Thromboembolic Complications Several Days After a Single-Dose Administration of Aspirin

Aguejouf, Omar; Belougne-Malfatti, Emmanuelle; Zoutremepuich, F; Belon, Philippe; Doutremépuich, Christian

doi:10.1016/s0049-3848(97)00302-2

Cited by 34 publications

(22 citation statements)

References 13 publications

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“…When injected in a single high dose, aspirin induces a marked decrease in NE and DE, as shown in the present study [19]. A second effect of this high dose is achieved approximately 8 days after a single injection, in which a clear pro-thrombotic state is observed with an increase in NE and DE [12,19]. Aspirin at 100 mg/kg induced a decreased thrombi formation.…”

Section: Discussionsupporting

confidence: 77%

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Paradoxical Thrombotic Effects of Aspirin: Experimental Study on 1000 Animals

Doutremépuich¹,

Aguejouf²,

Desplat³

et al. 2010

CHDDT

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COX 2 inhibition induced a pro-thrombotic effect that was antagonized by aspirin at 1 mg/kg or 100 mg/kg. The administration of the lowest aspirin doses induced a pro-thrombotic effect stronger than the antithrombotic effect of COX 1 selective inhibition. The mechanism of this last pro-thrombotic effect is induced by residual aspirin and is independent of COX 1 inhibition. This study may explain the cause of the paradoxical thrombo-embolic complications observed after aspirin discontinuation, an effect of residual aspirin rather than a rebound effect, and highlights the importance of low doses of substances as a barely studied source of side-effects.

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Section: Discussionsupporting

confidence: 77%

“…The hypothesis of a rebound effect of aspirin was studied in a previous publication in which thrombi generation was increased at days 8 and 10 after injection of a single high dose of aspirin in rats [12].…”

Section: Introductionmentioning

confidence: 99%

Paradoxical Thrombotic Effects of Aspirin: Experimental Study on 1000 Animals

Doutremépuich¹,

Aguejouf²,

Desplat³

et al. 2010

CHDDT

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“…Further experiments with selective COX blockers are needed to clarify whether the modifications in the ULDA effect produced by indomethacin, where platelet activity is increased but at the same time the shortening of IHT in the PHIAS group is blocked, are due to this contradictory action of the nonselective block of COX. Interestingly, aspirin showed a late prothrombotic effect after 8 days of discontinuation, similar to its ultralowdose effect [22] . This effect could be the cause of an increased risk of ischemic stroke [23] .…”

Section: Discussionmentioning

confidence: 88%

Modifications Produced by Indomethacin and <i>L</i>-NAME in the Effect of Ultralow-Dose Aspirin on Platelet Activity in Portal Hypertension

Eizayaga

Aguejouf

Desplat

et al. 2006

Pathophysiol Haemos Thromb

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In our previous study, we demonstrated the effect of ultralow-dose aspirin (ULDA) on platelet activity and bleeding in rats with portal hypertension (PHT) produced by portal vein ligation (PVL). This paper reports modifications in this effect caused by blocking NO production by nitro arginine methyl ester (NAME) and cyclooxygenase (COX) activity with indomethacin. PVL rats and sham-operated controls were treated with placebo, indomethacin or NAME and 30 min thereafter with placebo or ULDA treatment. Platelet activity was studied by a model of in vivo laser-induced thrombus production in the mesenteric circulation, induced hemorrhage time (IHT) and platelet aggregation ex vivo induced by adenosine diphosphate in an aggregometer. The PVL group receiving placebo showed a decreased platelet activity with prolonged IHT, an effect that was reversed by ULDA. Indomethacin induced a decreased platelet activity in the control rats and a prolonged IHT. In PHT with ULDA, in vivo platelet activity was enhanced but the normalization of IHT observed in rats without indomethacin was blunted. The addition of NAME normalized the diminished in vivo platelet aggregation and increased the IHT observed in PVL animals. These changes decreased the effect of ULDA in both sham-operated and PVL animals. The effect of indomethacin was more clearly modified by ULDA than the effect of NAME, thus suggesting that modifications in the COX pathway might alter the effect of ULDA. The simultaneous administration of indomethacin and ULDA could inhibit its beneficial effect on bleeding in rats with PHT.

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“…However, early spontaneous recanalization of an extracranial arterial occlusion (especially an IA occlusion) has rarely been reported. of aspirin administration, whereas an increased thromboembolic effect appears at eight to ten days after drug cessation due to new platelet formation with increased COX-1 activity and rebound inflammation (9)(10)(11). The studies of Sibon and Orgogozo (12) and Maulaz et al (13), have demonstrated that recent aspirin discontinuation is associated with increased stroke risk, with most strokes occurring between six and 10 days after aspirin cessation.…”

Section: Discussionmentioning

confidence: 99%