Acute coronary syndrome (ACS) is associated with significant morbidity,
mortality and it is a major public health problem. The primary pathophysiological
mechanism of the ACS is the response to vascular injury such as atherosclerotic plaque
rupture or endothelial monolayer erosion that triggers platelet activation and
aggregation leading to platelet-rich thrombi. These platelet-rich thrombi impair blood
flow and result in ischemia. Inhibition of platelet aggregation by medical treatment
prevents formation and progression of thrombotic process. Antiplatelet therapy is
indispensible in the early and long-term management of patients with ACS. Current
platelet inhibitors are thromboxane inhibitors (aspirin), P2Y12 inhibitors (ticlopidine,
clopidogrel, prasugrel, ticagrelor, cangrelor and elinogrel) and protease-activated
receptor antagonists (vorapaxar and atopaxar). The aim of this chapter is to discuss anti
platelet therapy in ACS.
Keywords: Acute coronary syndrome, antiplatelet therapy, aspirin, atherosclerosis,
atoxapar, cangrelor, coronary artery disease, clopidogrel, elinogrel, inflammation,
irreversible, platelets, prasugrel, protease-activated receptor, reversible,
thienopyridine, thrombosis, thromboxane, ticagrelor, voraxapar.
