Detection of a rise and/or fall of cardiac troponin (cTn) is the cornerstone in the diagnosis of myocardial infarction (MI). For the acute risk, it is hypothesized that cTn mirrors activated coagulation and platelet reactivity and indicates the presence of a ruptured plaque, which may help to identify patients at high risk who benefit particularly from aggressive pharmacological treatment and early invasive strategy. High-sensitivity assays using the 99th percentile as the threshold for positivity can achieve sensitivity at presentation of 90 % or more, and performance further improves with subsequent measurements within 3 to 6 h. By 3 h, negative predictive values of almost 100 % have been reported. However, use of assays with higher sensitivity lead ultimately to a loss of clinical specificity. Thus, other conditions than MI, such as stroke, pulmonary embolism, sepsis, acute perimyocarditis, Takotsubo, acute heart failure and tachycardia also can go with elevated troponin levels. The detection of brief rise and subsequent fall of troponin concentration in marathon runners, and even in healthy subjects, after a standardized exercise test has cast doubts on the hypothesis that troponin is released only upon irreversible damage. This kind of troponin leakage may originate from a cytosolic compartment of the cells and not from the necrosis of thin filaments.