Why the study?
Cardiomyocyte injury can elevate serum cTnT and cTnI in conditions other than AMI, making knowledge of non-infarct causes essential to avoid diagnostic errors and guide patient management.
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Design
Review article
Non-ischemic troponin elevations warrant differential consideration to reduce misdiagnosis; review extends mechanistic synthesis but leaves prospective validation open.
The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI) (ischemic necrosis of cardiac myocytes). Any type of reversible or irreversible cardiomyocyte injury can result in elevated serum cTnT and cTnI levels. Researchers and practitioners involved in the diagnosis and treatment of cardiovascular disease, including AMI, should know the key causes and mechanisms of elevated serum cTnT and cTnI levels. This will allow to reduce or completely avoid diagnostic errors and help to choose the most correct tactics for further patient management. The purpose of this article is to discuss the main causes and mechanisms of increase in cardiac troponins concentrations in frequently occurring physiological (physical exertion, psycho-emotional stress) and pathological conditions (inflammatory heart disease, pulmonary embolism, chronic renal failure and sepsis (systemic inflammatory response)) not related to myocardial infarction. Keywords: diagnostics, differential diagnosis, causes of increased concentration, mechanisms of increase, cardiac troponins, troponin T, troponin I, acute myocardial infarction, physical activity, psycho-emotional stress, myocarditis, endocarditis, pericarditis, sepsis, pulmonary embolism, chronic renal failure Corrigendum for this paper has been published
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Aleksey Chauin (2021) studied this question.
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