EVALUATION ON EFFECTIVENESS OF LOW DOSE ASPIRIN THERAPY FOR PROTECTION OF THROMBUS FORMATION

1987 ◽  
Author(s):  
S Kariyone ◽  
M Hirakuri ◽  
T Yui ◽  
T Uchida
Keyword(s):  
Platelet Aggregation ◽  
Oral Dose ◽  
Time Course ◽  
Low Dose ◽  
Thrombus Formation ◽  
Platelet Factor ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Before And After

In order to protect thrombus formation, administration of low dose aspirin has become common. However, its significance for this purpose is still not clear. Effect of small dose of aspirin (ASA) onplatelet aggregation and ability of malondialdehyde(MDA) formation in platelet by the addition of arachidonic acid in vitro were investigated. In clinical study, platelet aggregation, MDA formation of platelet, serum P-thromboglobulin(p-TG), platelet factor 4(PF4) and thromboxane B2(TX-B2) levelswere measured before and after low doseaspirin therapy.Platelet aggregations by ADP, collagen, epinephrin and arachidonate as inducers were significantly suppressed under 12.5 ug/ml ASA in the medium. MDA formation of platelet was remarkably inhibited under 1.6 ug/ml of ASA in the medium in vitro.In patients, single oral dose of 50 mg ASA showed no change on platelet aggregation while the ability of MDA formation decreased 50# of the before. Serum concentration of ASA after oral dose of 50 mg ASA only showed 1.5 to 6.0 ug/ml at maximum.Daily dose of 50 mg ASA was continued during 10 days. Changes of various factors due to the time course were observed. Inhibitions of platelet aggregation were seen from 5th day on ADP and collagenand from 2nd day on epinephrin and arachidonate as inducers during the therapy. MDA formations of platelet were decreased quickly and it became almost zero at 5th day. ASA levels in the patient serum reached plateau as 8 or 9 ug/ml from 3rdday.Various patients with a possibility of thrombus formation were administered daily 50 mg ASA during 10 days. Platelet aggregations and MDA production, serum β-TG, PF4 and TXB2 levels were measured before and after the therapy. Platelet aggregations by ADP, collagen and epinephrin as inducers were significantly suppressed after the therapyand MDA production of platelet was also markedly decreased after the therapy. There were no significant changes in serumβ-TG and PF4 levels while TXB2 level tended to decrease after the therapy.From these results, it was concluded that daily 50 mg ASA oral dose was certainly effective for protection of thrombus formation.

Effects of low-dose aspirin on in vitro platelet aggregation in the early minutes after ingestion in normal subjects

1994 ◽  
Vol 74 (7) ◽  
pp. 720-723 ◽  
Author(s):  
Salim F. Dabaghi ◽  
Suraj G. Kamat ◽  
John Payne ◽  
Gary F. Marks ◽  
Robert Roberts ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Low Dose ◽  
Normal Subjects ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Effect of Diltiazem and Low-Dose Aspirin on Platelet Aggregation and ATP Release Induced by Paired Agonists

1993 ◽  
Vol 70 (02) ◽  
pp. 332-335 ◽  
Author(s):  
Marjorie L Zucker ◽  
Susan E Budd ◽  
Lawrence E Dollar ◽  
Steven B Chernoff ◽  
Raul Altman
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Low Dose ◽  
Atp Release ◽  
Thromboxane B2 ◽  
Platelet Response ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Significant Difference

