Thrombosis and Inflammation in Acute Coronary Syndromes

Platelet Inhibitors for the Treatment of Acute Coronary Syndromes

Author(s): Hasan Gungor and Ceyhun Ceyhan

Pp: 105-120 (16)

DOI: 10.2174/9781681080291115010009

* (Excluding Mailing and Handling)

Abstract

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.

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