Haemostasis is a complex phenomenon defined as the chain of mechanisms able to maintain the integrity of a closed, high-pressure circulatory system after vascular damage.1 Thrombogenesis represents the main process assuring haemostasis at each level of the vascular system, and its accurate regulation guarantees the correct balance between blood flow and damage repair. An uncontrolled thrombin formation may occur in different pathological situations, finally leading to the dangerous process of thrombosis.
Atherosclerosis development and its complication into an acute coronary syndrome (ACS) recognises different pathogenetic mechanisms that involve inflammation, endothelial dysfunction, platelet activation and, finally, thrombus formation.2 ST-segment elevation myocardial infarction (STEMI) is paradigmatic of inappropriate thrombogenic response. In fact, a complete thrombotic occlusion of epicardial coronary vessels is present in the vast majority of cases.3
The currently recommended treatment of ACS is based upon early mechanical reperfusion and prompt use of potent antithrombotic drugs aimed to obtain the best chances of vessel patency restore and significant reduction of acute and late cardiovascular events.4–6 Furthermore, the widespread use of intracoronary devices, such as drug-eluting stents during percutaneous coronary intervention (PCI), also implies the necessity for prevention of potentially lifethreathening device-related complications, such as early, late and very late stent thrombosis. On the other hand, the need for fast reperfusion and thrombosis inhibition must be balanced with the individual risk of bleeding for each subject, as this complication is a well-recognised cause of morbidity and mortality in post-PCI patients.7 With the development of more potent and rapidly acting antithrombotic agents, the choice of the right therapy for each patient should be the result of a careful consideration of the individual clinical and operative risk.