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N‐terminal pro-brain natriuretic peptide in patients with acute pulmonary embolism

Plasma brain natriuretic peptide (BNP), released from myocytes of ventricles upon stretch, has been reported to differentiate pulmonary from cardiac dyspnoea. Limited data have shown elevated plasma BNP levels in acute pulmonary embolism (APE), frequently accompanied by dyspnoea and right ventricular (RV) dysfunction. The aim of this study was to assess plasma N‐terminal proBNP (NT‐proBNP) in APE, and to establish whether it reflects the severity of RV overload and if it can be used to predict adverse clinical outcome. On admission, NT‐proBNP and echocardiography for RV overload were performed in 79 APE patients (29 males), aged 63±16 yrs. Plasma NT‐proBNP was elevated in 66 patients (83.5%) and was higher in patients with (median 4,650 pg·mL−1 (range 61–60,958)) than without RV strain (363 pg·mL−1 (16–16,329)). RV‐to-left ventricular ratio and inferior vena cava dimension correlated with NT‐proBNP. All 15 in-hospital deaths and 24 serious adverse events occurred in the group with elevated NT‐proBNP, while all 13 (16.5%) patients with normal values had an uncomplicated clinical course. Plasma NT‐proBNP predicted in-hospital mortality. Plasma N‐terminal pro-brain natriuretic peptide is elevated in the majority of cases of pulmonary embolism resulting in right ventricular overload. Plasma levels reflect the degree of right ventricular overload and may help to predict short-term outcome. Acute pulmonary embolism should be considered in the differential diagnosis of patients with dyspnoea and abnormal levels of brain natriuretic peptide.