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• W199423752 abstract "The use of highly sensitive and very specific measurements of cardiac troponin I and troponin T has revolutionized the detection of cardiac injury. Although the most common use of these tests is the diagnosis of acute myocardial infarction, it has become clear that there are a large number of other disease entities capable of causing troponin release. The process of supply/demand imbalance is a part of many of these other pathophysiologies and, therefore, could, in one sense, be considered ischemia. This suggests that the cardiac myocyte is sensitive to a variety of pathological stresses on the cardiopulmonary system. It is feasible that these stresses are reflected in the posttranslational degradation and disease-specific processing of the troponins within the myocyte prior to release into the blood. To further facilitate and improve the diagnostic yield of the cardiac troponins, one can increase the sensitivity of the assays to allow for detection of still lower levels. Another possibility is to determine whether or not there is the potential to detect specific cardiac troponin fragments, with the idea that they might be more specific for the certain types of cardiac injury and thus specific disease processes. This chapter discusses potential disease-related degradation; why there might be different fragments for different pathological processes; and, finally, the potential clinical use in monitoring these modifications. The attempt to distinguish disease entities based on fragment analysis has the potential to further advance the field by allowing more specific diagnoses." @default.
• W199423752 created "2016-06-24" @default.
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• W199423752 date "2006-01-01" @default.
• W199423752 modified "2023-09-26" @default.
• W199423752 title "Degradation of Cardiac Troponins" @default.
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• W199423752 doi "https://doi.org/10.1007/978-1-59745-051-5_11" @default.
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