 12 months of admission without interval history, electrocardiography changes, or cardiac biomarkers to suggest a cardiac event (myocardial infarction, myocarditis, pericarditis) that may have resulted in a decline in cardiac function. Patients with systolic blood pressure (SBP) <90 mm Hg, estimated glomerular filtration rate (eGFR), as determined by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) threshold, ≤15 ml/min/1.73 m2 (22), or other primary cardiac diagnosis (myocarditis, hypertrophic cardiomyopathy, severe valvular disease, infiltrative cardiomyopathy, congenital heart disease, constrictive cardiomyopathy), and those with severe pulmonary hypertension were excluded. All participants provided informed consent, and the study was approved by the Johns Hopkins Institutional Review Board.
Randomization and treatment assignments
Patients were randomized in a 1:1:1:1 ratio to 1 of 4 treatment strategies for a treatment course of at least 72 h: strategy 1 consisted of intermittent bolus furosemide (every 12 h); strategy 2 consisted of continuous infusion furosemide; strategy 3 consisted of intermittent bolus plus low-dose intravenous dopamine (3 μg/kg/min); and strategy 4 consisted of continuous infusion plus low-dose intravenous dopamine (3 μg/kg/min). A block randomization scheme was performed using an automated Web-based system, stratified by the following criteria: race (African American vs. non-African American), chronic kidney disease status (CKD defined as eGFR <60 ml/min/1.73 m2 vs. ≥60 ml/min/1.73 m2, according to the CKD-EPI equation) (22), and whether intravenous contrast had been administered to the patient prior to hospital admission.
All patients received an open-label, intravenous loop diuretic (furosemide) with a recommended total daily dose equal to 2.0 times their total daily outpatient oral furosemide-equivalent dose, at the discretion of the primary team. It was recommended that patients naïve to outpatient loop diuretics receive a starting intravenous furosemide dose of 80 mg/day. Patients randomized to the intermittent bolus treatment arms received the total daily diuretic dose divided into 2 doses, every 12 h. Patients randomized to the continuous infusion treatment arms received the total diuretic dose as a continuous infusion over 24 h without a bolus dose. Use of other medications and diuretic dosages after the first 24 h were administered at the discretion of the clinician. All patients received a standard 2,000-mg sodium-restricted diet, and a 2,000-ml fluid-restricted diet (13). Following assessment of the primary endpoint at 72 h, subsequent treatment was prescribed at the clinician’s discretion. Investigators were blinded to treatment assignment at the time of enrollment, at 72 h and at discharge. The patient, the primary care providing team, and the nursing staff were not blinded to treatment assignment.
After patients gave consent, they underwent baseline assessment, which included history and physical examination, recording vital signs, tests for biomarkers (N-terminal pro–B-type natriuretic peptide [NT-proBNP], plasma cystatin C) and electrolytes, and a 6-min walk test. Patient-reported global assessment of symptoms and of dyspnea were measured using a visual analog scale. Study assessments were repeated at 72 h and at discharge (Online Table 2). A transthoracic echocardiogram was obtained during admission. Frailty was assessed at enrollment and at discharge by using the Johns Hopkins Frailty Assessment Tool (23). All patients received assessments of vital status and rehospitalization at 30 and 180 days and at 1 year by telephone. Hospitalizations for HF were adjudicated by 2 physicians.
The primary endpoint of the study was percent change in creatinine at 72 h. Secondary endpoints (Online Table 2) included markers of renal function (change in cystatin C, development of WRF) and congestion (cumulative urine output, change in weight, and change in NT-proBNP). Treatment failure was defined as exceeding the maximum dose of furosemide permitted (total dose of furosemide was 400 mg given intravenously over 24 h); development of worsening renal function requiring renal replacement therapy; or discontinuation of study drug for significant hypotension, hypertension, or tachyarrhythmia.
The trial used a 2 × 2 factorial design to evaluate 2 simultaneous interventions. Primary analysis was conducted on an intention-to-treat basis. A total sample size of 140 participants was determined to provide 80% power to detect a treatment difference of >30% in creatinine at 72 h, using a Type I error rate of 0.05, including dropouts. Due to a slow enrollment rate, the study was stopped prematurely.
