Clinical investigation
Brain natriuretic peptide predicts right heart failure in patients with acute pulmonary embolism

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Abstract

Background

Plasma levels of brain natriuretic peptide (BNP) are increased in patients with left heart failure. In patients with severe pulmonary embolism (PE), primary right ventricular (RV) dysfunction is frequent. Little is known about BNP secretion in acute RV failure.

Methods

We prospectively studied 50 consecutive patients with confirmed PE (age range, 57 ± 19 years; 36 men). PE was confirmed with pulmonary angiography, spiral computed tomography, or echocardiography and subsidiary analyses. On admission, echocardiography and BNP measurements were performed in all patients.

Results

Patients without RV dysfunction had significantly lower BNP levels than patients with RV dysfunction (55 ± 69 pg/mL vs 340 ± 362 pg/mL, P <.001). There was a significant correlation between RV end-diastolic diameter and BNP (r = 0.43, P <.05). BNP discriminated patients with or without RV dysfunction (area under the receiver operating characteristic curve, 0.78; 95% CI, 0.64–0.92). A BNP >90 pg/mL was associated with a risk ratio of 28.4 (95% CI, 3.22–251.12) for the diagnosis of RV dysfunction. All patients without LV systolic dysfunction who had syncope necessitating cardiopulmonary resuscitation had normal BNP levels. Patients with RV dysfunction had significantly more in-hospital complications (cardiogenic shock, inotropic therapy, mechanical ventilation). However, BNP levels were not predictive of mortality or in-hospital complications.

Conclusions

BNP levels are frequently increased in patients with PE who have RV dysfunction, whereas patients without RV dysfunction show reference range BNP levels in the absence of left ventricular dysfunction. In acute PE, BNP elevation is highly predictive of RV dysfunction, but not of in-hospital complications and mortality.

Section snippets

Patients

We prospectively studied all patients with confirmed acute PE who were admitted to the intensive care unit of our department between September 2000 and May 2002. Patients examined later than 3 days after the onset of symptoms were excluded. The diagnosis of PE was confirmed with computed spiral tomography, pulmonary angiography, or high-probability lung perfusion scintigraphy.18 In the absence of preexisting chronic pulmonary disease, a combination of abnormal echocardiography results and

Patients

Fifty consecutive patients with acute PE were studied. The baseline clinical variables of the study population are displayed in Table I.

Ten patients (20%) were diagnosed as having massive PE, 21 patients (42%) with moderate to large PE and 19 patients (38%) with small PE. The principal symptoms were dyspnea (86%), chest pain (56%), and syncope (16%). Risk factors included major surgery within 2 weeks of diagnosis (20% of patients), history of prior deep vein thrombosis or thromboembolism

Discussion

In this study, we demonstrated that in acute PE: 1) pathological BNP levels are frequently found in patients with RV dysfunction, but not in patients without RV dysfunction; 2) BNP is discriminative for the detection of RV dysfunction; 3) BNP determination is not helpful in patients with LV systolic dysfunction; and 4) pathological BNP levels are not predictive of in-hospital complications and the mortality rate of PE.

References (33)

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