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J Am Coll Cardiol, 2003; 41:1264-1272, doi:10.1016/S0735-1097(03)00168-2 © 2003 by the American College of Cardiology Foundation |





* Cardiovascular Division, Department of Medicine, Brigham & Womens Hospital, Boston, Massachusetts, USA
Donald W. Reynolds Cardiovascular Research Center, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Harvard Clinical Research Institute, Boston, Massachusetts, USA
Merck & Co, West Point, Pennsylvania, USA
Manuscript received October 27, 2002; revised manuscript received December 4, 2002, accepted December 26, 2002.
* Reprint requests and correspondence: Dr. David A. Morrow, Cardiovascular Division, Brigham and Womens Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA.
dmorrow{at}partners.org
OBJECTIVES: This study was designed to evaluate B-type natriuretic peptide (BNP) for risk assessment and clinical decision making over a range of cut points, alone and with cardiac troponin I (cTnI), in patients with nonST-elevation acute coronary syndromes (ACS).
BACKGROUND: B-type natriuretic peptide holds promise for risk stratification. Additional evidence regarding optimal decision limits, use in combination with troponin, and use in targeting therapy is needed before acceptance into clinical use for ACS.
METHODS: We evaluated BNP at baseline in 1,676 patients with nonST-elevation ACS randomized to early invasive versus conservative management.
RESULTS: Patients with elevated BNP (>80 pg/ml; n = 320) were at higher risk of death at seven days (2.5% vs. 0.7%, p = 0.006) and six months (8.4% vs. 1.8%, p < 0.0001). The association between BNP and mortality at six months (adjusted odds ratio [OR] 3.3; 95% confidence interval [CI] 1.7 to 6.3) was independent of important clinical predictors, including cTnI and congestive heart failure (CHF). Patients with elevated BNP had a fivefold higher risk of developing new CHF by 30 days (5.9% vs. 1.0%, p < 0.0001). B-type natriuretic peptide added prognostic information to cTnI, discriminating patients at higher mortality risk among those with negative (OR 6.9; 95% CI 1.9 to 25.8) and positive (OR 4.1; 95% CI 1.9 to 9.0) baseline cTnI results. No difference was observed in the effect of invasive versus conservative management when stratified by baseline levels of BNP (pinteraction
0.6).
CONCLUSIONS: Elevated BNP (>80 pg/ml) at presentation identifies patients with nonST-elevation ACS who are at higher risk of death and CHF and adds incremental information to cTnI. Additional work is needed to identify therapies that may reduce the risk associated with increased BNP.
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