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Editorial |
1 Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia, PA.
aAddress correspondence to the author at: University of Pennsylvania School of Medicine, Rm. 608 BRB II/III, 421 Curie Blvd., Philadelphia, PA 19104.
| The first 20% of the full text of this article appears below. |
The search for new biomarkers of cardiovascular disease remains a large and growing enterprise. Biomarkers are used to identify the risk, presence, and/or severity of disease; to guide diagnostic and therapeutic interventions; and to provide clues to disease mechanisms and pathophysiological distinctions within clinically similar populations. Among cardiovascular biomarkers, those used for identifying the presence or severity of myocardial injury have the most extensive history. Beginning with the first report 55 years ago that circulating transaminases are increased in acute myocardial infarction (1), the search for new and better biomarkers of myocardial injury has continuously evolved. As recently reviewed (2), cardiac troponin has emerged after decades of clinical and laboratory investigation as a highly diagnostically sensitive and specific biomarker of myocardial injury, with a currently indispensable role in the accurate and timely diagnosis of patients with suspected acute coronary syndromes (ACSs).1 Central to this preeminence is the tissue specificity of cardiac troponin isoforms, increases in assay sensitivity, and an extensive body of evidence validating the diagnostic, prognostic, and therapy-guiding utility of cardiac troponins in diverse clinical settings. Because the benefits of ACS treatments are favorably influenced by the speed with which they are applied, the ideal myocardial injury biomarker must also permit rapid measurement; cardiac troponin assays have also proved satisfactory in this regard.
Despite the established strengths of cardiac troponins for prompt and reliable detection of myocardial injury, the ability to reliably detect ischemia in the absence of myocyte necrosis and the ability to distinguish alternative causes and mechanisms of myocyte damage (inflammation, oxidative stress, apoptosis) represent unmet needs and opportunities for new biomarkers, which have been highlighted in recent reviews (2)(3). Resistance to inaccuracy caused
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