P2Y12 Receptor Inhibitors in Acute Coronary Syndromes: From the Research Laboratory to the Clinic and Vice Versa

Alexopoulos, Dimitrios

doi:10.1159/000357399

Cited by 15 publications

(9 citation statements)

References 47 publications

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“…ADP receptors may be important therapeutic targets. Moreover ADP receptor antagonists are in wide clinical use [11][12][13][16][17][18]. However, several limitations of known synthetic ADP receptors antagonist have recently been discussed including inter-patient variability in antiplatelet effects and a relatively slow onset of action [19][20][21].…”

Section: Methodsmentioning

confidence: 99%

Effects of novel quinoid thiosulfonate derivative on ADP-induced platelet aggregation

et al. 2014

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Recently, in a large scale screening test, we have found that S-((1,4-dimethoxy-9,10-dioxo-9,10-dihydroanthracen-2-yl)methyl)4-aminobenzenesulfonothioate, a chemically synthesized thiosulfonate derivative of quinone, possessed an antiplatelet activity. To elucidate the mechanism of its antiplatelet action, a series of experiments were performed. The compound was found to inhibit the ADP-induced platelet aggregation. The inhibitory effect was dose-dependent on concentration and preincubation time. The derivative also disaggregated the preformed platelet aggregates induced by ADP.

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Section: Methodsmentioning

confidence: 99%

Effects of novel quinoid thiosulfonate derivative on ADP-induced platelet aggregation

et al. 2014

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“…The activated platelets then release adenosine diphosphate (ADP) from their dense granules, which activates surrounding platelets via the G-protein coupled receptors, P2Y1 and P2Y12 [120]. Though a weak platelet agonist itself, ADP amplifies the platelet response induced by stronger agonists (collagen and vWF) [121]. The P2Y1 receptor mediates cytoplasmic calcium mobilization, which plays a major role in platelet activation and stabilization.…”

Section: Platelet Function and Hematoma Expansionmentioning

confidence: 99%

Hematoma Expansion Following Intracerebral Hemorrhage: Mechanisms Targeting the Coagulation Cascade and Platelet Activation

Burchell

Tang

Zhang

2017

CDT

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Hematoma expansion (HE), defined as a greater than 33% increase in intracerebral hemorrhage (ICH) volume within the first 24 hours, results in significant neurological deficits, and enhancement of ICH-induced primary and secondary brain injury. An escalation in the use of oral anticoagulants has led to a surge in the incidences of oral anticoagulation-associated ICH (OAT-ICH), which has been associated with a greater risk for HE and worse functional outcomes following ICH. The oral anticoagulants in use include vitamin K antagonists, and direct thrombin and factor Xa inhibitors. Fibrinolytic agents are also frequently administered. These all act via differing mechanisms and thus have varying degrees of impact on HE and ICH outcome. Additionally, antiplatelet medications have also been increasingly prescribed, and result in increased bleeding risks and worse outcomes after ICH. Aspirin, thienopyridines, and GPIIb/IIIa receptor blockers are some of the most common agents in use clinically, and also have different effects on ICH and hemorrhage growth, based on their mechanisms of action. Recent studies have found that reduced platelet activity may be more effective in predicting ICH risk, hemorrhage expansion, and outcomes, than antiplatelet agents, and activating platelets may thus be a novel target for ICH therapy. This review explores how dysfunctions or alterations in the coagulation and platelet cascades can lead to, and/or exacerbate, hematoma expansion following intracerebral hemorrhage, and describe the mechanisms behind these effects and the drugs that induce them. We also discuss potential future therapy aimed at increasing platelet activity after ICH.

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“…By blocking this receptor, prasugrel modulates "platelet procoagulant activity, thrombin generation, P-selectin expression, soluble CD40L, and inflammation marker release." 9 Additionally, prasugrel shows increased potency, faster onset, and more consistent action across patients compared with clopidogrel. 9 The TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel -Thrombolysis In Myocardial Infarction-38) compared the efficacy and safety of prasugrel and clopidogrel in combination with aspirin.…”

Section: Case Reportmentioning

confidence: 99%

Retrobulbar hemorrhage and prasugrel

Matharu

Smith

Lee

2016

Canadian Journal of Ophthalmology

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Retrobulbar hemorrhage and prasugrelRetrobulbar hemorrhage (RBH) is the accumulation of blood in the orbit behind the globe. Although some hemorrhages are minor and do not result in significant mass effect, an RBH is an ophthalmologic emergency requiring immediate surgical intervention. An RBH manifests as acute ipsilateral orbital pain and proptosis and can be variably associated with loss of vision, ophthalmoplegia, subconjunctival hemorrhage, and increased intraocular and intraorbital pressure. 1 Most cases of RBH are traumatic or postsurgical, but some occur spontaneously in patients with bleeding diatheses. Another etiology for RBH is retrobulbar anesthesia injection. 1 The use of antiplatelet therapy has not been considered to be a significant risk factor for RBH 1,2 ; yet newer, more potent antiplatelet agents may carry significantly more risk for RBH. We report a case of RBH causing blindness in a patient taking aspirin and prasugrel. To our knowledge, this is the first such case reported in the English-language ophthalmic literature. DISCUSSIONRBH is a potentially visually devastating complication of retrobulbar anesthesia. Although older literature

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P2Y12 Receptor Inhibitors in Acute Coronary Syndromes: From the Research Laboratory to the Clinic and Vice Versa

Cited by 15 publications

References 47 publications

Effects of novel quinoid thiosulfonate derivative on ADP-induced platelet aggregation

Effects of novel quinoid thiosulfonate derivative on ADP-induced platelet aggregation

Hematoma Expansion Following Intracerebral Hemorrhage: Mechanisms Targeting the Coagulation Cascade and Platelet Activation

Retrobulbar hemorrhage and prasugrel

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