Contemporary Decongestion Strategies in Patients Hospitalized for Heart Failure: A National Community-Based Cohort Study

Jimmy Zheng; Andrew P. Ambrosy; Ankeet S. Bhatt; Sean P. Collins; Kelsey M. Flint; Gregg C. Fonarow; Marat Fudim; Stephen J. Greene; Anuradha Lala; Jeffrey M. Testani; Anubodh S. Varshney; Ryan S.K. Wi; Alexander T. Sandhu

Disclosures

JACC Heart Fail. 2024;12(8)

Abstract and Introduction

Abstract

Background: Heart failure (HF) is a leading cause of hospitalization in the United States. Decongestion remains a central goal of inpatient management, but contemporary decongestion practices and associated weight loss have not been well characterized nationally.

Objectives: This study aimed to describe contemporary inpatient diuretic practices and clinical predictors of weight loss in patients hospitalized for HF.

Methods: The authors identified HF hospitalizations from 2015 to 2022 in a U.S. national database aggregating deidentified patient-level electronic health record data across 31 geographically diverse community-based health systems. The authors report patient characteristics and inpatient weight change as a primary indicator of decongestion. Predictors of weight loss were evaluated using multivariable models. Temporal trends in inpatient diuretic practices, including augmented diuresis strategies such as adjunctive thiazides and continuous diuretic infusions, were assessed.

Results: The study cohort included 262,673 HF admissions across 165,482 unique patients. The median inpatient weight loss was 5.3 pounds (Q1-Q3: 0.0-12.8 pounds) or 2.4 kg (Q1-Q3: 0.0-5.8 kg). Discharge weight was higher than admission weight in 20% of encounters. An increase of ≥0.3 mg/dL in serum creatinine from admission to inpatient peak occurred in >30% of hospitalizations and was associated with less weight loss. Adjunctive diuretic agents were utilized in <20% of encounters but were associated with greater weight loss.

Conclusions: In a large-scale U.S. community-based cohort study of HF hospitalizations, estimated weight loss from inpatient decongestion remains highly variable, with weight gain observed across many admissions. Augmented diuresis strategies were infrequently used. Comparative effectiveness trials are needed to establish optimal strategies for inpatient decongestion for acute HF.

Introduction

Acute heart failure (HF) is among the leading causes of hospitalization in the United States.^[1] Despite advances in guideline-directed medical therapy, HF readmission rates have worsened over the past decade.^[2] Given inadequate decongestion is associated with worse postdischarge outcomes, optimizing decongestion continues to be an important therapeutic goal of inpatient HF management.^[3] However, few effective strategies for acute HF decongestion have emerged, and intravenous loop diuretic agents remain the cornerstone of treatment.^[4]

Contemporary HF decongestion practices across the U.S. are not well-described. Nearly 20 years ago, the ADHERE (Acute Decompensated Heart Failure National Registry) registry described inpatient HF treatment patterns and decongestion outcomes in a prospective national database of HF hospitalizations across 275 community and academic medical centers.^[5] Although most patients in the ADHERE registry presented with congestion, one-third lost fewer than 5 pounds or 2.3 kg and 16% actually gained weight. Since then, several clinical trials investigating adjunctive diuretic agents have also reported decongestion outcomes.^[6,7,8] However, clinical trial cohorts often differ in patient characteristics, disease burden, and treatment conditions from those in routine practice.^[9] The GWTG-HF (Get With The Guidelines–Heart Failure) registry captures inpatient HF care but lacks detailed data on inpatient medications.^[10] An analysis of Optum electronic health record data described in-hospital diuretic treatment patterns, including dose changes and combination therapy use, but did not report changes in weight.^[11]

We developed a national observational cohort to assess the TREAT-AHF (Trajectory and Response to Emergently Administered Therapy for Acute Heart Failure) registry. As the national burden of HF hospitalizations continues to increase,^[12,13] optimization of acute inpatient decongestion is critical in mitigating HF morbidity and mortality. In this large longitudinal analysis, we aimed to characterize contemporary patterns of decongestion strategies and identify clinical predictors of weight loss in acute HF hospitalizations in the United States.

