## 1 Introduction  
Diagnosing cardiac emergencies is one of the most crucial tasks in the emergency department. It is imperative to expeditiously and precisely narrow down the wide differential diagnosis of chest discomfort in order to administer the necessary life-saving treatments to patients [1]. To distinguish between the various causes of chest discomfort, a number of crucial diagnostic instruments are employed in addition to the history and physical examination [2]. Troponins are regulatory proteins in muscle tissue and their measurement is a tool that is now crucial to cardiac workups and diagnosis [3]. Troponins are located in the cytosol of the myocyte as a small free pool as well as structural proteins [4]. There are three different molecular forms of troponin that are associated with different isotypes that are present in heart tissue, slow-twitch skeletal muscle, and fast-twitch skeletal muscle [5]. The cardiac isotype exhibits about 40% sequence heterogeneity with respect to the skeletal isotypes and has an additional 31 residues at the amino terminus [6]  
Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are crucial protein molecules involved in muscle contraction, particularly in the regulation of cardiac and skeletal muscles. However, there are several key differences between the two: cTnI has not been identified outside the myocardium, indicating its specificity to the heart muscle. On the other hand,cTnT is expressed to a small extent in skeletal muscle, but the current cTnT assays do not detect skeletal troponins [7]. There are also some differences in function: cTnI binds to actin in thin microfilaments to hold the troponin-tropomyosin complex, and it inhibits ATPase activity of actomyosin. Meanwhile, cTnT binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex, and it regulates the interaction of the troponin complex with thin filaments. Since cardiac troponin is not a constitutive blood protein, healthy subjects without heart injury will have extremely low blood levels of this protein. Therefore, the clinical interest in cardiac troponin levels is limited to elevated levels, unlike many other blood indicators that can demonstrate both unusually low and high levels. The clinical significance of cTnI and cTnT levels lies in their ability to indicate heart muscle damage, particularly as a result of a myocardial infarction or other heart-related problems. These proteins, which are specific to the heart, are normally found inside cardiac muscle cells. However, when cardiac muscle damage occurs, such as during a myocardial infarction, these proteins leak into the bloodstream. Therefore, higher levels of cTnI or cTnT in the blood indicate more severe heart damage. Additionally, troponin levels can be used to estimate the extent of heart damage. The more damage there is to the heart, the greater the amount of cTnI and cTnT there will be in the blood. A multicenter study involving 2226 patients reported that both troponins, despite differences in biochemical characteristics and release kinetics, have high diagnostic accuracy for acute myocardial infarction [8]. Cardiac troponins are released into the circulation as a consequence of an acute cardiac shock and a brief period of local ischemia. Patients usually experience a dull discomfort in their arms or chest within the first several hours following the trauma. Usually, between two and three hours after the onset of chest discomfort, troponin levels in the blood begin to rise. The levels will continue to rise until a peak is reached, generally between 12 and 48 h [9]. However, the peak can appear anywhere between 6 h and 3 days, depending on the kind of myocardial infarction [10]. Blood levels of cTnI often rise much higher than that of cTnT in myocardial infarction, whereas cTnT is often higher in patients with stable conditions such as atrial fibrillation [11].