Risk Stratification in Pulmonary Embolism Based on Biomarkers and Echocardiography

Abstract

Since the initial observation that elevated cardiac troponin T levels are closely associated with mortality in acute pulmonary embolism,1 several reports have confirmed the prognostic role of cardiac troponins in this setting.2,3 More recently, yet another group of biomarkers, the natriuretic peptides B-type natriuretic peptide (BNP) and N-terminal-pro-B-type natriuretic peptide (NT-proBNP), emerged to confer additional prognostic information.4–7 See p 1573 The role of cardiac troponins as indicators of irreversible cell injury is well established.8 Although in myocardial infarction circulating troponins result from continuous degradation of the contractile machinery of irreversibly injured cardiomyocytes, the reason for elevated blood levels in pulmonary embolism is less well defined. In pulmonary embolism the time period of marker elevation is 7 days despite the short half-life of cardiac troponin T of 90 minutes.8 It is highly likely that in pulmonary embolism most of the detectable troponin in circulation corresponds to the unbound cytosolic fraction, which may egress rapidly after membrane damage from injured cells. Because prolonged elevation of troponins in blood is not commonly found in pulmonary embolism, irreversible degradation of the sarcomeric protein complex, which …