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

Abstract

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 Ͼ30 mm, RV/left ventricular end-diastolic diameter ratio Ͼ1, 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 Ͼ90 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 al 1 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 Ͼ2 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.

Prospective Study of the Clinical Features and Outcomes of Emergency Department Patients with Delayed Diagnosis of Pulmonary Embolism

“…The data show that patients with a delayed diagnosis had hemodynamically significant PE. As part of the protocol, we measured multiple biomarkers and imaging parameters associated with worsened outcome for every patient in all three groups (e.g., elevated troponin level and D-dimer, abnormal echocardiogram, higher electrocardiogram score, lower pulse oximetry, and distribution of intrapulmonary clots) 14,[16][17][18][19][20][21][22][23][24][25][26][27][29][30][31] Taken together, the data in Table 4 and Figure 2 suggest that patients with a delayed diagnosis had PE of at least equal severity to patients with ED-diagnosed PE. Patients with a delayed diagnosis of PE had a higher in-hospital adverse outcome rate compared with the other groups.…”

“…15 We also compared between groups the frequency of measurements associated with worsened PE severity: an elevated troponin measurement, an abnormal RV observed on echocardiography, RV strain indicated by the Daniel electrocardiogram score >8, abnormal systolic function of the left ventricle (ejection fraction >45%), a D-dimer concentration >8.0 mg/mL, and the percentage occlusion and distribution of intrapulmonary clots. 14,[16][17][18][19][20][21][22][23][24][25][26][27][28][29]…”

Clinical Characteristics, Management, and Outcomes of Patients Diagnosed With Acute Pulmonary Embolism in the Emergency Department

“…Cause of death was adjudicated by the primary investigator at each participating center, based upon available medical records. All clinical data, including protocols for performing diagnostic imaging studies and the tests used to risk-stratify PE (including troponins, natriuretic peptides, and echocardiography), were evaluated using local standards (11)(12)(13). A Pulmonary Embolism Severity Index (PESI) score was calculated for all patients for whom sufficient data was available.…”

Cardiothoracic CT: one-stop-shop procedure? Impact on the management of acute pulmonary embolism

“…There is increasing evidence that the BNP and NT-proBNP levels are directly related to the severity of RVD [16, 17]. In a systematic review, Sanchez et al found a relative risk for predicting 30-day mortality of 9.5 for BNP and 5.7 for pro-BNP in patients with proven PE [18].…”