Risk stratification of pulmonary embolism: clinical evaluation, biomarkers or both?

The concept of risk-stratification is one of the cornerstones of the recent guidelines on pulmonary embolism (PE), which were issued by the European Society of Cardiology (ESC) and endorsed by the European Respiratory Society [1]. According to these guidelines, patients with PE are divided in three groups with increasing risk of death or adverse outcome following a three-step process that is based on clinical data, assessment of anatomical right ventricular dysfunction on echocardiography or spiral computed tomography (CT), and of myocardial injury by dosage of cardiac biomarkers [1]. The first step is based on the measurement of blood pressure to determine whether cardiogenic shock is present, or not. For the vast majority of patients with acute PE who present with normal blood pressure, the second step consists of a simple clinical evaluation, summarised in the Pulmonary Embolism Severity Index (PESI) or its simplified version (sPESI) [2, 3]. These scores are able to select low-risk patients, defined as PESI class I or II or sPESI=0 who have a mortality risk <3% at 1 month. Cohort studies and one randomised clinical trial have confirmed that low-risk patients can safely be treated at home [4, 5]. Implementing PESI enables the identification of ∼45% of patients with acute PE as low-risk patients and reduces the length of hospitalisation without significantly increasing the risk of death, recurrent PE or major bleeding [4, 6]. Patients with normal blood pressure, but higher values of PESI or sPESI, have a mortality risk of ∼5–7% and should be treated at hospital according to ESC guidelines [1, 7, 8]. The goal of further risk stratification is to select the patients with the highest risk of an adverse event among those with normal blood pressure. This can be done by the combination of cardiac biomarkers dosing and/or the search for right ventricular dysfunction (RVD) by echocardiography or spiral CT. Several cohort studies strongly suggest that clinical variables, RVD and biomarkers have independent and complementary prognostic values in normotensive patients with acute PE [8–10].