## 4 Discussion  
Troponin tests have been developed over time with ever-lower 99 th percentiles and ever-increasing sensitivity. As a result, more recent troponin test generations are able to identify elevated levels sooner, which is linked to heightened sensitivity for myocardial damage and quicker ACS rule-in and rule-out times. The pattern of cTnT concentration, characterized by an initial drop, followed by a plateau, and then another drop [12] is different from cTnI. The reason for the difference may be attributed to the unique properties of cTnT and the kinetics of its release into the bloodstream. cTnT is partially present as an unbound form or cytosolic fraction that can be released quickly after cell damage [23], but the majority of cTnT (94%) is bound to the myofibrils and is released more slowly (especially in the case of irreversible injury). This is one of the hypotheses for the biphasic curve of cTnT and not cTnI. Alternatively, immune-reactive cTnT fragments with a prolonged half-life and lack of discernibility may be the cause of the biphasic curve's shape [24]. According to the current data, troponin tests function extremely similarly in clinical settings. Combining the two biochemical signals from cTnT and cTnI may overcome preanalytical, analytical, and pathophysiological differences between the biomarkers and enhance clinical decision-making, according to the Advantageous Predictors of Acute Coronary Syndromes Evaluation (APACE) study group's hypothesis. After eliminating patients with ST-segment elevation myocardial infarction, they enrolled 2256 patients with suspected AMI; of these, 18% had an adjudicated diagnosis of AMI. At admission, the entire cohort was assessed for cTnT (Roche Diagnostics, Mannheim, Germany) and cTnI (Abbott Laboratories, Abbott Park, IL, USA), and there was a r = 0.89 correlation between the two measures. When both assays were presented, the area under the curve (diagnostic accuracy) was 0.93 (95% confidence interval, 0.92-0.94) [25]. Preliminary data from the cross-sectional Maastricht study suggests that troponin assays might not be interchangeable in the general population. The association between the aforementioned methods for cTnI and cTnT was only r = 0.54 in 1540 middle-aged members of the general population who did not have a substantial baseline disease. Although this association is obviously significant in most biological contexts, it is far from being regarded as a stand-in for assays that are purportedly detecting the same biomarker [26]. The association between cTnI and cTnT assays is clearly dependent on population. In our study, the correlation was strong in the Type 2 group (r = 0.75) and in the NSTEMI group (r = 0.70) while no correlation was found in the control group (r = \(-\)0.06). Unfortunately, the STEMI group was too small for the calculation. Our study presents the elevation of two proteins, cTnI and cTnT, in different cardiac events. In the case of NSTEMI, which is characterized by partial blockage of the coronary artery, there is a moderate increase in the levels of both cTnI and cTnT. This is due to the damage inflicted on part of the heart muscle. On the other hand, STEMI is caused by a complete blockage of a coronary artery, leading to more extensive damage to the heart muscle. This results in a significant elevation of both cTnI and cTnT levels. Type 2 myocardial infarction, which occurs when the heart muscle demands more oxygen than the body can supply, can result in variable elevations of cTnI and cTnT. This type of event can occur in situations like severe illness, surgery, or severe emotional stress. The elevation of these proteins may not be as high as in STEMI or NSTEMI. The ratios of cTnI and cTnT relative to their cut-off values are lower in Type 2 myocardial infarction than in NSTEMI. This difference can be attributed to the nature of these two types of heart conditions. The most common cause of NSTEMI is a partial blockage of one or more coronary arteries, which provide the heart with blood.