## 1 Introduction
STEMI is considered a more serious event than NSTEMI due to the larger blockage and the resulting impact on the heart's blood supply. This results in more long-term heart health problems and increases the risk of death in the short term. The severity of myocardial injury in STEM is typically more extensive due to the complete blockage of a coronary artery. In STEMI, both cTnI and cTnT levels are typically elevated at presentation and are associated with a worse prognosis in terms of both short-term and long-term mortality. Higher troponin values generally correlate with a larger infarct, providing an estimate of the infarct size and the severity of myocardial damage. In NSTEMI, elevated levels of cTnI and cTnT at presentation are also associated with a worse prognosis in terms of both short-term and long-term mortality. Peak troponin values can provide an estimate of the infarct size and the severity of myocardial damage, with higher values generally correlating with a larger infarct. In Type 2 myocardial infarction, an elevated troponin in the first blood sample is expected in patients with renal failure. A rising concentration of troponin indicates acute injury and may be due to an acute myocardial infarction. It is crucial to classify the etiology of a troponin elevation and treat patients accordingly [19]. Particularly in the current era of high-sensitivity troponin tests, the number of situations known to cause myocardial injury by pathways other than myocardial ischemia is increasing [20]. Elevated troponin levels can be indicative of heart damage, but they are not specific to myocardial infarction. Other conditions, such as congestive heart failure, abnormally fast heartbeat, and kidney disease, can also cause elevated troponin levels, leading to potential misinterpretation. Elevated troponin levels can also result from conditions such as acute coronary syndrome, acute myocarditis, and infiltrative diseases like amyloidosis. Additionally, medications, toxins, transplant vasculopathy, and critical illness can also lead to elevated troponin levels. Acute ventricular wall stretch or strain is typically the cause of acute (or chronic) systolic or diastolic heart failure. Troponin trajectories are typically more indolent, with milder troponin increases. Myocardial inflammation directly causes pericarditis and myocarditis. Cardiopulmonary resuscitation is another possibility, where the heart injury can be caused by electrical shocks from an external defibrillator or by mechanical chest compressions. Stress-induced release of neurohormonal hormonesand catecholamines also results in myocyte damage and temporary dilation of the ventricle, which is known as stress-induced cardiomyopathy. Acute pulmonary embolism is not from cardiac ischemia, but rather from an acute stretch or strain of the right ventricle. Renal failure due to chronic kidney disease or severe renal injury is at least somewhat associated with decreased troponin clearance from the kidneys. Both cTnI and cTnT were associated with adverse classical cardiovascular disease (CVD) risk factors. The Spearman correlation coefficient between cTnT and cTnI was found to be 0.443 (\(p<0.001\)) [21]. Previous cohort studies have examined either cTnI or cTnT but rarely both of them, most likely due to the assumption that assays can be interchanged in diagnosis of an acute cardiac event. This has resulted in an evidence base that does not directly show which biomarker is actually better. A meta-analysis, which included 13 studies that measured cTnI and 7 studies that measured cTnI--none of which measured both--reflects this. The risk of future CVD events was greater for cTnT than cTnI in the top versus bottom third of the distribution (hazard ratio = 1.60 versus 1.36; \(p=0.171\)), and cTnT was more significantly related to fatal CVD (\(p=0.027\)) [22]. The aim of our study was to determine cTnI and cTnT in patients admitted to the emergency department with chest pain and to correlate the results of the two troponins.