Pharmacodynamic Evaluation of Switching From Ticagrelor to Prasugrel in Patients With Stable Coronary Artery Disease

Angiolillo, Dominick J.; Curzen, Nicholas; Gurbel, Paul A.; Vaitkus, Paul T.; Lipkin, Fred; Li, Wei; Jakubowski, Joseph A.; Zettler, Marjorie E.; Effron, Mark B.; Trenk, Dietmar

doi:10.1016/j.jacc.2013.11.032

Cited by 86 publications

(53 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Between ticagrelor and clopidogrel 35,38 > A need for a switch between prasugrel and ticagrelor is rare but may be needed for compliance issues since ticagrelor is a twice daily drug and prasugrel is taken once a day. > Patients who develop troublesome dyspnoea with ticagrelor may be better off on prasugrel.…”

Section: Switching Between P2y 12 Inhibitorsmentioning

confidence: 99%

Antiplatelet therapy – a summary for the general physicians

Thachil¹

2016

Clinical Medicine

View full text Add to dashboard Cite

APlatelets play a very important role in physiological haemostasis and thrombus formation. Platelet aggregation is the key pathophysiological factor in the development of arterial ischaemic events, including coronary artery disease, cerebrovascular accidents and peripheral arterial disease. As such, antiplatelet therapy plays a very important role in preventing recurrent events in the individuals who are affected by one of these conditions. Until recently, the repertoire of antiplatelet therapy was limited to aspirin and clopidogrel. However, this landscape has changed dramatically with the advent of newer and more potent agents, prasugrel and ticagrelor and also the glycoprotein IIb/IIIa antagonists. This armamentarium is likely to expand further with the advent of protease-activated receptor-1 antagonists and the intravenous cangrelor. This review summarises the different agents available and some practical considerations for their use from a general physician's perspective.

show abstract

Section: Switching Between P2y 12 Inhibitorsmentioning

confidence: 99%

Antiplatelet therapy – a summary for the general physicians

Thachil¹

2016

Clinical Medicine

View full text Add to dashboard Cite

show abstract

“…In light of the multiple chemical and pharmacological differences existing between the 3 currently available oral P2Y 12 inhibitors, including potency, 11 consistency and reversibility of the P2Y 12 inhibition, 12 binding site in the target receptor, and off-target effects, 13,14 caution should be used in interpreting the value of these compounds as class effects.…”

Section: Response By Collet Et Al On P 1903mentioning

confidence: 99%

Pretreatment With P2Y ₁₂ Inhibitors in Non–ST-Segment–Elevation Acute Coronary Syndrome Is Clinically Justified

Valgimigli¹

2014

Circulation

View full text Add to dashboard Cite

“…Breet et al [44] Paniccia et al [51,65] Tantry et al [116] Marcucci et al [119] Price et al [120] Angiolillo et al [121] HIT: Heparin-Induced Thrombocytopenia; plt: Platelet; RIPA: Ristocetin-Induced Platelet Aggregation; VWD: Von Willebrand Disease.…”

Section: Platelet Aggregation On Platelet-rich Plasmamentioning

confidence: 99%

“…For the VerifyNow P2Y12 assay results are expressed as P2Y12 Reaction Units (PRU). Different laboratory and clinical studies relative to patient on different thienopyridines have tried to choose a cutoff value for discriminating patients not responsive to drug [44,51,[119][120][121][122] . The potential role of this system for prediction of postoperative bleeding in surgical practice remains placed for the evaluation of the extent of inhibition of platelet function in response to antiplatelet medication [123] .…”

Section: Verifynow Systemmentioning

confidence: 99%

Assessment of platelet function: Laboratory and point-of-care methods

Paniccia¹

2014

WJTM

View full text Add to dashboard Cite

In the event of blood vessel damage, human platelets are promptly recruited on the site of injury and, after their adhesion, activation and aggregation, prevent blood loss with the formation of a clot. The consequence of abnormal regulation can be either hemorrhage or the development of thrombosis. Qualitative and/or quantitative defects in platelets promote bleeding, whereas the residual reactivity of platelets, despite antiplatelet therapies, play an important role in promoting arterial thrombotic complications. Platelet function is traditionally assessed to investigate the origin of a bleeding syndrome, to predict the risk of bleeding prior surgery or during pregnancy or to monitor the efficacy of antiplatelet therapy in thrombotic syndromes that, now, can be considered a new discipline. "Old" platelet function laboratory tests such as the evaluation of bleeding time and the platelet aggregation analysis in platelet-rich plasma are traditionally utilized to aid in the diagnosis and management of patients with platelet and hemostatic disorders and used as diagnostic tools both in bleeding and thrombotic diathesis in specialized laboratories. Now, new and renewed automated systems have been introduced to provide a simple, rapid assessment of platelet function including point of care methods. These new methodologies are also suitable for being used in non-specialized laboratories and in critical area for assessing platelet function in whole blood without the requirement of sample processing. Some of these methods are also beginning to be incorporated into routine clinical use and can be utilized as not only as first panel for the diagnosis of platelet dysfunction, but also for monitoring anti-platelet therapy and to potentially assess risk of both bleeding and/or thrombosis.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Platelets; Method; Test; Point of care testing; Laboratory assessment; Bleeding; Thrombosis; Platelet function Core tip: This review discussed the scenario of available platelet function laboratory and point-of-care methods suitable in different clinical setting. As this matter has become of crucial importance in the bleeding management and for monitoring antiplatelet therapies, improved ability to assess platelet function in a timely and efficient manner is essential. Traditional platelet function methods, requiring a fair degree of expertise, have been limited to specialized laboratory. Many efforts have been carried out for improving platelet function assays for centralized laboratory, such as different point-of-care testing methodologies have been developed. Moreover, different guidelines and recommendations for their method standardization are growing.

show abstract

Pharmacodynamic Evaluation of Switching From Ticagrelor to Prasugrel in Patients With Stable Coronary Artery Disease

Abstract: Compared with continued ticagrelor therapy, switching from ticagrelor to prasugrel therapy was associated with an increase in platelet reactivity that was partially mitigated by the administration of an LD.

Cited by 86 publications

References 25 publications

Antiplatelet therapy – a summary for the general physicians

Antiplatelet therapy – a summary for the general physicians

Pretreatment With P2Y ₁₂ Inhibitors in Non–ST-Segment–Elevation Acute Coronary Syndrome Is Clinically Justified

Assessment of platelet function: Laboratory and point-of-care methods

Contact Info

Product

Resources

About

Pharmacodynamic Evaluation of Switching From Ticagrelor to Prasugrel in Patients With Stable Coronary Artery Disease

Abstract: Compared with continued ticagrelor therapy, switching from ticagrelor to prasugrel therapy was associated with an increase in platelet reactivity that was partially mitigated by the administration of an LD.

Cited by 86 publications

References 25 publications

Antiplatelet therapy – a summary for the general physicians

Antiplatelet therapy – a summary for the general physicians

Pretreatment With P2Y 12 Inhibitors in Non–ST-Segment–Elevation Acute Coronary Syndrome Is Clinically Justified

Assessment of platelet function: Laboratory and point-of-care methods

Contact Info

Product

Resources

About

Pretreatment With P2Y ₁₂ Inhibitors in Non–ST-Segment–Elevation Acute Coronary Syndrome Is Clinically Justified