Primary and secondary endpoints consisted of comparisons between diuretic strategy (intermittent bolus vs. continuous infusion) and dopamine strategy (no-dopamine vs. low-dose dopamine). Summaries of continuous variables are displayed using mean ± SD for normally distributed variables or median and interquartile ranges for variables with a skewed distribution. Nonparametric testing for the continuous primary endpoint (percent change in creatinine) was performed using the Wilcoxon-Mann-Whitney U test. Secondary endpoints were compared by chi-square test for categorical variables and by Student’s t-test for continuous variables. Patient-reported global well-being and dyspnea scores were quantified as the area under the curve (AUC) of assessments from baseline to 72 h. Statistical results with p values <0.05 were considered statistically significant.
For both the primary endpoint and select secondary endpoints, multivariate linear and logistic regression analyses were performed, with adjustments for age, sex, race, body mass index (BMI), smoking, hypertension, diabetes, history of atrial fibrillation, eGFR at baseline, SBP change at 72 h, heart rate change at 72 h, and fluid balance at 72 h, with the level of significance specified at a p value of <0.05. Covariates were selected based on prior knowledge. Subgroup analyses of treatment effect were performed for both diuretic (intermittent bolus vs. continuous infusion) and dopamine (no-dopamine vs. low-dose dopamine) strategies. Tests for interaction between dopamine and diuretic strategies were performed with regression analysis by creation of a dopamine*diuretic term and a p value of 0.10 for significance. Correlation plots of the association between the primary endpoint and change in SBP by treatment strategy were created, with significance specified at p < 0.05. All statistical analyses were conducted with R version 3.3.1 software (R Foundation for Statistical Computing, Vienna, Austria).
Ninety patients were enrolled between October 2013 and December 2016. As shown in Table 1, the mean age of the population was 66 ± 13 years, 68% were female, and 62% were African American. The patient population had many co-morbidities including 94% with hypertension, 59% with diabetes, and 36% with history of atrial fibrillation or flutter. Patients were morbidly obese with a mean BMI of 40.8 ± 12.9 kg/m2. Median SBP was 134 mm Hg (interquartile range [IQR]: 115 to 152 mm Hg); median eGFR was 50.0 ml/min/1.73 m2 (eGFR IQR: 39.0 to 76.8 ml/min/1.73 m2); and median NT-proBNP was 1,257 pg/ml (IQR: 367 to 2,656 pg/ml). There were no significant differences between treatment groups apart from baseline heart rate (Table 1).
All patients who were randomized were included in assessments of treatment effects, with performance of intention-to-treat analyses (Figure 1). A total of 7 patients did not receive treatment as assigned: 3 patients in the dopamine arm had treatment stopped early due to new atrial arrhythmias, but none were hemodynamically unstable; 4 patients were dropped early or did not continue to treatment due to refusal (n = 2), or because they were too ill (n = 1), or by decision of the primary team (n = 1).
Continuous infusion treatment strategy was associated with significantly greater percent increase in creatinine at 72 h than intermittent bolus treatment strategy (continuous infusion: 16.01%; 95% confidence interval [CI]: 8.58% to 23.45%, vs. intermittent bolus: 4.62%; 95% CI: −1.15% to 10.39%; p = 0.02) (Figure 2).
Continuous infusion treatment strategy was associated with a greater proportion of WRF (rise in serum creatinine: ≥0.3 mg/dl at 72 h) than intermittent bolus strategy (continuous infusion: 36.2% vs. intermittent bolus: 11.6%; p = 0.01) (Table 2). There were no significant differences between diuretic strategy in change in cystatin C at 72 h, however (p = 0.13). There were also no differences between intermittent bolus and continuous infusion strategies in measurements of congestion, including cumulative urine output at 72 h (p = 0.62), change in weight at 72 h (p = 0.46), and change in NT-proBNP at 72 h (p = 0.99). Continuous infusion strategy was associated with a trend toward a greater drop in SBP at 72 h than intermittent bolus strategy (continuous infusion: −11.49 ± 22.65 mm Hg vs. intermittent bolus, −3.37 ± 29.86 mm Hg; p = 0.15). There were no differences in symptoms assessed by Global Well-Being score (p = 1.00) and dyspnea score (p = 0.58) at 72 h between diuretic strategies. Also, there were no differences in change in 6-min walk distances at 72 h between patients receiving intermittent bolus and those receiving continuous infusion strategies (p = 0.77) (Table 2).