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Abstract and Introduction
Methods
Results
Discussion
Conclusions
References
Sidebar

Table 1. Baseline Characteristics of the TREAT-AHF Registry Compared With Other HF Registries
	TREAT-AHF (N = 262,673)	GWTG-HF (N = 423,333)	ADHERE (N = 97,794)
Study period	2015-2022	2010-2016	2001-2004
Admission age, y	73.6 ± 13.2	72.2 ± 14.6	72.3 ± 13.9
Female	50.4	48.2	50.2
Race/ethnicity
Non-Hispanic White	74.0	69.1	72.0
Hispanic	3.9	7.6	—
Black	12.0	19.3	20.7
Other^a	10.2	3.9
Short-term outcomes
Discharge home	62.5	77.5	—
Discharge to other health care facility	23.5	19.7	—
Length of stay, d	5.8 (3.7-9.6)	4.0 (3.0-6.0)	4.4 (2.8-7.0)
Weight loss >10 pounds or >4.5 kg	32.5	—	26.1
Inpatient mortality	6.2	2.8	4.0
HF characteristics^b
History of HF	68.9	—	76.1
Number of HF hospitalizations in past year	0.6 ± 1.1	—	1.0 ± 1.1
Systolic dysfunction^c	37.7	43.4	50.8
Clinical characteristics^b
Atrial fibrillation	44.8	39.2	31.2
Chronic kidney disease	38.4	24.9	30.2
COPD	35.3	33.6	30.9
Diabetes	44.5	45.0	44.1
Hyperlipidemia	58.6	54.1	35.3
Hypertension	81.6	81.1	72.6
Ischemic heart disease	48.5	49.6	57.5
Peripheral vascular disease	23.1	12.4	17.9
Valvular disorder	26.4	—	22.7
Ventricular arrhythmia	8.1	—	8.4
Admission vitals
Systolic blood pressure, mm Hg	133 ± 24	142 ± 30	143 ± 32
Diastolic blood pressure, mm Hg	72 ± 14	78 ± 19	78 ± 20
Heart rate, beats/min	86 ± 18	86 ± 20	88 ± 22
Admission laboratory values
Sodium, mEq/L	137 ± 5	138 ± 7	—
Creatinine, mg/dL	1.4 ± 0.9	1.3 ± 0.6	1.8 ± 1.6
Blood urea nitrogen, mEq/L	30 ± 20	—	32 ± 21
BNP, pg/mL	867 (359-2,344)	838 (408-1,669)	—
Baseline medications^d
ACEI	24.1	33.7	41.2
ARB	18.2	14.5	12.0
ARNI	4.2	—	—
BB	59.2	68.5	48.4
MRA	16.2	12.7	10.5
SGLT2i	1.9	—	—
Loop diuretic	56.7	60.0	70.5
Digoxin	6.7	10.8	28.2

Values are range, median (Q1-Q3), n (%), or mean ± SD, unless otherwise indicated. ^aIncludes Asian, American Indian or Alaskan Native, Native Hawaiian or Pacific Islander, and unknown. ^bBased on ICD-9/ICD-10 and SNOMED-CT codes during 24-month lookback. ^cRegistry classification based on left ventricular ejection fraction. TREAT-AHF classification based on diagnostic codes. ^dExcludes patients not prescribed any of fifty common outpatient medications during 12-month lookback due to likelihood of receiving prescriptions from outside sources.

ACEI = angiotensin-converting enzyme inhibitor; ADHERE = Acute Decompensated Heart Failure National Registry; ARB = angiotensin receptor blocker; ARNI = angiotensin receptor-neprilysin inhibitor; BB = beta-blocker; BNP = B-type natriuretic peptide; COPD = chronic obstructive pulmonary disease; GWTG-HF = Get With The Guidelines–Heart Failure; ICD-9 = International Classification of Diseases–9th Revision; ICD-10 = International Classification of Diseases–10th Revision MRA = mineralocorticoid receptor antagonist; SGLT2i = sodium glucose co-transporter 2 inhibitor; SNOMED-CD = Systematized Nomenclature of Medicine Clinical Terms.

Table 2. Inpatient Management in the TREAT-AHF Registry (N = 262,673)
Oral therapies
ACEI/ARB/ARNI	43.1
ARNI	4.8
BB	73.0
MRA	18.1
SGLT2i	1.1
Digoxin	9.1
Loop diuretic	56.7
Adjunctive diuretic	17.1
Metolazone	10.3
Chlorothiazide	1.6
Hydrochlorothiazide	2.4
Chlorthalidone	0.4
Acetazolamide	4.0
Tolvaptan	0.7
Intravenous therapies
Loop diuretic^a	100.0
Furosemide	94.0
Bumetanide	15.8
Torsemide	0.0
Continuous infusion	6.6
Vasoactives	14.5
Inotropes	7.7
Dobutamine	4.5
Dopamine	2.5
Milrinone	1.8
Vasodilators	8.5
Nesiritide	<0.1
Nitroglycerin	8.2
Nitroprusside	0.5

Values are n (%). Not all category percentages equal the sum of their parts due to use of multiple therapies within a single category. ^aFurosemide and bumetanide frequencies include bolus and continuous dosing of respective therapies.

