Recent therapeutic approaches to platelet activation in coronary artery disease.
We have examined the role of platelets and platelet activation, and related emerging therapeutic approaches, in acute coronary syndromes (ACS). The role of platelets in atherothrombosis and ACS is critical, since platelet activation is a key step in the manifestation of these syndromes. Adhesion of sub-endothelial collagen and von Willebrand Factor (vWF) to the glycoprotein (GP) platelet receptors (GPIaIIa and GPIb/IX/V respectively) stimulates platelet activation. During activation, platelets present pseudopodia, which ensures a tighter adhesion to the sub-endothelial matrix and, via GPIIbIIIa receptors, facilitates platelet aggregation and platelet binding to fibrinogen and vWF. Although all laboratory methods estimating platelet activation and antiplatelet therapy have specific limitations, the use of antiplatelet agents such as aspirin, clopidogrel, and GPIIbIIIa inhibitors remains essential in ACS prevention and treatment. Platelet-related genetic polymorphisms can modulate the response to these agents. Presently, antiplatelet intervention remains an important therapeutic modality, with novel antiplatelet therapies, such as prasugrel and ticagrelor under clinical investigation.
Tousoulis
Dimitris
D
1st Cardiology Unit, Hippokration Hospital, Athens University Medical School, Greece. drtousoulis@hotmail.com
Paroutoglou
Ioannis Ph
IP
Papageorgiou
Nikolaos
N
Charakida
Marietta
M
Stefanadis
Christodoulos
C
D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D011110:Polymorphism, Genetic; D013927:Thrombosis / Q000209:etiology / Q000517:prevention & control
D010975:Platelet Aggregation Inhibitors