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Cardiac Markers: A Chest Pain Center Focus

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Short Stay Management of Chest Pain

Part of the book series: Contemporary Cardiology ((CONCARD))

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Abstract

Use of cardiac biomarkers for care of patients presenting to the emergency department has a rich history beginning in the 1950s. Aspartate aminotransferase, lactate dehydrogenase isoenzymes, creatine kinase and its MB isoenzyme and myoglobin have all been utilized over the years. However a sentinel event occurred in the 1990s with the availability of assays for the myocardial specific biomarkers cardiac troponin T (cTnT) and cardiac troponin I (cTnI). Along with clinical features and the electrocardiogram, cTnI and cTnT measurements are now a cornerstone for early risk stratification, the diagnosis of myocardial infarction and clinical decision-making in the context of suspected acute coronary syndrome patients in the emergency department. Point-of-care measurements of cardiac troponin and other markers have been implemented at many institutions where the central laboratory is unable to provide results in one hour or less from the time of collection. Because cTnT and cTnI are believed to be released only upon myocardial necrosis, there has been substantial effort in identifying markers of myocardial ischemia that do not necessarily have irreversible cell death. Promising markers include ischemia modified albumin, C-reactive protein, myloperoxidase as well as B-type natriuretic peptide and its biologically inactive co-metabolite NT-proBNP. Also, attention has turned to measurement of very low troponin concentrations measured using assays that are able to measure troponin reliably at concentrations 10- to 100-fold lower than the best conventional troponin assays, with the idea of specifically detecting subtle cardiac injury associated with unstable angina. There are a number of clinical confounders for measurements including renal insufficiency, end stage renal disease, blunt chest trauma, pulmonary embolism, chemotherapy and recent cardiac procedures. Interpretation of cardiac marker results in these clinical circumstances can be complicated and the clinical course of the patient relative to temporal increase in biomarkers must be taken into account.

Few tests have the clinical value and impact of cTnT and cTnI, and it is unlikely that these tests will be replaced for the diagnosis of MI in the foreseeable future. For risk stratification and patient management, however, other markers of inflammation, heart dysfunction or the coagulation process may provide complementary information. Some of these novel markers may come from the proteomic, metabolomic and molecular diagnostic studies. However, it is critical to note that the real value of any new or existing markers will hinge on evidence that their utilization can be shown to improve clinical and/or economic outcomes.

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Christenson, R.H. (2009). Cardiac Markers: A Chest Pain Center Focus. In: Cannon, C., Peacock, W. (eds) Short Stay Management of Chest Pain. Contemporary Cardiology. Humana Press. https://doi.org/10.1007/978-1-60327-948-2_7

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