At 30 days, there were no significant differences in all-cause hospitalization (p = 0.43) or HF hospitalization rates (p = 0.35) between intermittent bolus and continuous infusion strategy groups (Table 2). At 1 year, there were no significant differences in HF hospitalizations (p = 0.58) or overall mortality (intermittent bolus: 21.4% vs. continuous infusion: 13.6%; p = 0.34) between the 2 diuretic strategies (Table 2).
In subgroup analyses, we assessed whether the effects of continuous infusion versus intermittent bolus on the primary endpoint of percent change in creatinine differed by subgroups defined by age (≤65 years of age), sex, race, elevated SBP, eGFR ≤60 ml/min/1.73 m2, or cystatin C ≥1.42 mg/l (Figure 3). Women, African Americans, and those with CKD showed statistically significant worsening of creatinine concentrations with continuous infusion compared to patients undergoing intermittent bolus treatment (Figure 3A). There were no significant interactions between these subgroups and diuretic strategy (Figure 3A). There were no significant differences between diuretic strategies the secondary outcome of volume of diuresis within any of the subgroups (Figure 3B).
In multivariate linear regression analyses, continuous infusion strategy was associated with greater percent rise in creatinine than intermittent bolus strategy (continuous infusion: 11.15%; 95% CI: 0.92% to 21.37%; p = 0.03) (Table 3). Continuous infusion strategy showed a trend toward greater percent change in cystatin C than intermittent bolus in linear regression analysis (p = 0.10). Continuous infusion was associated with greater risk of WRF than intermittent bolus (odds ratio [OR]: 4.32; 95% CI: 1.26 to 14.74; p = 0.02). There were no significant differences in volume of diuresis at 72 h between continuous infusion and intermittent bolus strategies in linear regression analysis (continuous infusion: 21 ml; 95% CI: −1,757 to 1,799 ml; p = 0.98) (Table 3).
Low-dose dopamine strategy
There were no significant differences in percent change in creatinine between low-dose dopamine and no-dopamine treatment strategies at 72 h (low-dose dopamine: 12.79%; 95% CI: 5.66% to 19.92% vs. no-dopamine: 8.03%; 95% CI: 1.44% to 14.62%; p = 0.33) (Figure 2).
There were no significant differences in renal outcomes including development of WRF (low-dose dopamine: 25.0% vs. no-dopamine: 23.8%; p = 1.00) and change in cystatin C at 72 h (p = 0.82), with low-dose dopamine versus no-dopamine (Table 2). There were also no differences in measurements of congestion, including cumulative urine output at 72 h (p = 0.68), change in weight at 72 h (p = 0.27), and change in NT-proBNP at 72 h (p = 0.14) with low-dose dopamine versus no dopamine. There were no differences in SBP at 72 h with low-dose dopamine versus no-dopamine (p = 0.75). Furthermore, there were no significant differences in symptoms assessed by Global Well-Being score (p = 0.19) and dyspnea score (p = 0.50) with low-dose dopamine versus no-dopamine. There were also no significant differences in change in 6-min walk distances with low-dose dopamine versus no-dopamine (p = 0.55) (Table 2).
At 30 days, there were no significant differences in all-cause hospitalizations (p = 0.29) or HF hospitalization rates (p = 0.14) with low-dose dopamine versus no-dopamine (Table 2). At 1 year, there were no significant differences in HF hospitalizations (p = 0.32) or overall mortality (low-dose dopamine of 15.6% vs. no-dopamine of 19.5%; p = 0.63) in association with low-dose dopamine (Table 2).
