Introduction
Coronary artery disease is a widespread cardiac disease that occurs by plaque formation on coronary artery wall. Coronary artery disease is the first and most important death reason in today’s societies. In addition, this disease leads to disability and high morbidity. What conventionally was called a heart attack, is more precisely called acute coronary syndrome nowadays. Patients who go to the emergency room with acute coronary syndromes (ACS) will divided into Two groups include ST-segment elevation myocardial infarction (STEMI) and coronary syndromes without ST-segment elevation (NSTE ACS) (1,2).
Despite the decrease in mortality rate due to STEMI in recent years, this disease still remains a common clinical and challenging condition with high mortality risk. Each year, approximately 258,000 patients in the United States present to the emergency department with a diagnosis of STEMI, with an incidence of 7.3 per 10,000 (3).
STEMI is usually caused by a rupture or erosion in the atherosclerotic plaque, followed by platelet aggregation and thrombosis which ultimately leads to acute coronary artery occlusion and myocardial damage and therefore requires emergency treatment. The preferred treatment strategy includes emergency reperfusion through primary percutaneous coronary intervention (PPCI). Reperfusion of coronary blood flow as soon as possible after acute ST-segment elevation myocardial infarction improves disease outcomes (4).
Of course, despite reperfusion of blood flow in the coronary arteries that caused the infarct, there is myocardial perfusion disorder in some patients who have undergone successful PCI, which is associated with a larger infarct size and an increase in long-term cardiac mortality (4,5). One of the main causes of myocardial reperfusion disorder is the embolization of thrombotic substances including platelet aggregations in the distal microcirculation. Widespread use of PCI may also create a thrombotic condition due to wounding the vessel wall and stimulate platelet activation and proliferation of new intima (6).
The first step to initiate arterial thrombosis is endothelial damage and exposure of subendothelial matrix glycoprotein (GP) to circulating platelets, followed by platelet adhesion (7). GP IIb/IIIa are the most abundant integrins on the surface of platelets, which turn into a ligand-accepting form after the activation of platelets. Ligands such as fibrinogen bind to GP IIb/IIIa of adjacent platelets and lead to platelet aggregation and thrombus formation. (8)
In recent years, the implementation of adjunctive mechanical and pharmacological therapies during PPCI has significantly improved clinical outcomes in STEMI patients. Among these treatments, aspirin and P2Y12 inhibitors can be mentioned, which play an essential role in the medical treatment of STEMI patients (9, 10).
Among other treatments, thrombus aspiration and the use of GP IIb/IIIa inhibitors can be mentioned, which have significantly reduced the incidence of distal embolization and improved reperfusion of capillary blood flow and clinical outcomes in STEMI patients. However, this approach may also have disadvantages, meaning that any effective antiplatelet regimen may be associated with an increased risk of bleeding, and often discontinuation of long-term therapy potentially worsens outcomes (11-14).
Three intravenous drugs of GP IIb/IIIa inhibitors namely Abciximab, Eptifibatide and Tirofiban are widely used in PCI and in the treatment of ACS. Eptifibatide is a peptide containing the amino acid sequence of arginine, glycine and aspartate with a half-life of 2.7 hours, which binds to GP IIb/IIIa receptors and prevents the binding of fibrinogen to receptor and causes an anti-platelet effect. On the other hand, inhibition of GP IIb/IIIa reduces the activation of prothrombin replication factors. Therefore, inhibition of GP IIb/IIIa may have both antiplatelet and anticoagulant effects (7,8,15,16). The dose used in the treatment of STEMI is intravenous bolus dose of 180µg/kg and infusion of 2µg/kg/min for a maximum time of 18 hours (9).
According to European and American guidelines, intravenous injection of GP IIb/IIIa inhibitors in patients with STEMI who underwent PPCI and have evidence of high thrombosis or no-reflow phenomenon seems reasonable (Class: IIa, LoE: C) (9,10). However, so far few studies (Low Level of Evidence) have investigated the effect of maintenance dose of Eptifibatide in STEMI patients who underwent PPCI. Therefore, in this study, we investigated the effect of maintenance dose of Eptifibatide in patients with STEMI who underwent PPCI.