Utility of Brain Natriuretic Peptide to Predict Right Ventricular Dysfunction and Clinical Outcome in Patients With Acute Pulmonary Embolism

To the Editor: We read the paper by Kucher et al,1 which demonstrated the association between high levels of pro-brain natriuretic peptide (BNP) and increased risk of adverse clinical outcome (death, resuscitation, mechanical ventilation, pressors, thrombolysis, catheter fragmentation, and surgical embolectomy) in patients with acute pulmonary embolism. The authors concluded that patients with acute pulmonary embolism and low pro-BNP levels have an uneventful course and good prognosis. We studied 50 patients with confirmed acute pulmonary embolism prospectively and followed them up for their inhospital course and complications.2 Echocardiography and BNP measurement were performed in all patients at admission. Thirtyone patients (62%) of our study population had right ventricular (RV) dysfunction (dilatation of the right ventricle with a diastolic diameter 30 mm, RV/left ventricular end-diastolic diameter ratio 1, or hypokinesis of the right ventricle). We found that patients without RV dysfunction had significantly lower BNP levels compared with patients with RV dysfunction. There was a significant correlation between RV end-diastolic diameter and BNP. In addition, BNP discriminated between patients with and those without RV dysfunction (area under the receiver operating characteristic, 0.78). A BNP 90 pg/mL was associated with a risk ratio of 28.4 for the diagnosis of RV dysfunction. However, all patients presenting with syncope necessitating cardiopulmonary resuscitation showed normal BNP levels. Thus, normal BNP levels do not exclude severe pulmonary embolism. This might be due to an insufficient time span for right ventricular BNP production and secretion as a consequence of sudden RV pressure overload resulting in syncope with cardiac arrest in these patients. All of the patients with syncope and normal BNP levels showed elevated troponin T levels, stressing the value of troponin T measurements in identifying patients with severe pulmonary embolism. Kucher et al1 mention that a possible limitation of their study lies in the absence of serial pro-BNP testing and thus in an underestimation of pro-BNP elevation given the possible transient nature of its release. Indeed, in our study, we found highly dynamic BNP release kinetics with rapidly falling BNP levels after initiation of therapy aimed at improving RV dysfunction, especially after thrombolysis. On the other hand, in patients admitted with subacute pulmonary embolism 2 days after onset of symptoms, we still found BNP levels significantly elevated. Overall, we found BNP levels not to be predictive for mortality or in-hospital complications. Patients with RV dysfunction as determined by echocardiography had significantly more in-hospital complications, confirming that echocardiography remains the bedside gold standard for the detection of RV dysfunction. Further studies in larger patient populations possibly comparing pro-BNP and BNP kinetics and their respective predictive values appear warranted.