Pulmonary embolism biomarkers

Resident Survival Guide

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]

Overview[edit | edit source]

Although the usefulness of brain natriuretic peptide (BNP) concentrations to diagnose pulmonary embolism (PE) is limited,^[1] elevated BNP and pro-BNP levels are associated with right ventricular dysfunction and increased mortality, and are therefore useful prognostic markers.^[2] The evaluation of troponin concentration also serves as a useful prognostic marker to identify myocardial necrosis^[3][4] and mortality associated with acute PE.^[5]

Biomarkers[edit | edit source]

Brain Natriuretic Peptide (BNP)[edit | edit source]

• BNP levels can be elevated among patients with PE.^[6] However, the routine assessment of BNP levels to diagnose PE is not indicated as it is non-specific and has reduced sensitivity secondary to the presence of other etiologies which falsely elevate BNP levels in acute case scenarios.^[1]

• In 2006 Sohne et al, demonstrated that the presence of elevated BNP levels at admission were associated with early fatal venous thromboembolism in hemodynamically stable patients with acute PE. This relationship appeared to be clinically insignificant when used as a guide to initiate early thrombolysis in this population.^[1]

• BNP and pro-BNP levels are beneficial as a prognostic marker;^[2] in fact, elevated BNP levels is associated with right ventricular dysfunction and associated mortality in the setting of a PE.^[7][8][9] The presence of right ventricular dysfunction is one of the criteria used to classify a PE as submassive or intermediate risk.^[10][11]

• The following values are considered a marker of right ventricular dysfunction:^[10][11]
  • BNP > 90 pg/mL
  • N-terminal pro-BNP >500 pg/mL

Troponin[edit | edit source]

• Measurement of troponin subtype levels, particularly troponin I and troponin T, may be of value in patients presenting with undifferentiated chest pain and/or dyspnea.^[12]

• Serum troponin concentrations can be elevated in patients with an acute PE, however its use in diagnosing a PE is very limited. The role of troponin in PE is to risk stratify patients and to optimize management strategies. In fact, elevated troponins are a marker of myocardial necrosis, one of the criteria used to classify PE into submassive or intermediate risk. Myocardial necrosis in PE is defined as the presence of:^[10][11]
  • Elevation of troponin I (>0.4 ng/mL), OR
  • Elevation of troponin T (>0.1 ng/mL)

• Troponins are also a prognostic marker of right ventricular dysfunction in patients with a confirmed PE.^[13][14][15] Troponin I specifically may be assessed to identify patients with right ventricular dysfunction who have a significant amount of segmental defects on V/Q scan.^[3][4][3]

• When compared to patients with myocardial infarction (MI), the variation in troponin concentration among patients with acute PE follow a different pattern.^[16] A study on 9 patients with elevated troponins revealed that elevation in troponins has a lower peak levels and remains detectable for a shorter period of time compared to that in acute MI.^[16]

References[edit | edit source]

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