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Troponins as biomarkers of cardiac injury

Allan S Jaffe, MD
David A Morrow, MD, MPH
Section Editor
Juan Carlos Kaski, DSc, MD, DM (Hons), FRCP, FESC, FACC, FAHA
Deputy Editor
Gordon M Saperia, MD, FACC


Cardiac injury occurs when there is disruption of normal cardiac myocyte membrane integrity. This results in the loss into the extracellular space (including blood) of intracellular constituents including detectable levels of a variety of biologically active cytosolic and structural proteins, referred to as biomarkers, such as troponin, creatine kinase, myoglobin, heart-type fatty acid binding protein, and lactate dehydrogenase. Injury is usually considered irreversible (cell death), but definitive proof that cell death is an inevitable consequence of the process is not available. (See 'Ischemia and troponin elevation' below.)

When a sufficient number of myocytes have died (myocyte necrosis) or lost function, acute clinical disease is apparent. Ischemia, with or without infarction, consequent to an imbalance between the supply and demand of oxygen (and nutrients) is the most common cause of cardiac injury. Other causes include trauma, toxins, and viral infection.

The biochemical characteristics and utility of troponins, the diagnosis of cardiac injury, and acute myocardial infarction (MI) in particular will be reviewed here. The other biomarkers of cardiac injury and disease states, other than an acute MI, in which elevation of biomarkers are seen are discussed separately. (See "Biomarkers of cardiac injury other than troponin" and "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)


There is considerable debate about whether troponin is released with reversible as well as irreversible ischemia. If this phenomenon occurs, it should be seen with all cardiac biomarkers, and it would not be possible biochemically to distinguish reversible from irreversible injury [1].

Those in favor of the hypothesis that cardiac biomarker elevations occur with reversible injury suggest that the minor elevations seen after triathlons and/or marathons in some individuals and with severe pulmonary embolism reflect reversible injury since they tend to be transient and do not have the persistence seen with an acute myocardial infarction [2-4]. The development of more highly sensitive assays may allow for a better evaluation of this issue in the future since increases from normal values may persist but not be detected without highly sensitive assays. (See "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome", section on 'Myocardial strain'.)


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Literature review current through: Sep 2016. | This topic last updated: Oct 14, 2015.
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