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J Am Coll Cardiol, 2002; 39:202-209 © 2002 by the American College of Cardiology Foundation |
* Division of Cardiology, Veterans Affairs Medical Center, and the Department of Medicine, University of California, San Diego, California, USA
Manuscript received June 18, 2001; revised manuscript received October 4, 2001, accepted October 26, 2001.
* Reprint requests and correspondence: Dr. Alan Maisel, Veterans Affairs Medical Center, Cardiology 111-A, 3350 La Jolla Village Drive, San Diego, California 92161, USA.
amaisel{at}ucsd.edu
OBJECTIVES: Since B-type natriuretic peptide (BNP) is secreted by the left ventricle (LV) in response to volume elevated LV pressure, we sought to assess whether a rapid assay for BNP levels could differentiate cardiac from pulmonary causes of dyspnea.
BACKGROUND: Differentiating congestive heart failure (CHF) from pulmonary causes of dyspnea is very important for patients presenting to the emergency department (ED) with acute dyspnea.
METHODS: B-natriuretic peptide levels were obtained in 321 patients presenting to the ED with acute dyspnea. Physicians were blinded to BNP levels and asked to give their probability of the patient having CHF and their final diagnosis. Two independent cardiologists were blinded to BNP levels and asked to review the data and evaluate which patients presented with heart failure. Patients with right heart failure from cor pulmonale were classified as having CHF.
RESULTS: Patients with CHF (n = 134) had BNP levels of 758.5 ± 798 pg/ml, significantly higher than the group of patients with a final diagnosis of pulmonary disease (n = 85) whose BNP was 61 ± 10 pg/ml. The area under the receiver operating curve, which plots sensitivity versus specificity for BNP levels in separating cardiac from pulmonary disease, was 0.96 (p < 0.001). A breakdown of patients with pulmonary disease revealed: chronic obstructive pulmonary disease (COPD): 54 ± 71 pg/ml (n = 42); asthma: 27 ± 40 pg/ml (n = 11); acute bronchitis: 44 ± 112 pg/ml (n = 14); pneumonia: 55 ± 76 pg/ml (n = 8); tuberculosis: 93 ± 54 pg/ml (n = 2); lung cancer: 120 ± 120 pg/ml (n = 4); and acute pulmonary embolism: 207 ± 272 pg/ml (n = 3). In patients with a history of lung disease but whose current complaint of dyspnea was seen as due to CHF, BNP levels were 731 ± 764 pg/ml (n = 54). The group with a history of CHF but with a current COPD diagnosis had a BNP of 47 ± 23 pg/ml (n = 11).
CONCLUSIONS: Rapid testing of BNP in the ED should help differentiate pulmonary from cardiac etiologies of dyspnea.
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