The term ischemia denotes an inadequate blood supply to tissues due to blockage of arterial inflow, while reperfusion injury is defined as damage caused by the return of blood flow after an ischemic period, leading to the death of cells that had been damaged only reversibly upon return of blood flow. [63]. The final infarct size after an MI event is therefore the result of ischemic and reperfusion injury. For this reason, the term that best describes this process of myocyte death in reperfused MI is myocardial ischemia/reperfusion (I/R) injury [64]. In the first hours following myocardial ischemia, damaged cardiac cells can release several molecules, including adenosine, opioids and bradykinin, which activate G protein signaling pathways thereby promoting myocardial survival. While in the late phase, myocardial ischemia induces an upregulation of growth factors and cytokines, including VEGF, ILGF, and SDF-1, in the damaged myocardium, thus promoting a cardioprotective state. The liver also participates in cardioprotection through the regulation and release of secretory proteins, including FGF21 and TFF3, which also promote cardiomyocyte survival. [65]. Seminal studies conducted approximately three decades ago with animal models demonstrated that early reperfusion was able to limit infarct size [66]. Thus fibrinolysis was indisputably associated with decreased mortality in STEMI patients [67].A decade later; primary angioplasty has been shown to be more superior than fibrinolysis [68]. Currently, primary coronary angioplasty (PCI) has been established as the basic treatment for patients with STEMI. The period between the onset of myocardial infarction symptoms (representative of the time of coronary occlusion) and reperfusion...... half of the article...... the need for duplicate revascularization compared to angioplasty with balloon [75]. Both pre- and postconditioning appear to protect cardiomyocytes at the time of reperfusion therapy. Ischemic post-conditioning is a chain of repetitive interruptions of coronary blood flow administered after a period of ischemia. Inhibition of ONOO-induced nitro-oxidative stress could play a critical role in postconmediate cardioprotection [76]. Iliodromitis et al also reported that postcon-mediated cardioprotection was in cohorts with reduced nitro-oxidative stress in vivo. The recognition that iNOS activation in cardiac myocytes might be beneficial, and that nitrate/NO might have both beneficial and detrimental effects, led to the selection of the 1400 W iNOS inhibitor dose to significantly inhibit, but not limit, l Increased activity level of iNOS in the myocardium after MI [77]