Abbreviations as in Table 1.

Authors and Disclosures

From the ^aDepartment of Medicine, Stanford University, Stanford, California, USA; ^bDepartment of Cardiology, Kaiser Permanente San Francisco Medical Center, San Francisco, California, USA; ^cDivision of Research, Kaiser Permanente Northern California,Oakland, California, USA; ^dDepartment of Emergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA; ^eGeriatric Research, Education and Clinical Center, VA Tennessee Valley Healthcare System, Nashville, Tennessee, USA; ^fRockyMountain Regional VA Medical Center, University of Colorado School of Medicine, Aurora, Colorado, USA; ^gDivision of Cardiology,Department of Medicine, Geffen School of Medicine at UCLA, Los Angeles, California, USA; ^hDepartment of Medicine, DukeUniversity Medical Center, Durham, North Carolina, USA; ⁱDuke Clinical Research Institute, Durham, North Carolina, USA; ^jDivision of Cardiology, Duke University School of Medicine, Durham, North Carolina, USA; ^kZena and Michael A. Wiener Cardiovascular Institute and Department of Population Health Science and Policy, Mount Sinai, New York, New York, USA; ^lSection ofCardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA; ^mDivision of Cardiovascular Medicine, Department of Medicine, Stanford University, Stanford, California, USA; ⁿDepartment ofMedicine, Albany Medical College, Albany, New York, USA; and the ^oDivision of Cardiology, Veterans Affairs Palo Alto Health CareSystem, Palo Alto, California, USA.

Address for Correspondence: Dr AlexanderSandhu, Division of Cardiovascular Medicine,Department of Medicine, Stanford University, 870Quarry Road, Stanford, California 94305, USA. E-mail: ats114@stanford.edu.

Funding Support and Author Disclosures: Dr Zheng has served as a consultant for Reprieve Cardiovascular. Dr Ambrosy has received relevant research support through grants to his institution from the National Heart, Lung, and Blood Institute (number K23HL150159), the American Heart Association (Second Century Early Faculty Independence Award), The Permanente Medical Group, Northern California Community Benefits Programs, Garfield Memorial Fund, Abbott Laboratories, Amarin Pharma, Edwards Lifesciences LLC, Esperion Therapeutics, and Novartis. Dr Bhatt has received relevant research support through grants to his institution from the National Heart, Lung, and Blood Institute, National Institute on Aging, the Centers for Disease Control and Prevention, and the American College of Cardiology Foundation; and previously received consulting fees from Sanofi Pasteur. Dr Collins has received research support from the National Institutes of Health, Patient-Centered Outcomes Research Institute, Department of Defense, and Beckman Coulter; and consulting fees from Abbott, Redesign Health, and Reprieve Cardiovascular, Inc. Dr Flint has received relevant grant funding from Abbott. Dr Fonarow has served as a consultant for Abbott, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Eli Lilly, Johnson and Johnson, Medtronic, Merck, Novartis, and Pfizer. Dr Greene has received research support from the Duke University Department of Medicine Chair’s Research Award, American Heart Association (number 929502), Amgen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Cytokinetics, Merck, Novartis, Pfizer, and Sanofi; served on the advisory board or as a consultant for Amgen, AstraZeneca, Bayer, Boehringer Ingelheim/Lilly, Bristol Myers Squibb, Corteria, CSL Vifor, Cytokinetics, Lexicon, Merck, Roche Diagnostics, Sanofi, scPharmaceuticals, Tricog Health, and Urovant Pharmaceuticals; and received speaker fees from Boehringer Ingelheim, Cytokinetics, Lexicon, and Roche Diagnostics. Dr Varshney has received consulting fees from Broadview Ventures. Dr Sandhu has received relevant research support from the National Heart, Lung, Blood Institute (number 1K23HL151672) and the American Heart Association; and served as a consultant for Reprieve Cardiovascular, Lexicon Pharmaceuticals, and Cleerly. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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