## 4 Discussion
Increased troponin levels in the blood are not directly related to any of these diagnoses, but they can affect the heart and cause indirect effects that may affect troponin levels. In cellulitis, pneumonia, cholangitis, and exacerbations of COPD, troponin increases due to the systemic inflammatory response that follows. Inflammation can cause increased cardiac workload and stress on the heart muscle, which in turn can lead to increased troponin levels. Also, the lack of oxygen in the blood as a result of these conditions can put stress on the heart, which can affect its function and lead to increased troponin levels. In the large multicenter BASEL study in Switzerland, it was shown that measuring cardiac troponin levels is helpful in predicting death among patients presenting with pneumonia to the emergency room; cTnT was found to be superior for predicting prognosis [30],which is in contrast to our results, where cTnT was normal while cTnI was elevated in patients with this diagnosis. In patients with chronic kidney disease, cTnT was found to be more commonly elevated. These elevations are not necessarily associated with myocardial infarction. However, they may be a sign of heart problems or damage to the cardiac muscle, which may develop as a complication of kidney disease [31]. The authors of [PERSON]'s study concluded that while cTnI is more frequently raised as a result of coronary reasons, cTnT is more frequently linked to mortality that is not caused by coronary causes [21]. During an acute myocardial infarction, cTnI concentrations often rise to greater levels than cTnT concentrations. The molecular structures of cTnI and cTnT differ, which could have an impact on both their release and clearance from circulation. Compared to cTnT (37 kDa), cTnI has a lower molecular weight (35 kDa) and faster release kinetics. Higher amounts of cTnI relative to cTnT may be explained by this. All of the patients have increased cTnI, which raises the possibility of cardiac injury of some kind. Normal cTnT levels, however, may suggest that the injury is either relatively recent (since cTnT levels may not have had time to develop) or not severe enough to result in a noticeable increase in cTnT levels. Our study has some limitations. Because of the small number of patients in the STEMI subgroup, the statistical comparisons for this group were not performed. As this was a single-center study with no external validity, the applicability of the results to different populations or clinical settings would still have to be confirmed. Future research could include long-term follow-up, which might provide insights into the prognostic value of troponin measurements. The present analytical challenges could give an opportunity to alternative technologies [32], which include POCT with shorter turn-around times. Today, no single marker satisfies all of the requirements for being a perfect biomarker of myocardial infarction. Novel promising biomarkers, such as urine and salivary cardiac troponins, heart-type fatty acid binding protein, and miRNAs [33] could reduce the amount of time that passes between myocardial infarction and suggested treatment. The novel biomarkers have been the subject of relatively few clinical trials and have not yet been used in emergency departments.