Abstract
The definition of myocardial infarction was updated in 2000 to include an elevation of cardiac troponin T or I (cTnT or xTnI) alongside clinical evidence of myocardial infarction. The redefinition was jointly done by the American College of Cardiology Committee and the European Society of Cardiology. Since then, cardiac troponin T and I have assumed the position as the primary biochemical markers for diagnosing myocardial infarction. The high sensitivity of cardiac troponin for myocardial necrosis influenced the decision to include cardiac troponins (cTn) in the diagnostic pathway. An elevated cTn level indicates the presence of myocardial injury. However, it does not give the underlying reason for the damage. Apart from acute myocardial infarction (AMI), a range of potential diseases feature troponin release, including heart failure, acute pulmonary embolism, end-stage renal disease, and myocarditis. However, regardless of the mechanism that triggers the release from cardiac myocytes, elevated cTnI and cTnT typically implies a poor prognosis. This review attempts to explain both the cardiac and non-cardiac causes of increased cTnT in emergency department patients.