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.