Abciximab, ticlopidine, and concomitant abciximab-ticlopidine therapy: Ex vivo platelet aggregation inhibition profiles in patients undergoing percutaneous coronary interventions

Kleiman, Neal S.; N, Grazeiadei; Maresh, Kelly; Taylor, Rebecca J.; Frederick, Bart; Lance, Ellen T.; Effron, Mark B.; Jordan, Robert E.; Mascelli, Mary Ann

doi:10.1067/mhj.2000.109220

Cited by 16 publications

(6 citation statements)

References 38 publications

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“…Abciximab in combination with ticlopidine, a thienopyridine, has a prolonged inhibitory effect on mural thrombosis by decreasing platelet aggregates [25]. The effect on the expression of glycoprotein IIb/IIIa has been controversial [12].…”

Section: Effect Of Abciximab On Activated Platelet Glycoprotein Iib/iiiamentioning

confidence: 99%

Platelet–monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab

Ray

Walters

Bett

et al. 2005

International Journal of Cardiology

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Section: Effect Of Abciximab On Activated Platelet Glycoprotein Iib/iiiamentioning

confidence: 99%

Platelet–monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab

Ray

Walters

Bett

et al. 2005

International Journal of Cardiology

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“…Besides in vivo systems, ex vivo models have been used to some extent for studying human microvessels under various conditions. 24,25 Under these ex vivo conditions, however, the preservation of real whole human blood and tissue can restrict the output of experimental results, and biases can arise during donor selection. [25][26][27] Fortunately, by recreating human microvessels in vitro, these in vivo and ex vivo barriers can be overcome.…”

Section: Introductionmentioning

confidence: 99%

“…24,25 Under these ex vivo conditions, however, the preservation of real whole human blood and tissue can restrict the output of experimental results, and biases can arise during donor selection. [25][26][27] Fortunately, by recreating human microvessels in vitro, these in vivo and ex vivo barriers can be overcome. For instance, microuidic devices have been found to enable the precision control of dynamic-ow environments, endothelial cell culture, and physiological properties of an in vitro 3D microvasculature system for days on end.…”

Section: Introductionmentioning

confidence: 99%

Manufacturing of poly(ethylene glycol diacrylate)-based hollow microvessels using microfluidics

et al. 2020

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“…9 The thienopyridines can be administered after the use of the parenteral IIb/IIIa inhibitors to provide consistent platelet blockade over several weeks. 66,67 The findings from the cardiology literature suggest that these drugs could be useful following renal, visceral, superficial femoral artery, and other small vessel interventions. Patients are often anticoagulated with heparin for a short time after infrainguinal angioplasty as well as renal and visceral artery stenting, and further investigation into potentially substituting clopidogrel would seem justified.…”

Section: Oral Antiplatelet Agentsmentioning

confidence: 99%

Use of Antiplatelet Inhibitors in Peripheral Vascular Interventions

Stavropoulos

Shlansky-Goldberg²

2005

Semin intervent Radiol

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In the past decade, a tremendous amount of information has been gathered about platelet function and its impact on percutaneous vascular interventions. Strategies for prevention of platelet aggregation have moved beyond aspirin administration. Powerful oral antiplatelet agents such as ticlopidine (Ticlid) and clopidogrel (Plavix) have been developed to prevent platelet aggregation and thrombosis. The discovery of the glycoprotein IIb/IIIa receptor, which is responsible for platelet aggregation, has led to the development of receptor antagonists. These drugs include abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Several large studies have demonstrated that these drugs can improve outcomes in coronary interventions. Because most of the data regarding antiplatelet agents in percutaneous interventions comes from studies of coronary interventions, knowledge of these studies is necessary before using the antiplatelet drugs in peripheral vascular interventions. This article reviews the use of these agents in percutaneous coronary artery interventions and discusses their potential use in peripheral interventions.KEYWORDS: Blood, platelets, arteries, transluminal angioplasty, thrombosis, drugsObjectives: Upon completion of this article, the reader will understand the use of antiplatelet agents in percutaneous coronary artery interventions and be able to discuss their potential use in peripheral interventions. Accreditation: Tufts University School of Medicine (TUSM) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Credit: TUSM designates this educational activity for a maximum of 1 Category 1 credit toward the AMA Physicians Recognition Award. Each physician should claim only those credits that he/she actually spent in the activity.Over the past decade, our understanding of the role of the platelet in acute vascular events including those associated with percutaneous interventions has increased dramatically. Although aspirin was introduced in the late 1890s, its antiplatelet effect was not discovered until the 1960s.1,2 Aspirin primarily affects the biosynthesis of cyclic prostanoids such as thromboxane A 2 (TXA 2 ) by irreversibly inhibiting both the function of cyclooxygenase (COX-1) in platelets and the vascular synthesis of prostacyclin. 3,4 Although the efficacy of aspirin in preventing thrombotic complications during percutaneous coronary interventions (PCIs) is well established, 5-8 aspirin is a relatively weak platelet antagonist and some patients may be resistant to its effects. Other non-TXA 2 -dependent activators of platelet aggregation such as thrombin, adenosine diphosphate (ADP), and collagen 3,4 are not affected by aspirin. The current general recommendation for 584-4662. 0739-9529,p;2005,22,02,080,087,ftx,en;sir00297x. 80 aspirin use during PCI is an empirical dose of aspirin, 80 to 325 mg, given at least 2 hours prior to an intervention. 9Pharmacologic therapy during peripheral vascu...

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Abciximab, ticlopidine, and concomitant abciximab-ticlopidine therapy: Ex vivo platelet aggregation inhibition profiles in patients undergoing percutaneous coronary interventions

Cited by 16 publications

References 38 publications

Platelet–monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab

Platelet–monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab

Manufacturing of poly(ethylene glycol diacrylate)-based hollow microvessels using microfluidics

Use of Antiplatelet Inhibitors in Peripheral Vascular Interventions

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