Modern antiplatelet agents in coronary artery disease

Abstract

Dual antiplatelet therapy is well recognized in the prevention of thrombotic complications of acute coronary syndrome and percutaneous coronary interventions. Despite clinical benefits of aspirin and clopidogrel therapy, a number of limitations curtail their efficacy: slow onset of action, variability in platelet inhibitory response and potential drug-drug interactions. Furthermore, the single platelet-activation pathway targeted by these agents allows continued platelet activation via other pathways, ensuring incomplete protection against ischemic events, thus, underscoring the need for alternate antiplatelet treatment strategies. A number of novel antiplatelet agents are currently in advance development and many have established superior effects on platelet inhibition, clinical outcomes and safety profile than clopidogrel in high-risk patients. The aim of this review is to provide an overview of the current status of P2Y12 receptor inhibition and PAR-1 antagonists in determining a future strategy for individualized antiplatelet therapy.

Role of Pannexin-1 hemichannels and purinergic receptors in the pathogenesis of human diseases

“…The P2Y12 platelet receptor plays an important role in the genesis of platelet aggregation (Power et al, 2012; Tam et al, 2012). Current treatments blocking adenosine diphosphate (ADP) binding to the P2Y12 receptor, which inhibits platelet aggregation, are commercially available as well as in clinical trials.…”

“…However, its toxicity led to the development of second-generation thienopyridine clopidogrel (Ji and Hou, 2011). Clopidogrel also has its limitations, such as a delay in platelet block because the prodrug requires activation in the liver, and clopidogrel therapy is irreversible which can lead to increase bleeding and transfusion risk in cardiothoracic surgery (Power et al, 2012; Tam et al, 2012). Third generation thienopyridine prasugrel addressed the issue of delayed platelet blocking by being relatively independent of hepatic activation, however, it still remained irreversible and patients were still at risk for increase bleeding (Ferraris et al, 2012).…”

Is There a Relationship Between the Arterial Stiffness and Effectiveness of Acetylsalicylic Acid in Patients with Stable Coronary Artery Disease?

“…Yeni antiplatelet ilaçların gelişmesine rağmen asetilsalisilik asit hala birincil ve ikincil koruma amaçlı kullanılmaktadır (1) . Asetilsalisilik asit siklooksijenaz enzimini inhibe ederek tromboksan (Tx) A2 sentezini bloke eder.…”