著者: Alan S Maisel, Padma Krishnaswamy, Richard M Nowak, James McCord, Judd E Hollander, Philippe Duc, Torbjørn Omland, Alan B Storrow, William T Abraham, Alan H B Wu, Paul Clopton, Philippe G Steg, Arne Westheim, Catherine Wold Knudsen, Alberto Perez, Radmila Kazanegra, Howard C Herrmann, Peter A McCullough, Breathing Not Properly Multinational Study Investigators
雑誌名: N Engl J Med. 2002 Jul 18;347(3):161-7. doi: 10.1056/NEJMoa020233.
Abstract/Text
BACKGROUND: B-type natriuretic peptide is released from the cardiac ventricles in response to increased wall tension.
METHODS: We conducted a prospective study of 1586 patients who came to the emergency department with acute dyspnea and whose B-type natriuretic peptide was measured with a bedside assay. The clinical diagnosis of congestive heart failure was adjudicated by two independent cardiologists, who were blinded to the results of the B-type natriuretic peptide assay.
RESULTS: The final diagnosis was dyspnea due to congestive heart failure in 744 patients (47 percent), dyspnea due to noncardiac causes in 72 patients with a history of left ventricular dysfunction (5 percent), and no finding of congestive heart failure in 770 patients (49 percent). B-type natriuretic peptide levels by themselves were more accurate than any historical or physical findings or laboratory values in identifying congestive heart failure as the cause of dyspnea. The diagnostic accuracy of B-type natriuretic peptide at a cutoff of 100 pg per milliliter was 83.4 percent. The negative predictive value of B-type natriuretic peptide at levels of less than 50 pg per milliliter was 96 percent. In multiple logistic-regression analysis, measurements of B-type natriuretic peptide added significant independent predictive power to other clinical variables in models predicting which patients had congestive heart failure.
CONCLUSIONS: Used in conjunction with other clinical information, rapid measurement of B-type natriuretic peptide is useful in establishing or excluding the diagnosis of congestive heart failure in patients with acute dyspnea.
Copyright 2002 Massachusetts Medical Society.
PMID
12124404 N Engl J Med. 2002 Jul 18;347(3):161-7. doi: 10.1056/NE･･･
著者: James L Januzzi, Carlos A Camargo, Saif Anwaruddin, Aaron L Baggish, Annabel A Chen, Daniel G Krauser, Roderick Tung, Renee Cameron, J Tobias Nagurney, Claudia U Chae, Donald M Lloyd-Jones, David F Brown, Stacy Foran-Melanson, Patrick M Sluss, Elizabeth Lee-Lewandrowski, Kent B Lewandrowski
雑誌名: Am J Cardiol. 2005 Apr 15;95(8):948-54. doi: 10.1016/j.amjcard.2004.12.032.
Abstract/Text
The utility of aminoterminal pro-brain natriuretic peptide (NT-proBNP) testing in the emergency department to rule out acute congestive heart failure (CHF) and the optimal cutpoints for this use are not established. We conducted a prospective study of 600 patients who presented in the emergency department with dyspnea. The clinical diagnosis of acute CHF was determined by study physicians who were blinded to NT-proBNP results. The primary end point was a comparison of NT-proBNP results with the clinical assessment of the managing physician for identifying acute CHF. The median NT-proBNP level among 209 patients (35%) who had acute CHF was 4,054 versus 131 pg/ml among 390 patients (65%) who did not (p <0.001). NT-proBNP at cutpoints of >450 pg/ml for patients <50 years of age and >900 pg/ml for patients >or=50 years of age were highly sensitive and specific for the diagnosis of acute CHF (p <0.001). An NT-proBNP level <300 pg/ml was optimal for ruling out acute CHF, with a negative predictive value of 99%. Increased NT-proBNP was the strongest independent predictor of a final diagnosis of acute CHF (odds ratio 44, 95% confidence interval 21.0 to 91.0, p <0.0001). NT-proBNP testing alone was superior to clinical judgment alone for diagnosing acute CHF (p = 0.006); NT-proBNP plus clinical judgment was superior to NT-proBNP or clinical judgment alone. NT-proBNP measurement is a valuable addition to standard clinical assessment for the identification and exclusion of acute CHF in the emergency department setting.
PMID
15820160 Am J Cardiol. 2005 Apr 15;95(8):948-54. doi: 10.1016/j.･･･
著者: W Frank Peacock, Gregg C Fonarow, Charles L Emerman, Roger M Mills, Janet Wynne, ADHERE Scientific Advisory Committee and Investigators, Adhere Study Group
雑誌名: Cardiology. 2007;107(1):44-51. doi: 10.1159/000093612. Epub 2006 May 4.
Abstract/Text
BACKGROUND: Since most acute decompensated heart failure (ADHF) patients present for hospital care via the emergency department (ED), we sought to determine the impact of early ED initiation of ADHF-specific therapy, as indicated by nesiritide use, on subsequent outcomes.
METHODS: We queried the Acute Decompensated Heart Failure National Registry (ADHERE) to identify patients with initial systolic blood pressure >90 mm Hg and negative cardiac biomarkers, hospitalized after presentation to the ED, who received nesiritide but no other intravenous vasoactive drugs. Intensive care unit use and total hospital length of stay were compared based on the hospital unit where nesiritide therapy was initiated after multivariate adjustment for baseline differences in study populations.
RESULTS: Nesiritide was started in the ED in 1,613 patients (EDN group) and after admission to an inpatient unit in 2,687 patients (INN group). EDN patients had higher baseline systolic and diastolic blood pressure (both p < 0.001); while INN patients were more likely to be male and have baseline renal dysfunction (both p < 0.001). Nesiritide was initiated a median of 2.8 and 15.5 h after presentation in EDN and INN patients, respectively (p < 0.001). Compared to INN, EDN patients had a shorter adjusted mean total hospital length of stay (5.4 vs. 6.9 days; p < 0.001), were less likely to require transfer to the intensive care unit from another inpatient unit (odds ratio [OR]: 0.301; 95% confidence interval [CI]: 0.206-0.440), and were more likely to be discharged home (OR: 1.154; 95% CI: 1.005-1.325).
CONCLUSIONS: Initiation of ADHF-specific therapy early, while the patient is in the ED, is associated with improved clinical outcomes.
PMID
16741357 Cardiology. 2007;107(1):44-51. doi: 10.1159/000093612. ･･･
