The potential of new and old biomarkers for risk stratification in pulmonary embolism

Pulmonary embolism (PE) is a common cardiovascular emergency that has a non-specific clinical presentation and is difficult to diagnose. Its severity must be promptly assessed by stratifying the risk of in-hospital and short-term (30-day) mortality on an individual basis using risk markers. Rapid and accurate risk stratification in PE has tended to focus on thrombus size and location, as well as its effects on systemic blood pressure and heart rate, and evidence of right ventricular (RV) dilatation and/or dysfunction on imaging studies. However, PE induces a wide range of biochemical changes, including the release of neurohormonal factors such as serotonin, which may partly explain increased pulmonary artery pressures. The same cardiac biomarkers used to assess myocardial necrosis in acute coronary syndromes can be useful for risk stratification of patients with PE. Measurement of serum troponins is included in the stratification algorithm to quantify RV micronecrosis and microinfarction.1 Assessment of brain natriuretic peptide (BNP) or its N-terminal fraction (NTproBNP) levels may also be important to quantify acute RV overload, although clinical decisions based on these results have yet to be standardized.2,3 Obviously, no biomarker can be used without taking account of the clinical context. While the cost of assessing biomarkers may not be great, we cannot allow ourselves the luxury of using them indiscriminately if we want to