Abstract 3730: Celecoxib Does Not Deteriorate Antiplatelet Effects of Aspirin and Clopidogrel in Healthy Volunteers

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Wonjae Lee ◽  
Dong-A Kwon ◽  
Hyun-Ju Cho ◽  
Jung-Won Suh ◽  
Su-Yeon Choi ◽  
...  

Background: Celecoxib, cyclooxygenase (COX)-2 inhibitor, has been reported to inhibit neointimal hyperplasia in animal studies and to reduce restenosis after coronary stenting in COREA-TAXUS clinical trial. The main concern is that celecoxib would increase thrombogenecity by inhibiting the synthesis of prostacyclin in endothelial cells. However, it is not known whether the administration of celecoxib would weaken antiplatelet effects of aspirin and clopidogrel which are used after stenting. Methods: We recruited healthy volunteers (n=40) and randomized them into five subgroups. Each subject received the medication for 6 days and blood samples were taken day 0 and 7. Celecoxib 200mg twice a day, and/or aspirin 100mg daily, and/or clopidogrel 75 mg daily was administered. We compared platelet function by using light transmittance aggregometry and arachidonic acid metabolite assay among subgroups. Results: Celecoxib single treatment did not significantly affect platelet aggregation. Dual asprin and Plavix treatment inhibited platelet aggregation by 53%, which was not affected by addition of celecoxib showing 52% inhibition (t-test: p = 0.873). The changes of prostacyclin level did not differ among each treatment group (ANOVA: p=0.193). Although statistically not significant, celecoxib seems to lower the thromboxane level further when added to antiplatelet agents. Conclusion: Celecoxib treatment did not interfere with antiplatelet effect of aspirin or clopidogrel, suggesting that celecoxib as anti-restenosis agent would be administered safely during coverage of dual antiplatelet therapy in patients with coronary stenting without increasing thrombogenecity.

1984 ◽  
Vol 51 (01) ◽  
pp. 037-041 ◽  
Author(s):  
K M Weerasinghe ◽  
M F Scully ◽  
V V Kakkar

SummaryCollagen mediated platelet aggregation caused -5.6 ± 6.7% inhibition and +39.1 ± 15.2% potentiation of prekallikrein activation in plasma from normal healthy volunteers between 20–40 and 50–65 years of age, respectively (n = 15, p <0.01). The amouns of platelet factor-four (PF4) released in the two groups were not significantly different. Collagen treatment in the presence of indomethacin caused +11.5 ± 3.6% and +59.6 ± 19.5% potentiation in the 20–40 and 50–65 age groups respectively (p <0.02). Adrenaline mediated platelet aggregation caused -55.2 ± 7.1% and -35.2 ± 8.3% inhibition in the 20–40 and 50–65 age groups, respectively. Collagen treatment of platelet-deficient-plasma and platelet-rich-plasma in EDTA also caused potentiation of prekallikrein activation.The results indicate that the observed degree of prekallikrein activation after platelet aggregation is a net result of the inhibitory effect of PF4 and the potentiatory effect of activated platelets. The potentiatory effect was greater after collagen treatment as compared to adrenaline treatment, and in the 50–65 age group as compared to the 20–40 age group.


Platelets ◽  
2014 ◽  
Vol 26 (6) ◽  
pp. 608-609 ◽  
Author(s):  
Paul A. Gurbel ◽  
Martin G. Gesheff ◽  
Christopher J. Franzese ◽  
Kevin P. Bliden ◽  
Udaya S. Tantry

1997 ◽  
Vol 3 (3) ◽  
pp. 196-202 ◽  
Author(s):  
Alexander Kaplan ◽  
Svetlana Kaplan ◽  
Karen F. Marcoe ◽  
Lester R. Sauvage ◽  
William P. Hammond

The turbidimetric method of Bom is the current approach for assessing the aggregation behavior of platelets. It has been of modest practical value, due to difficulty in standardizing laboratory techniques for plasma preparation and inadequate quantification of the aggregation process. We report a new technique of sedimented platelet rich plasma (SPRP) preparation that reduces the irregularities caused by factors associated with procuring and preparing blood samples and permits a more flexible protocol for laboratory practice. We quantified results with a platelet aggregation score, which is calculated by multiplying the ratio of the height of the initial wave of aggregation to the maximum height of the aggregation pattern by the total area under the aggregation curve and by the ratio of the whole blood platelet count and the number of platelets in the sample. Comparative analysis of platelet aggregation scores (n = 95) obtained with both plasma preparation techniques using a paired t test demonstrated no statistical differences ( t = 1.368, p = 0.174). To demonstrate the application of this modified method to evaluation of antiplatelet agents, the effects of aspirin and aspirin combined with citric acid on platelet aggregation were studied in vitro. The antiaggregatory effect of aspirin combined with citric acid was dependent on the pH and on their molar ratio, and was greater than the effect of aspirin alone. The SPRP protocol with platelet aggregation scoring methodology could be a valid alternative for measurement of the platelets' propensity to aggregate and the effect of antithrombotic treatments. Key Words: Platelet aggregation— Aspirin—Citric acid.


2018 ◽  
Vol 46 (12) ◽  
pp. 5074-5082 ◽  
Author(s):  
Thomas Kander ◽  
Erik Lindblom ◽  
Ulf Schött

Objective This study aimed to evaluate the dose-response effects of supplemental omega-3 fatty acids on platelet function in healthy volunteers. Methods Twelve healthy volunteers ingested a normal supplemental dose of 1260 mg omega-3 fatty acids daily for 5 days, followed by a high dose of 2520 mg daily for another 5 days. Multiple electrode aggregometry (MEA) with four different agonists was used to measure platelet aggregation before and after the normal- and high-dose regimes. In vitro spiking using physiological doses of omega-3 fatty acids was also performed to determine whether MEA is capable of detecting a platelet-inhibiting effect due to omega-3 fatty acids. Results There were no differences in platelet aggregation measured by the MEA assay in healthy volunteers after intake of either the normal or high dose of omega-3 fatty acids. In the in vitro experiment, a platelet-inhibiting effect of omega-3 fatty acids was shown by an arachidonic acid agonist in MEA . Conclusions Supplemental omega-3 fatty acids do not evoke their positive health effects through inhibition of platelet aggregation measurable with MEA.


2020 ◽  
pp. 101-104
Author(s):  
E Osuch ◽  
TL Rasakanya

Antiplatelet agents prevent clot formation and growth through prevention of platelet aggregation. Antiplatelet agents are essential for the prophylaxis and pharmacological management of arterial thrombosis. Appropriate use of these agents requires knowledge of their pharmacology and therapeutic uses with appropriate assessment of risks and benefits.


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