Macrophage Migration Inhibitory Factor Gene Polymorphism in Acute Coronary Syndrome.

Background Acute coronary syndrome (ACS) is a result of the interplay between genetic and environmental risk factors. A unique cytokine macrophage migration inhibitory factor (MIF), expressed by inflammatory cells, acts via a cluster of differentiation 74 (CD74) and a cluster of differentiation 44 (CD44) receptors, leading to the recruitment of mononuclear neutrophils and lymphocytes. This cascade results in exaggerated inflammation and atherosclerosis. MIF's distinctive characteristics and functions make it an essential target for achieving therapeutic atherosclerosis regression, setting it apart from other cytokines. Hence, this study aims to detect the MIF gene polymorphism in ACS patients and to assess the incidence of in-hospital major adverse cardiac events (MACE). Methodology This study was conducted in a tertiary care hospital. A total of 90 patients who had ACS were enrolled, of which 83 were included, and seven patients were excluded based on exclusion criteria (four cases of old myocardial infarction, two cases of valvular heart disease, and one case of dilated cardiomyopathy). After detailed clinical examination, laboratory evaluation, and genetic test, patients were divided into two groups based on MIF gene mutation. Five patients who had positive MIF gene mutation were termed as group A (n=5), and 78 patients with negative MIF gene mutation were termed as group B (n=78). The statistical analysis for the collected data was done using IBM SPSS Statistics for Windows, Version 20 (Released 2011; IBM Corp., Armonk, New York, USA). Results Out of the 83 patients in this study, the male gender was predominant; there were three male patients in group A (n=3; 60%) and 48 male patients in group B (n=48; 61.5%). The most common age group was between 60 and 69 years; two of five patients (n=2; 40%) in group A and 30 out of 78 patients (n=30; 38.4%) in group B belonged to this age group. The common symptom was chest pain present in five patients in group A (n=5; 100%) and 76 patients (n=76; 97.5%) in group B. A common risk factor in group A patients was tobacco chewing, seen in three patients (n=3; 60%), and group B smoking was the most common risk factor seen in 30 patients (n=30; 38.5%). The most common ECG finding in group A was ST-elevation myocardial infarction (STEMI), seen in three patients (n=3; 60%), and in group B, the commonest ECG finding was non-ST-elevation myocardial infarction (NSTEMI) seen in 23 patients (n=23; 29.5%). The most common MACE was heart failure seen in two patients in group A (n=2; 40%) and in 50 patients in group B (n=50; 64.1%), followed by arrhythmias seen in one patient in group A (n=1; 20%), and eight patients in group B (n=8; 10.3%). Conclusion This study demonstrated a significant positive association between MIF gene polymorphism and the occurrence of cardiovascular events like myocardial infarction, with a statistically significant p-value (p=0.001). This study showed the presence of the disease in young age groups and individuals without conventional risk factors, underscoring the importance of genetic studies. Genetic risk factors independently contribute to the pathophysiology of coronary artery disease; hence, understanding the mechanisms of these genes and incorporating genetic testing into standard clinical practice can help future research to develop therapeutic agents that can specifically target these genes.