The term ischemia refers to insufficient blood supply to tissues due to blockage of arterial inflow, while reperfusion injury is defined as damage caused by the restoration of blood flow after a period ischemic, leading to death. of cells that were only reversibly injured when blood flow was restored. [63]. The final infarct size after an MI event is therefore the result of ischemic and reperfusion damage. 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 after myocardial ischemia, injured cardiac cells can release several molecules, including adenosine, opioids, and bradykinin, which activate G protein signaling pathways, thereby promoting myocardial survival. At the late phase, myocardial ischemia induces upregulation of growth factors and cytokines, including VEGF, ILGF, and SDF-1, in the injured myocardium, thereby promoting a cardioprotective state. The liver also participates in cardioprotection through the upregulation and release of secretory proteins, including FGF21 and TFF3, which also promote cardiomyocyte survival. [65]. Fundamental studies carried out approximately thirty years ago in animal models demonstrated that early reperfusion was capable of limiting infarct size (66). Then, fibrinolysis was undoubtedly associated with a reduction in mortality in patients with STEMI [67]. A decade later; Primary angioplasty has been shown to be superior to fibrinolysis [68]. Currently, primary coronary angioplasty (PCI) has been established as the mainstay treatment for STEMI patients. The period from the onset of MI symptoms (representative of the time of coronary occlusion) and reperfusion...... middle of article ...... the need for revascularization in duplicate on balloon angioplasty [75]. Preconditioning and postconditioning appear to protect cardiomyocytes at the time of reperfusion treatment. Ischemic postconditioning 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 an essential role in post-preservation cardioprotection (76). Iliodromitis et al also reported that post-preservation cardioprotection existed in cohorts with reduced nitro-oxidative stress in vivo. Recognition that activation of iNOS in cardiac myocytes might be advantageous, and that nitrate/NO might have both beneficial and detrimental effects, led to the iNOS inhibitor dose of 1400 W to significantly inhibit, but not restrict, increased myocardial iNOS activity level. after MI [77]