UTILITY OF A RAPID B-NATRIURETIC PEPTIDE ASSAY IN DIFFERENTIATING CONGESTIVE HEART FAILURE FROM LUNG DISEASE IN PATIENTS PRESENTING WITH DYSPNEA.

Morrison LK, et alJ Am Coll Cardiol 2002 Jan 16;39(2):202-9.

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.

COMMENTS: While BNP demonstrates an episode of CHF, it does not rule out a concurrent COPD exascerbation in those patients with both diseases.

DYSPNEA DIFFERENTIATION INDEX: A NEW METHOD FOR THE RAPID SEPARATION OF CARDIAC VS PULMONARY DYSPNEA.

Ailani RK, et al. Chest 1999 Oct;116(4):1100-4.

STUDY OBJECTIVE: To assess the utility of a new parameter in the differentiation of dyspnea of cardiac origin from dyspnea of pulmonary origin.

METHODS: The peak expiratory flow (PEF) rate and the partial pressure of oxygen in arterial blood (PaO(2)) were measured in 71 patients with the chief complaint of dyspnea. The patients were treated in the hospital, and the final diagnosis (cardiac or pulmonary) of the cause of dyspnea was made at discharge. We defined a new measure, the dyspnea differentiation index (DDI), as (PEF x PaO(2))/1,000. We performed a receiver operating characteristic (ROC) curve analysis of the data to define the measure that best distinguished cardiac from pulmonary dyspnea. The curves also allowed us to establish an optimal cut-off point to distinguish between cardiac and pulmonary dyspnea.

RESULTS: Patients with pulmonary dyspnea had a significantly lower mean PEF than patients with cardiac dyspnea (144 +/- 66 vs 267 +/- 97 L/min, respectively; p < 0.001). They also had a lower DDI than patients with cardiac dyspnea (8.4 +/- 4.0 vs 18.4 +/- 7.9 L-mm/min, respectively; p < 0.001). These two measures, PEF and DDI, also best distinguished pulmonary from cardiac dyspnea. PEF was able to diagnose the correct cause of dyspnea in 72% of patients, and DDI was correct in 79% of patients. This compares favorably to the performance of the emergency department physicians, who were able to predict the correct diagnosis in only 69% of patients.

CONCLUSION: These results demonstrate that the PEF by itself is useful in differentiating between cardiac and pulmonary causes of dyspnea, but that the calculation of DDI is superior in this regard.