Cardiac Biomarkers in Pulmonary Embolism: Revealing or Redundant?

Pulmonary embolism (PE) is common, with an incidence of 39–115 per 100 000 population. In 6 European countries (population 454.4 million) PE caused an estimated 370 000 deaths in 2004 (1). Thirty four percent died early, either before therapy could be initiated or before it could take effect. Among the 41% diagnosed pre-mortem, 15% deteriorated with hemodynamic collapse and 10% died suddenly (2, 3). Even among those given recommended therapy, 7%–8% died early (1). There is a need for improved risk stratification to guide any escalation beyond standard anticoagulant management to thrombolytic pharmacotherapy or trans-vascular/surgical thrombus disruption/removal. Matthews et al. assessed the value of cardiac biomarkers for risk stratification of initially stable patients with PE (4). Currently recommended assessment in acute PE comprises (a) risk stratification according to hemodynamic status, (b) a clinical score, (c) right heart imaging, and (d) circulating cardiac biomarkers (1). Recommended thresholds warranting upgrading of risk are based on values used in acute coronary syndromes for cardiac troponin (cTn) [e.g., 14 ng/L for high sensitivity (hs)-cTnT] and from observational cohorts for BNP/NT-proBNP (e.g., 500–600 ng/L for NT-proBNP) (5, 6). Guidelines reflect reports dating back 10 to 20 years with little recent refinement of optimal cardiac marker cut points.