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(Circulation. 2005;112:1520-1521.)
© 2005 American Heart Association, Inc.

Editorial

Risk Stratification in Pulmonary Embolism Based on Biomarkers and Echocardiography

Evangelos Giannitsis, MD, FESC; Hugo A. Katus, MD, FESC

From Abteilung Innere Medizin III, Medizinische Klinik, Universitätsklinikum Heidelberg, Heidelberg, Germany.

Correspondence to Evangelos Giannitsis, Abteilung Innere Medizin III, Medizinische Klinik, Universitätsklinikum Heidelberg, 69120 Heidelberg, Germany. E-mail evangelos_giannitsis@med.uni-heidelberg.de

Key Words: Editorials • echocardiography • pulmonary heart disease • prognosis • risk factors

An extract of the first 250 words of the full text is provided, because this article has no 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 <2 to 3 days in most cases, whereas even in patients with small non–ST-segment–elevation acute myocardial infarction (NSTEMI) cardiac troponins remain elevated for >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 is a surrogate for irreversible cell necrosis, apparently does not often occur in patients who survive pulmonary embolism. Regardless of the exact pathomechanism, at present it is believed that cardiac troponins are being released as the consequence of myocardial damage resulting from the acute increase of . . . [Full Text of this Article]

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Circulation 2005 112: 1573-1579. [Abstract] [Full Text]

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