Author + information
- Received August 22, 2018
- Revision received September 26, 2018
- Accepted September 29, 2018
- Published online December 31, 2018.
- Ravi B. Patel, MDa,∗ (, )@RBPatelMD,
- Muthiah Vaduganathan, MD, MPHb,
- Aruna Rikhi, MPHc,
- Hrishikesh Chakraborty, DrPHc,
- Stephen J. Greene, MDc,d,
- Adrian F. Hernandez, MDc,d,
- G. Michael Felker, MD, MHSc,d,
- Margaret M. Redfield, MDe,
- Javed Butler, MD, MPH, MBAf and
- Sanjiv J. Shah, MDa
- aDepartment of Medicine, Division of Cardiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois
- bHeart and Vascular Center, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts
- cDuke Clinical Research Institute, Durham, North Carolina
- dDivision of Cardiology, Duke University Medical Center, Durham, North Carolina
- eDepartment of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota
- fDepartment of Medicine, University of Mississippi School of Medicine, Jackson, Mississippi
- ↵∗Address for correspondence:
Dr. Ravi B. Patel, Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, 676 North Saint Clair Street, Suite 600, Chicago, Illinois 60611.
Objectives This study sought to characterize the course of decongestion among patients hospitalized for acute heart failure (AHF) by history of atrial fibrillation (AF) and/or atrial flutter (AFL).
Background AF/AFL and chronic heart failure (HF) commonly coexist. Little is known regarding the impact of AF/AFL on relief of congestion among patients who develop AHF.
Methods We pooled patients from 3 randomized trials of AHF conducted within the Heart Failure Network, the DOSE (Diuretic Optimization Strategies) trial, the ROSE (Renal Optimization Strategies) trial, and the CARRESS-HF (Cardiorenal Rescue Study in Acute Decompensated Heart Failure) trial. The association between history of AF/AFL and in-hospital changes in various metrics of congestion was assessed using covariate-adjusted linear and ordinal logistic regression models.
Results Of 750 unique patients, 418 (56%) had a history of AF/AFL. Left ventricular ejection fraction was higher (35% vs. 27%, respectively; p < 0.001), and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels were nonsignificantly lower at baseline (4,210 pg/ml vs. 5,037 pg/ml, respectively; p = 0.27) in patients with AF/AFL. After adjustment of covariates, history of AF/AFL was associated with less substantial loss of weight (−5.7% vs. −6.5%, respectively; p = 0.02) and decrease in NT-proBNP levels (−18.7% vs. −31.3%, respectively; p = 0.003) by 72 or 96 h. History of AF/AFL was also associated with a blunted increase in global sense of well being at 72 or 96 h (p = 0.04). There was no association between history of AF/AFL and change in orthodema congestion score (p = 0.67) or 60-day composite clinical endpoint (all-cause mortality or any rehospitalization; hazard ratio: 1.21; 95% confidence interval: 0.92 to 1.59; p = 0.17).
Conclusions More than half of the patients admitted with AHF had a history of AF/AFL. History of AF/AFL was independently associated with a blunted course of in-hospital decongestion. Further research is required to understand the utility of specific therapies targeting AF/AFL during hospitalization for AHF.
Supported by National Heart, Lung, and Blood Institute/National Institutes of Health awards U10 HL084904, U10 HL110297, U10 HL110342, U10 HL110309, U10 HL110262, U10 HL110338, U10 HL110312, U10 HL110302, U10 HL110336, and U10 HL110337. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Dr. Patel is supported by NHLBI T32 postdoctoral training grant T32HL069771. Dr. Vaduganathan is supported by KL2/Catalyst Medical Research Investigator Training award, Harvard Catalyst, Harvard Clinical and Translational Science Center, National Center for Advancing Translational Sciences, NIH award KL2 TR002542; and serves on advisory boards for Bayer AG and Baxter Healthcare. Dr. Greene is supported by NHLBI T32 postdoctoral training grant T32HL069749-14 and Heart Failure Society of America/Emergency Medicine Foundation Acute Heart Failure Young Investigator Award, Novartis; and has received research support from Amgen and Novartis. Dr. Felker has received research support from NHLBI, the American Heart Association, Novartis, Cytokinetics, Amgen, and Merck; and has consulted for Amgen, Novartis, Bristol-Myers Squibb, Stealth, SC Pharma, Innolife, Cytokinetics, VWave, EBR Systems, and Cardionomic. Dr. Butler has received research support from NIH and European Union; and has consulted for Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, CVRx, Janssen, Luitpold Pharmaceuticals, Medtronic, Merck, Novartis, Relypsa, Vifor Pharma, and ZS Pharma. Dr. Shah has received research grants from Actelion, AstraZeneca, Corvia, and Novartis; and is a compensated consultant for Actelion, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cardiora, Eisai, Ironwood, Merck, Novartis, Sanofi, and United Therapeutics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Barry Greenberg, MD, served as Guest Editor for this paper.
- Received August 22, 2018.
- Revision received September 26, 2018.
- Accepted September 29, 2018.
- 2019 American College of Cardiology Foundation
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