Tumor Necrosis Factor-alpha (TNF-α) is a key player in systemic inflammation and plays a pivotal role in the pathophysiology of myocardial infarction (MI) . When TNF-α is released by activated macrophages, monocytes, and other cells at the site of injury, it triggers inflammation and exacerbates myocardial damage . High levels of TNF-α can induce apoptosis in cardiomyocytes and are also involved in the post-MI remodeling process of the heart, often leading to heart failure . Additionally, TNF-α contributes to endothelial dysfunction, impairing vasodilation and promoting thrombosis . As a result, TNF-α can be used as a biomarker for diagnosing and predicting MI . Elevated blood levels of TNF-α signify a continuous inflammatory process, but elevated levels following myocardial infarction are linked to unfavorable consequences .