SummaryThe authors studied the effects of diltiazem, administered alone and together with low-dose aspirin, on the platelet response to paired agonists. After a baseline period, 25 healthy volunteers were given oral diltiazem for 1 week (120, 240, or 360 mg/day), and then crossed over randomly between 1 week on diltiazem plus aspirin (81 mg/day), and 1 week on aspirin (81 mg/day) alone. Platelet function was tested on 2 consecutive days in each period. Synergistic platelet aggregation and ATP release were obtained at baseline using a subthreshold concentration of arachidonic acid combined with platelet activating factor, ADP, or epinephrine. Diltiazem resulted in a significant decrease from baseline in platelet aggregation and ATP release using the arachidonic acid-epinephrine combination (35% and 40% decrease, respectively, p <0.01) and a significant decrease in aggregation using the arachidonic acid-ADP combination (22% decrease, p <0.01). The effects were neither dose-related, nor accompanied by any significant change in serum thromboxane B2 levels or bleeding times. There was no significant difference between the effects of aspirin alone and aspirin plus diltiazem on the synergistic platelet aggregation and ATP release induced by the paired agonists, or on thromboxane B2 levels or bleeding times. Diltiazem administered in vivo partially inhibits the synergistic platelet aggregation and ATP release induced by paired agonists; however, in contrast to a previous in vitro study it does not potentiate the platelet-inhibitory effect of aspirin.

scholarly journals Effect of low-dose aspirin on platelet aggregation inhibition in patients with rheumatoid arthritis

2019 ◽  
Vol 7 (4) ◽  
pp. 110-117
Author(s):  
Mehrzad Hajialilo ◽  
Amir Ghorbanihaghjo ◽  
Forough Ghassemi ◽  
Alireza Khabbazi ◽  
Aida Malek Mahdavi
Keyword(s):  
Rheumatoid Arthritis ◽  
Platelet Aggregation ◽  
Low Dose ◽  
Enzyme Linked Immunosorbent Assay ◽  
American College Of Rheumatology ◽  
Dose Aspirin ◽  
Framingham Risk ◽  
Low Dose Aspirin ◽  
Before And After ◽  
Artery Disease

Introduction : The risk for coronary artery disease (CAD) and mortality has increased in patients with rheumatoid arthritis (RA). Aspirin has anti-thrombotic effects and causes reduction in CAD occurrence in high-risk individuals. The objective of present project was evaluating the influence of low-dose aspirin on inhibition of platelet aggregation in patients with RA. Methods: Forty-eight subjects with RA diagnosed based on the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) 2010 criteria and age- and sex-matched healthy participants were studied. All subjects received 81 mg/day aspirin for 10 days. Level of the serum thromboxane B2 (sTxB2), a permanent metabolite of thromboxane A2 (TxA2), was measured before and after therapy using enzyme-linked immunosorbent assay (ELISA) kit. The impotency to decrease sTxB2 production to less than 10 ng/ml indicates suboptimal suppression of platelet aggregation via aspirin. Results: Low-dose aspirin decreased sTxB2 significantly compared with baseline in patients with RA [median interquartile range (IQR): 25.72 (11.78, 90.10) to 7.74 (5.80, 8.82), P < 0.001] and in healthy controls [median (IQR): 40.50 (33.25, 50.90) to 7.30 (4.75, 8.85), P < 0.001]. No remarkable changes were seen in sTxB2 between patients and controls after adjustment (P > 0.050). Pharmacologic influence of aspirin was suboptimal in 6.25% of cases in the presence of higher erythrocyte sedimentation rate (ESR) and in 2.7% of controls. Low-dose aspirin decreased sTxB2 significantly only in patients with Framingham Risk Score (FRS) < 10%. Conclusion: Low-dose aspirin decreased sTxB2 level and suppressed platelet aggregation and therefore, was effective in primary prevention of cardiovascular (CV) events in patients with RA; however, additional studies are required to reach accurate conclusions.

Increased prostacyclin production during exercise in untrained and trained men: effect of low-dose aspirin

1995 ◽  
Vol 78 (5) ◽  
pp. 1832-1838 ◽  
Author(s):  
R. H. Boger ◽  
S. M. Bode-Boger ◽  
E. P. Schroder ◽  
D. Tsikas ◽  
J. C. Frolich
Keyword(s):  
Platelet Aggregation ◽  
Prostaglandin E2 ◽  
Low Dose ◽  
Submaximal Exercise ◽  
Trained Subjects ◽  
Dose Aspirin ◽  
Low Dose Aspirin ◽  
Before And After ◽  
Excretion Rates ◽  
Prostacyclin Production

