P2Y12 platelet inhibition in clinical practice

Abstract

Platelet adhesion, activation and aggregation play a pivotal role in atherothrombosis. Intracoronary atherothrombosis is the most common cause of the development of acute coronary syndrome (ACS), and plays a central role in complications occurring around percutaneous coronary intervention (PCI) including recurrent ACS, procedure-related myocardial infarction or stent thrombosis. Inhibition of platelet aggregation by medical treatment impairs formation and progression of thrombotic processes and is therefore of great importance in the prevention of complications after an ACS or around PCI. An essential part in the platelet activation process is the interaction of adenosine diphosphate (ADP) with the platelet P2Y12 receptor. The P2Y12 receptor is the predominant receptor involved in the ADP-stimulated activation of the glycoprotein IIb/IIIa receptor. Activation of the glycoprotein IIb/IIIa receptor results in enhanced platelet degranulation and thromboxane production, and prolonged platelet aggregation. The objectives of this review are to discuss the pharmacological limitations of the P2Y12 inhibitor clopidogrel, and describe the novel alternative P2Y12 inhibitors prasugrel and ticagrelor and the clinical implications of the introduction of these new medicines.

Delayed targeting of CD39 to activated platelet GPIIb/IIIa via a single-chain antibody: breaking the link between antithrombotic potency and bleeding?

“…3 However, these drugs are also known to cause a significant increase in the rate of potentially detrimental bleeding complications. [4][5][6] An alternative therapeutic strategy to decrease ADP-induced platelet activation is the administration of a soluble form of CD39 (solCD39), an ecto-nucleoside triphosphate diphosphohydrolase, 7 which is constitutively expressed on endothelial cells and is described as a major physiological mechanism to maintain blood fluidity. [8][9][10][11] CD39 works by hydrolyzing ADP rather than by inhibition of platelet ADP receptors.…”

Status Quo of Hybrid Coronary Revascularization for Multi-Vessel Coronary Artery Disease

“…In case series of simultaneous HCR (CABG directly followed by PCI), a loading dose of clopidogrel (300 or 600 mg) is given either directly before surgery in the holding area [17], after LIMA insertion [28, 29], or after PCI is completed [17, 30, 31]. Interestingly, although maximal inhibition of platelet aggregation occurs only after a couple of hours [32], meaning there is incomplete platelet inhibition at the time of procedure, the reported rates of acute stent thrombosis are low (0% to 7%). Some authors suggest that in procedures performed with cardiopulmonary bypass, the use of cardiopulmonary bypass may be protective against the risk of stent thrombosis [33].…”

Hybrid minimally invasive myocardial revascularization in multivessel coronary disease . Current status of the issue

“…Недостатками являются возможность острых коронарных со-бытий в бассейнах нереваскуляризированных ОА и ПКА при проведении первого этапа, а также воз-можность неуспешного последующего ЧКВ при сложных техниках стентирования, риск рестеноза и тромбоза стента. При неуспешном ЧКВ возни-кает вопрос о необходимости повторной прямой реваскуляризации через срединную стернотомию [23,[43][44][45][46][47].…”