Annexin A1 is a Potential Novel Biomarker of Congestion in Acute Heart Failure.
Autor: | Adel FW; Cardiorenal Research Laboratory, Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota., Rikhi A; Department of Pediatrics, Duke University School of Medicine, Durham, North Carolina., Wan SH; Cardiorenal Research Laboratory, Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota., Iyer SR; Cardiorenal Research Laboratory, Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota., Chakraborty H; Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina., McNulty S; Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina., Tang WHW; Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio., Felker GM; Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina., Givertz MM; Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts., Chen HH; Cardiorenal Research Laboratory, Department of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota. Electronic address: Chen.Horng@mayo.edu. |
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Jazyk: | angličtina |
Zdroj: | Journal of cardiac failure [J Card Fail] 2020 Aug; Vol. 26 (8), pp. 727-732. Date of Electronic Publication: 2020 May 27. |
DOI: | 10.1016/j.cardfail.2020.05.012 |
Abstrakt: | Objectives: This study sought to identify the role of annexin A1 (AnxA1) as a congestion marker in acute heart failure (AHF) and to identify its putative role in predicting clinical outcomes. Background: AnxA1 is a protein that inhibits inflammation following ischemia-reperfusion injury in cardiorenal tissues. Because AHF is a state of tissue hypoperfusion, we hypothesized that plasma AnxA1 levels are altered in AHF. Methods: In the Renal Optimization Strategies Evaluation (ROSE) trial, patients hospitalized for AHF with kidney injury were randomized to receive dopamine, nesiritide, or placebo for 72 hours in addition to diuresis. In a subanalysis, plasma AnxA1 levels were measured at baseline and at 72 hours in 275 patients. Participants were divided into 3 tertiles based on their baseline AnxA1 levels. Results: The prevalence of peripheral edema 2+ increased with increasing AnxA1 levels (P < .007). Cystatin C, blood urea nitrogen, and kidney injury molecule-1 plasma levels were higher among participants in tertile 3 vs tertiles 1 or 2 (P< .05). Patients with a congestion score of 4 had a mean baseline AnxA1 level 8.63 units higher than those with a congestion score of 0 (P = .03). Patients in tertiles 2 and 3 were twice as likely to experience creatinine elevation as patients in tertile 1 (P = .03). Patients in tertiles 2 and 3 were at a higher risk of 60-day all-cause mortality or heart failure hospitalization and 180-day all-cause mortality (P < .05). Conclusions: Among patients hospitalized for AHF with impaired kidney function, elevated AnxA1 levels are associated with worse congestion, higher risk for further creatinine elevation, and higher rates of 60-day morbidity or all-cause mortality and 180-day all-cause mortality. Clinical Trial Registration: clinicaltrials.gov Identifier: NCT01132846. (Copyright © 2020 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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