Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure.
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OBJECTIVES: The purpose of this study was to assess the relationship between biomarkers of renin-angiotensin-aldosterone system (RAAS) activation and decongestion strategies, worsening renal function, and clinical outcomes. BACKGROUND: High-dose diuretic therapy in patients with acute heart failure (AHF) is thought to activate the RAAS; and alternative decongestion strategies, such as ultrafiltration (UF), have been proposed to mitigate this RAAS activation. METHODS: This study analyzed 427 AHF patients enrolled in the DOSE-AHF (Diuretic Optimization Strategies in Acute Heart Failure) and CARRESS-HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) trials. We assessed the relationship between 2 markers of RAAS activation (plasma renin activity [PRA] and aldosterone) from baseline to 72 h and 96 h and decongestion strategy: high- versus low-dose and continuous infusion versus bolus furosemide for DOSE-AHF and UF versus stepped pharmacologic care for CARRESS-HF. We determined the relationships between RAAS biomarkers and 60-day outcomes. RESULTS: Patients with greater RAAS activation at baseline had lower blood pressures, lower serum sodium levels, and higher blood urea nitrogen (BUN) concentration. Continuous infusion furosemide and UF were associated with greater PRA increases (median: +1.66 vs. +0.66 ng/ml/h with continuous vs. bolus infusion, respectively, p = 0.021; +4.05 vs. +0.56 ng/ml/h with UF vs. stepped care, respectively, p = 0.014). There were no significant differences in RAAS biomarker changes with high- versus low-dose diuretic therapy (both: p > 0.5). Neither baseline log PRA nor log aldosterone was associated with increased death or HF hospitalization (hazard ratio [HR] for a doubling of 1.05; 95% confidence interval [CI]: 0.98 to 1.13; p = 0.18; and HR: 1.13; 95% CI: 0.99 to 1.28; p = 0.069, respectively). The change in RAAS biomarkers from baseline to 72 and 96 h was not associated with outcomes (both: p > 0.5). CONCLUSIONS: High-dose loop diuretic therapy did not result in RAAS activation greater than that with low-dose diuretic therapy. UF resulted in greater PRA increase than stepped pharmacologic care. Neither PRA nor aldosterone was significantly associated with short-term outcomes in this cohort. (Determining Optimal Dose and Duration of Diuretic Treatment in People With Acute Heart Failure [DOSE-AHF]; NCT00577135; Effectiveness of Ultrafiltration in Treating People With Acute Decompensated Heart Failure and Cardiorenal Syndrome [CARRESS]; NCT00608491).
acute heart failure
Blood Urea Nitrogen
Dose-Response Relationship, Drug
Drug Administration Schedule
Published Version (Please cite this version)10.1016/j.jchf.2014.09.003
Publication InfoAbouEzzeddine, OF; Anstrom, Kevin J; Bart, BA; Braunwald, E; DeVore, Adam David; Felker, G Michael; ... Vader, JM (2015). Decongestion strategies and renin-angiotensin-aldosterone system activation in acute heart failure. JACC Heart Fail, 3(2). pp. 97-107. 10.1016/j.jchf.2014.09.003. Retrieved from https://hdl.handle.net/10161/11075.
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Professor of Biostatistics and Bioinformatics
My research interests include clinical trials, cost-benefit analysis, health economics, semiparametric estimation, and medical informatics.
Assistant Professor of Medicine
Adam D. DeVore, MD, MHS Dr. DeVore is a cardiologist and Assistant Professor of Medicine in the Department of Medicine, Division of Cardiology, at Duke University School of Medicine. His clinical interests include caring for patients and families with heart failure, including those with left ventricular assist devices and heart transplants. He is involved in and leads multiple large studies of patients with heart failure at both Duke University Medical Center and the
Professor of Medicine
Professor of Medicine
Associate Professor of Medicine
I am a cardiologist with a clinical and research interest in heart failure, including advanced therapies such as cardiac transplantation and mechanical assist devices or “heart pumps." I became a heart failure cardiologist in order to help patients manage their chronic disease over many months and years. I consider myself strongly committed to compassionate patient care with a focus on quality of life and patient preference.My research interests are focused on treating co-morbi
Richard Sean Stack, M.D. / Guidant Foundation Professor of Cardiology
Dr. O’Connor’s research interests include: acute heart failure; co-morbidities in heart failure; clinical trials; biomarkers; and novel pharmacological and non-pharmacological approaches for the treatment of heart failure.
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