Emerging antiplatelet agents, differential pharmacology, and clinical utility

Abstract

The aspirin–clopidogrel combination is the current gold standard antiplatelet regimen following percutaneous coronary intervention and for the treatment of acute coronary syndrome. Despite the clinical benefit of this combination, patients continue to have vascular events. Another purinergic (P2Y12) receptor antagonist, prasugrel, became available last year. Although prasugrel is superior to clopidogrel in reducing clinical endpoints, a higher bleeding rate has been identified particularly in high-risk patients. Ticagrelor, a reversible P2Y12 receptor antagonist currently being evaluated for approval, is also more potent than clopidogrel but has a similar bleeding risk. Two additional P2Y12 antagonists are being investigated that will be available as an intravenous formulation. Apart from the P2Y12 receptor antagonists, multiple other agents are being developed with unique mechanisms of platelet inhibition. These agents are being studied as an alternative to or in combination with clopidogrel. The antiplatelet agents currently under development include: thrombin receptor antagonists, phosphodiesterase inhibitors, a thromboxane–prostaglandin receptor antagonist, a serotonin receptor blocker, a platelet adhesion antagonist, nitric oxide-releasing aspirin, a glycoprotein VI antagonist, and a cyclooxygenase inhibitor. The purpose of this review is to describe the efficacy and safety profiles of the emerging antiplatelet agents and their role in the treatment of atherosclerotic cardiovascular diseases.

Antiplatelet Drugs in the Management of Cardiovascular Indications

“…It can be used in acute coronary syndrome and von Willebrand disease and related disorders such as thrombotic thrombocytopenic purpura (TTP) and other thrombotic microangiopathies. Its actions can be reversed by binding to complementary sequence of oligonucleotides (Das et al 2010). It has favorable safety profile in healthy individuals and patients with TTP.…”

Ticagrelor: An emerging oral antiplatelet agent

“…PLATO showed that treatment with ticagrelor as compared with clopidogrel in patients with ACS significantly reduced the mortality from vascular causes, myocardial infarction and stroke. [410]…”

“…[3] The thienopyridenes (clopidogrel, ticlopidine and prasugrel) are another class of antiplatelet agents that inhibit adenosine diphosphate induced platelet aggregation irreversibly via P2Y 12 receptor located on the surface of platelets. [45]…”

“…[3] The thienopyridenes (clopidogrel, ticlopidine and prasugrel) are another class of antiplatelet agents that inhibit adenosine diphosphate induced platelet aggregation irreversibly via P2Y 12 receptor located on the surface of platelets. [4,5] It has been seen that 1 in 3 ACS patient dies due to repeat MI despite intensive monitoring and prompt treatment of cardiac instability, thrombolytic activity, acute invasive interventions and dual antiplatelet therapy with aspirin and thienopyridines. [6] In patients with ACS, the most commonly used thienopyridine is clopidogrel.…”

Response to Letter Regarding Article, “Dabigatran and Thrombin Modulate Electrophysiological Characteristics of Pulmonary Vein and Left Atrium” by Chang et al

“…5,6 These differences might theoretically be caused by the deleterious electrophysiological effects of aspirin, which interfered prostacyclin and nitric oxide production or by beneficial effects of warfarin. 7 However, this study only treated healthy animals with dabigatran for 3 days, which is different from the long-term use of warfarin in clinical studies. It would be really helpful to compare the differences among various anticoagulant agents (warfarin, direct thrombin inhibitor, and factor Xa inhibitors) and antiplatelet agents (aspirin, clopidogrel, ticagrelor) on the electrophysiological and mechanical characteristics of the pulmonary veins and left atrium in models of disease and over longer durations.…”