Elevated admission urinary N-acetyl-β-D-glucosamidase level is associated with worse long-term clinical outcomes in patients with acute heart failure
Author(s) -
Sayaka Funabashi,
Kazunori Omote,
Toshiyuki Nagai,
Yasuyuki Honda,
Hiroki Nakano,
Satoshi Honda,
Naotsugu Iwakami,
Yasuhiro Hamatani,
Michikazu Nakai,
Kunihiro Nishimura,
Yasuhide Asaumi,
Takeshi Aiba,
Teruo Noguchi,
Kengo Kusano,
Hiroyuki Yokoyama,
Satoshi Yasuda,
Hisao Ogawa,
Toshihisa Anzai
Publication year - 2020
Publication title -
european heart journal acute cardiovascular care
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.42
H-Index - 33
eISSN - 2048-8734
pISSN - 2048-8726
DOI - 10.1177/2048872620901986
Subject(s) - heart failure , medicine , interquartile range , hazard ratio , acute decompensated heart failure , urinary system , renal function , inotrope , proportional hazards model , cardiology , adverse effect , confidence interval
Background: The prognostic significance of urinary N-acetyl-β-D-glucosamidase in acute heart failure has not been fully elucidated. Accordingly, this study investigated whether urinary N-acetyl-β-D-glucosamidase could be associated with subsequent adverse events in acute heart failure patients. Methods: We studied 708 consecutive acute heart failure patients who had accessible N-acetyl-β-D-glucosamidase data on admission from the National Cerebral and Cardiovascular Center Acute Decompensated Heart Failure registry. We assessed the relationship between the admission N-acetyl-β-D-glucosamidase level and the combined endpoint of all-cause death and worsening heart failure. Worsening heart failure was defined as worsening symptoms and signs of heart failure requiring intensification of intravenous therapy such as diuretics, vasodilators and inotropes or initiation of mechanical support after stabilisation with initial treatment during hospitalisation, or readmission due to heart failure after discharge. Results: During a median follow-up period of 763 (interquartile range 431–1028) days, higher urinary N-acetyl-β-D-glucosamidase was significantly related to increased events of all-cause death and worsening heart failure. In addition, patients with higher urinary N-acetyl-β-D-glucosamidase and lower estimated glomerular filtration rate on admission had the worst clinical outcomes. In multivariable Cox regression, urinary N-acetyl-β-D-glucosamidase on admission was independently associated with adverse events (hazard ratio 1.19, 95% confidence interval 1.04–1.35) even after adjustment by covariates including the baseline estimated glomerular filtration rate. Conclusions: Higher urinary N-acetyl-β-D-glucosamidase level on admission was independently associated with worse clinical outcomes. Our findings indicate the potential value of assessing urinary N-acetyl-β-D-glucosamidase on admission for further risk stratification in patients with acute heart failure.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom