Patients suffering from ST-segment elevation myocardial infarction (STEMI) continue to carry an elevated morbidity and mortality, despite advancements in percutaneous coronary intervention (PCI) technology and pharmacology . Post-infarct reperfusion injury likely contributes to this negative impact due to the development of a scar and creating a larger infarct size (IS). Post-infarct reperfusion injury is mediated by infiltration and activation of circulating inflammatory cell subsets (i.e., neutrophils) that enter the vulnerable area of myocardium and release proteases and reactive oxygen species . This pathophysiology is likely due to the neutrophil infiltration acting protectively, thus favoring a scar formation and potentially preventing negative left ventricle remodeling . Therapy targeting this inflammation cascade in theory could lead to a smaller infarct size and therefore better clinical outcomes, reducing the incidence of heart failure and malignant arrhythmias. That being said, previous studies have been mixed in regard to the administration of immunosuppressive drugs to treat this process .