The influence of a submaximal exercise on urinary 2,3-dinor-6-ketoprostaglandin F1 alpha (2,3-dinor-6-keto-PGF1 alpha), 2,3-dinor-thromboxane B2 (2,3-dinor-TxB2), and prostaglandin E2 excretion and on platelet aggregation was compared in untrained and trained subjects before and after low-dose aspirin administration (50 mg/day, 7 days). 2,3-Dinor-TxB2 excretion was significantly higher in the athletes at rest (P < 0.05). Submaximal exercise selectively increased 2,3-dinor-6-keto-PGF1 alpha excretion without affecting 2,3-dinor-TxB2 or prostaglandin E2 excretion rates or platelet aggregation. Low-dose aspirin inhibited platelet aggregation and 2,3-dinor-TxB2 excretion but reduced 2,3-dinor-6-keto-PGF1 alpha by only 24% in the untrained and by 51% in the trained subjects (P < 0.05). After low-dose aspirin administration, the selective stimulatory effect of submaximal exercise on urinary 2,3-dinor-6-keto-PGF1 alpha excretion was even more pronounced than before. The ratio of 2,3-dinor-6-keto-PGF1 alpha to 2,3-dinor-TxB2 was increased by exercise; this effect was significantly enhanced by low-dose aspirin (P < 0.05). Our results suggest that the stimulatory effect of submaximal exercise on prostacyclin production is mostly due to an activation of prostacyclin synthesis from endogenous precursors rather than the result of an enhanced endoperoxide shift from activated platelets to the endothelium. This effect is potentiated by low-dose aspirin pretreatment, indicating that 50 mg/day of aspirin do not impair exercise-induced endothelial prostacyclin production.

scholarly journals Lower incidence of hypertensive complications during pregnancy in patients treated with low-dose aspirin during in vitro fertilization and early pregnancy

2009 ◽  
Vol 24 (10) ◽  
pp. 2447-2450 ◽  
Author(s):  
M. J. Lambers ◽  
E. Groeneveld ◽  
D. A. Hoozemans ◽  
R. Schats ◽  
R. Homburg ◽  
...  
Keyword(s):  
In Vitro Fertilization ◽  
Early Pregnancy ◽  
Lower Incidence ◽  
Low Dose ◽  
Vitro Fertilization ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Cyclooxygenase-1 haplotype C50T/A-842G does not affect platelet response to aspirin

2009 ◽  
Vol 101 (04) ◽  
pp. 687-690 ◽  
Author(s):  
Caterina Pettinella ◽  
Mario Romano ◽  
Liborio Stuppia ◽  
Francesca Santilli ◽  
Rossella Liani ◽  
...  
Keyword(s):  
Low Dose ◽  
Ex Vivo ◽  
Aspirin Resistance ◽  
Platelet Response ◽  
Dose Aspirin ◽  
Cyclooxygenase 1 ◽  
Low Dose Aspirin ◽  
Induced Aggregation ◽  
Cox 1

SummaryCOX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment. Whether these polymorphisms exert an effect on response to aspirin both in vitro and ex vivo is still controversial. We geno-typed a population of 148 healthy individuals for the C50T/A-842G haplotype. Thirty of them underwent low-dose aspirin (100 mg daily) treatment for four weeks and were followed up for seven days after withdrawal. In this subgroup, we evaluated the thromboxane-dependence of biochemical and functional indexes used to monitor the antiplatelet effect of low-dose aspirin. Among the 148 subjects studied, 10 were heterozygous for the C50T/A-842G haplotype (6.7%) and only one was homozygous for the 50T/-842G haplotype (0.67%). In the group on low-dose aspirin, serum thromboxane (TX) B2 as well as urinary 11-dehydro-TXB2 and arachidonic acid (AA)-induced aggregation were similarly suppressed in carriers and non-carriers of the 50T/-842G haplotype, with an increase until basal levels of all the parameters within seven days after withdrawal. We found no relationship between the 50T/-842G haplotype and the so-called phenomenon of aspirin resistance. Platelet cyclooxygenase activity, as reflected by serum TXB2, was uniformly and persistently suppressed by low-dose aspirin in both carriers and non carriers of these polymorphisms.

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