ArticleThe open cardiovascular medicine journal2010
COX-2 Inhibition by Use of Rofecoxib or High Dose Aspirin Enhances ADP-Induced Platelet Aggregation in Fresh Blood.
Article in The open cardiovascular medicine journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- The Impact of pre-operative aspirin administration on free flap survival rate in lower extremity reconstructio n.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Article
- Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression.Metabolic brain disease · 2012Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimIncreased cardiovascular risk after use of selective or nonselective cyclooxygenase-2 (COX-2)-inhibitors might partly be caused by enhanced platelet aggregability. However, an effect of COX-2 inhibition on platelets has so far not been observed in humans.
methodsWe tested in healthy volunteers the effect of COX-2-inhibition nearly in-vivo, i.e. immediately after and even during blood sampling.
resultsMeasurement within 2 minutes after venipuncture, but not 60 minutes later, showed that 50 mg of rofecoxib (n=12) or 500 (n=8) or 1000 (n=8) mg of aspirin increased ADP-induced platelet aggregation in a whole-blood aggregometer to, respectively, 152, 176 and 204 % of basal level (p<0.01). No significant differences in aggregability were observed after ingestion of 80 mg of aspirin (n=16), or placebo (n=8). Plasma 6-keto-PGF1α was decreased to 74 % after rofecoxib and to 76 and 70 % after 500 and 1000 mg of aspirin but did not change after low dose aspirin. Continuous photometrical measurement of aggregation in blood flowing from a cannulated vein revealed that high dose aspirin did not elicit aggregation by itself, but increased ADP-induced aggregation in proportion to the decrease in prostacyclin formation (r=0.68, p = 0.004). Since in these experiments thromboxane production was virtually absent, the enhanced aggregation after partial COX-2 inhibition was not caused by unopposed thromboxane formation.
conclusionsWe conclude that both selective and nonselective COX-2 inhibition enhances ADP-induced platelet aggregation in humans. This effect can only be detected during or immediately after venipuncture, possibly because of the short half-life of prostacyclin.
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