In multivariate linear regression analyses, there was no significant effects of low-dose dopamine on percent change in creatinine (p = 0.34) or percent change in cystatin C (p = 0.92) at 72 h (Table 3). Additionally, there was no differences in risk of development of WRF with low-dose dopamine versus no-dopamine (low-dose dopamine OR: 1.09; 95% CI: 0.38 to 3.10; p = 0.92). Low-dose dopamine was associated with a trend toward greater volume of diuresis at 72 h than with no-dopamine; however, this was not statistically significant (low-dose dopamine: 687 ml; 95% CI: −997 ml to 2,371 ml; p = 0.42) (Table 3).
There were no significant differences in the effects of low-dose dopamine treatment on the primary outcome of percent change in creatinine or the secondary outcome of volume of diuresis across subgroups of age, sex, race, baseline SBP, eGFR, and cystatin C (Figures 3C and 3D).
Interaction testing was performed for dopamine and diuretic strategies and was not found to be significant for the primary outcome (pinteraction = 0.76 for percent change in creatinine) or secondary outcomes (Online Table 3).
In the intermittent bolus and continuous infusion groups, there was no significant correlation between SBP change and percent change creatinine, r = −0.06 (p = 0.73) and r = −0.16 (p = 0.28), respectively (Figure 4). In the low-dose dopamine group there was no significant correlation between SBP change and percent change creatinine, r = −0.01 (p = 0.96); however, in the no-dopamine group, there was a significant correlation between lower SBP and increased percent change creatinine, r = −0.41 (p = 0.0084).
In the first clinical trial of inpatient management strategies for the treatment of hospitalized HFpEF patients with acute HF, the ROPA-DOP study evaluated 2 treatment strategies for effect on renal function: intermittent bolus versus continuous infusion furosemide therapy, with and without low-dose (or “renal-dose”) dopamine. The study population was representative of the HFpEF clinical profile seen increasingly in urban communities: relatively younger patients with high rates of comorbidities including hypertension, diabetes, and morbid obesity, and included the largest percentage of African American enrollment in a HFpEF clinical trial to date (7,8). Low-dose dopamine did not significantly effect renal function and showed a non-significant trend toward greater diuresis in regression analyses, whereas continuous infusion furosemide diuretic strategy was associated with significant worsening of renal function at 72 h compared to intermittent bolus strategy.
Achieving adequate decongestion while avoiding renal injury is a primary goal in the treatment of acute HF, regardless of EF. Previous smaller studies in HFrEF patients have suggested that a continuous infusion strategy may augment diuresis with less renal injury (15,16,24). In the DOSE (Diuretic Optimization Strategies Evaluation) trial, however, there were no significant differences in patients’ global assessment of symptoms or in mean changes in creatinine between bolus versus continuous infusion strategies at 72 h of treatment (17). In contrast, our study showed a continuous infusion diuretic strategy was associated with a significant increase in percent creatinine and with a significantly higher rate of WRF at 72 h than with the intermittent bolus diuretic strategy. These findings persisted even after adjusting for common baseline demographics, co-morbidities, and hemodynamic parameters including change in blood pressure, heart rate, and volume of diuresis over the treatment period. Furthermore, we found that women, African Americans, and those with baseline CKD developed significantly worse renal function with continuous infusion strategy.
These findings suggest that a mechanism specific to continuous infusion diuretic strategy results in deleterious renal effects in HFpEF patients with acute HF. One possible explanation is that HFpEF patients may be more sensitive to preload and that a continuous infusion strategy may not allow for adequate re-equilibration of intravascular and extravascular volumes in the setting of congestion. This may lead to a state of transient pre-renal azotemia in the setting of acute HF, despite overall similarities in net volume of diuresis. In our clinical experience, we have observed this “yo-yo” effect consisting of a transient rise in creatinine with initiation of diuresis, followed by a decline when diuretic therapy is withheld, and then a rise in creatinine again after a few days of resuming therapy. Another potential factor may be hemodynamic responses to treatment, as the continuous infusion diuretic group showed a trend toward greater drop in SBP at 72 h than those in the intermittent bolus strategy group, potentially further exacerbating swings in preload, afterload, and volume distribution. Further investigation is needed to better understand why women, African Americans, and those with CKD in particular are more susceptible to renal injury with continuous infusion diuretic strategy than intermittent bolus diuretic strategy. Ongoing efforts to clinically and pathophysiologically phenotype HFpEF may provide clues as to why certain subgroups of HFpEF patients are more susceptible to volume and hemodynamic shifts than others (8,25).
