Use of antiplatelet therapies during primary percutaneous coronary intervention for acute myocardial infarction

Rupture of the vulnerable atherosclerotic plaque in the coronary artery wall leading to activation and aggregation of platelets to form an artery occluding thrombus is the most frequent cause of acute myocardial infarction (AMI) [1–3]. Cessation of blood flow in the infarct-related artery (IRA) launches the processes of irreversible myocardial injury, which can be stopped by prompt opening of the occluded artery. Primary percutaneous coronary intervention (PCI) defined as stented angioplasty without prior or concomitant fibrinolytic therapy is a preferred method of restoring IRA patency in ST-elevation MI (STEMI) [4,5]. The beneficial effect of primary PCI can be limited by complications related to thrombus defragmentation and distal macroembolization and/or by microembolization caused by aggregates of platelets and inflammatory cells [6]. Therefore, in order to reduce the thrombotic burden and prevent complications of primary PCI such as inadequate reperfusion (also known as no reflow or slow flow) and/or stent thrombosis it is crucial to provide high periand post-procedural platelet inhibition [4,5]. Various antiplatelet drugs have been shown to reduce the reperfusion injury and to help maintain patency of the culprit vessel after the procedure [4,7], which results in reduction of the infarct size and recurrent ischemic events as well as its consequences (death, recurrent MI and chronic heart failure). For many years, antiplatelet therapy in the setting of primary PCI included two oral antiplatelet drugs, which irreversibly block platelet activation (aspirin and clopidogrel) together with an inhibition of platelet aggregation by intravenous glycoprotein (Gp) IIb/IIIa blockers (preferably abciximab) [8]. For a long time, the only changes in this standard regimen involved modifications of dosing and timing of antiplatelet therapy. During the last 3 years, we have been witnessing a major change in the schemes of antiplatelet treatment for primary PCI comparable with the introduction of clopidogrel over a decade ago. The most important modifications of antiplatelet therapy presented in this manuscript are related to the development of new, more potent and fast-acting antiplatelet drugs, decreasing evidence for the use of Gp IIb/IIIa blockers, individualization of antiplatelet therapy based on patients and drug characteristics and the growing ability to o vercome drug resistance.