## 1 Introduction
When measured six to twelve hours after the onset of chest pain, troponin tests were found to have nearly 100% sensitivity and a considerably better specificity for cardiac muscle injury than earlier biomarkers [4]. Over the following four to ten days, the troponin level will return to normal, assuming no new cardiac injury occurs in the interim, but it can occasionally take as long as a few weeks for cardiac troponin levels to drop to baseline [9; 10]. Troponin T is found in a 3-unit complex of the contractile apparatus in myofibrils, and there is also a cytosolic pool of unbound troponin that is released acutely, mimicking the appearance kinetics of other cytosolic proteins. This pool represents about 6% of cTnT, which explains the late but not early release of troponin. The increased overall amount of troponin in the heart is not why troponin is more sensitive than other proteins. The increased early sensitivity likely reflects the fact that the percentage of troponin released that reaches the blood after cardiac injury is greater for troponin than for other proteins. The unique release kinetics and the presence of a cytosolic pool of unbound cTnT may contribute to the observed pattern of cTnT concentration, characterized by an initial drop, a plateau, and then another drop [12]. Both cTnI and cTnT have a short half-life in plasma, lasting around two hours. The apparent half-life is 24 h, with cTnT being slightly longer, due to the ongoing release of troponin from the necrotic myocardium [13]. Troponins have been measured using a variety of methods over time, each with unique benefits in terms of sensitivity and specificity. The clinical situation and the ideal balance between sensitivity and specificity--both necessary for a correct diagnosis--often influence the assay selection. Antibodies used in immunoassays can detect very low troponin concentrations with great sensitivity and specificity. Chemiluminescence detection is the most common choice and together with automated analysis provides quick results. Point-of-care testing (POCT), which offers rapid diagnostic results close to patient treatment sites, can have variable sensitivity and specificity and are less frequently used. The most recent international guidelines [14] suggest that high-sensitivity techniques should be used for measuring cardiac cTnI and cTnT in order to detect myocardial damage and differentiate between acute coronary syndromes. Acute myocardial infarction diagnosis requires the presence of myocardial damage, which is a separate condition. The 2018 Fourth Universal Definition of Myocardial Infarction states that myocardial injury is detected when at least one value above the 99 th percentile upper reference limit is measured in a patient with high-sensitivity methods for cTnI or cTnT [15; 16]. However, the primary justification for utilizing the 99 th percentile upper reference limit is the current deficiency in standardization and harmony among the many cardiac troponin assays. This means that a single numerical cut-off cannot be used as a physiological threshold for myocardial injury [17; 18]. With the development of troponin assays, the 99 th percentiles of the assays became ever lower, and the sensitivity became ever higher. In addition to providing a CV \(\leq\) 10% at the 99 th percentile, the most recent generation of high-sensitivity assays can now measure troponin concentrations above the level of detection in more than 50% of the healthy population. Additionally, gender-specific 99 th percentiles have been set with the value for females usually lower than for males. The levels of cTnI and cTnT can provide valuable insights into different types of myocardial infarction. ST-elevation myocardial infarction (STEMI) causes a larger blockage of one or more coronary arteries, leading to a complete deprivation of blood to the heart. On the other hand, non-ST-elevation myocardial infarction (NSTEMI) causes only partial or incomplete blockage of a coronary artery.