In order to mitigate some of the hemodynamic and volume shifts in the management of acute HF in HFpEF, we hypothesized that low-dose dopamine may facilitate diuresis without precipitating renal injury. Prior studies of low-dose dopamine in the treatment of acute decompensated HF in HFrEF patients have suggested several benefits of this treatment strategy, including increase in renal blood flow and improvement in renal function, while maintaining comparable if not improved urine output (19,26,27). In the DAD-HF (Dopamine in Acute Decompensated Heart Failure) study, the combination of low-dose dopamine (5 μg/kg/min) with low-dose furosemide resulted in equally efficacious diuresis with improved renal function compared to high-dose furosemide alone (28). This favorable effect of dopamine was not detected, however, in a follow-up study of high- versus low-dose furosemide infusion therapy, with or without the addition of low-dose dopamine (29). In the more recent ROSE (Renal Optimization Strategies Evaluation) trial, the addition of low-dose dopamine (3 μg/kg per min) to diuretic therapy had no significant effects on urinary volume or change in cystatin C at 72 h of treatment in a predominantly HFrEF population compared to placebo (21). Interestingly, a small subset of patients enrolled in the ROSE trial had an EF ≥50%, and in subgroup analysis this cohort had less urine output and a nonsignificant trend toward increased cystatin C with dopamine compared to placebo.
We found no differences in renal outcomes with low-dose dopamine. Of note, there were no significant differences in SBP changes or heart rate changes with low-dose dopamine. Interestingly, in our correlation analyses, lower SBP significantly correlated with rise in creatinine in the no-dopamine group; however, this correlation was not seen with low-dose dopamine. It is possible, therefore, that in a larger study with adequate power, dopamine may have a positive effect by mitigating the hemodynamic fluctuations seen during the treatment of acute HF in HFpEF patients.
ROPA-DOP was a single-center study that was not powered to detect clinical events. Furthermore, the study enrollment was stopped early due to slow enrollment rate. The investigator team was blinded to treatment assignment, but the patients and the primary care teams were not, which may be a source of possible bias. Finally, the trial allowed for adjustments in the diuretic dosages by the primary teams to replicate real-world practice, and this might have affected the observed differences at the 72-h endpoints.
In the first inpatient study to evaluate diuretic and renoprotective treatment strategies for the treatment of HFpEF patients hospitalized with acute HF, low-dose dopamine had a neutral effect on renal outcomes, whereas a continuous infusion diuretic strategy resulted in significantly worse renal function than intermittent bolus diuretic strategy.
COMPETENCY IN MEDICAL KNOWLEDGE: In the treatment of hospitalized HFpEF patients with acute HF, low-dose dopamine had a neutral effect on renal outcomes, whereas a continuous infusion diuretic strategy was associated with increased risk of renal injury compared to an intermittent bolus diuretic strategy.
TRANSLATIONAL OUTLOOK: Further studies are needed to better understand why HFpEF patients with acute HF are susceptible to renal injury and to help define best-practice strategies for the treatment of these patients.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- body mass index
- chronic kidney disease
- ejection fraction
- estimated glomerular filtration rate
- heart failure with preserved ejection fraction
- heart failure with reduced ejection fraction
- N-terminal pro–B-type natriuretic peptide
- systolic blood pressure
- worsening renal function
- Received January 30, 2018.
- Revision received April 12, 2018.
- Accepted April 17, 2018.
- 2018 American College of Cardiology Foundation
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