Low-dose aspirin and subsequent peripheral arterial surgery in the Physicians' Health Study

Goldhaber, Samuel Z.; Manson, JE; Stampfer, Meir J.; Lamotte, F; Rosner, Bernard; Buring, Julie E.; Hennekens, C

doi:10.1016/0140-6736(92)93216-a

Cited by 149 publications

(49 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The Physicians' Health Study, a primary prevention study, found that 325 mg ASA taken every other day decreased the need for surgical peripheral arterial reconstructive surgery. However, no difference was observed between the ASA and the placebo group with respect to the development of intermittent claudication [4].…”

Section: Introductionmentioning

confidence: 92%

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

et al. 2009

View full text Add to dashboard Cite

Edelgard Lindhoff-Last. Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up. Annals of Hematology, Springer Verlag, 2009, 88 (10) Abstract Non-responsiveness to aspirin as detected by laboratory tests may identify patients at high risk for future vascular events. The aim of this prospective study was to evaluate whether non-responsiveness to aspirin is stable over time. Ninety-eight patients with stable peripheral arterial occlusive disease (PAOD) treated with 100 mg/d aspirin were followed over a median timeframe of 17 months. Platelet function tests were performed initially and at follow-up using arachidonic acid-induced light transmittance aggregometry (LTA) in native platelet-rich plasma with the Behring Coagulation Timer® and by measuring the collagen−epinephrine closure time (CT) on a Platelet Function Analyzer (PFA-100®). When determining platelet function using LTA, four patients (4.1%) had residual platelet function (i.e., MaxAggr ≥78%) despite aspirin treatment, whereas, according to the PFA-100® results, 12 patients (12.2%) were identified as nonresponders (i.e., CT <192 s). Fifty-seven patients who were still under treatment with 100 mg/d aspirin at the time of follow-up provided a second blood sample. Further platelet function tests with the PFA-100® system identified a persistent non-responsiveness to aspirin over time in three patients (5.3%) whereas four (7.0%) and 15 (26.3%) patients had changes in response status when platelet function was assessed by LTA and on the PFA-100®, respectively. We conclude that true non-responsiveness to aspirin is a rare phenomenon in stable PAOD patients.Furthermore, we conclude that in a number of patients, aspirin non-responsiveness is not stable over time.

show abstract

Section: Introductionmentioning

confidence: 92%

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Indeed, although the evidence that aspirin prevents thrombotic events is overwhelming (3), it is now quite evident that it does not affect the progression of atherosclerosis (15). The expression by platelets of CD40L may represent one mechanism of aspirin-insensitive platelet contribution to the progression of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Interaction with damaged vessel wall in vivo in humans induces platelets to express CD40L resulting in endothelial activation with no effect of aspirin intake

Giannini

Falcinelli

Bury

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Activated platelets express CD40L on their plasma membrane and release the soluble fragment sCD40L. The interaction between platelet surface CD40L and endothelial cell CD40 leads to the activation of endothelium contributing to atherothrombosis. Few studies have directly demonstrated an increased expression of platelet CD40L in conditions of in vivo platelet activation in humans, and no data are available on its relevance for endothelial activation. We aimed to assess whether platelets activated in vivo at a localized site of vascular injury in humans express CD40L and release sCD40L, whether the level of platelet CD40L expression attained in vivo is sufficient to induce endothelial activation, and whether platelet CD40L expression is inhibited by aspirin intake. We used the skin-bleeding-time test as a model to study the interaction between platelets and a damaged vessel wall by measuring CD40L in the blood emerging from a skin wound in vivo in healthy volunteers. In some experiments, shed blood was analyzed before and 1 h after the intake of 500 mg of aspirin. Platelets from the bleeding-time blood express CD40L and release soluble sCD40L, in a time-dependent way. In vivo platelet CD40L expression was mild but sufficient to induce VCAM-1 expression and IL-8 secretion in coincubation experiments with cultured human endothelial cells. Moreover, platelets recovered from the bleedingtime blood activated endothelial cells; an anti-CD40L antibody blocked this effect. On the contrary, the amount of sCD40L released by activated platelets at a localized site of vascular injury did not reach the concentrations required to induce endothelial cell activation. Soluble monocyte chemoattractant protein-1, a marker of endothelium activation, was increased in shed blood and correlated with platelet CD40L expression. Aspirin intake did not inhibit CD40L expression by platelets in vivo. We concluded that CD40L expressed by platelets in vivo in humans upon contact with a damaged vessel wall activates endothelium; aspirin treatment does not inhibit this mechanism. bleeding time; flow cytometry; atherosclerosis; platelet activation CD40L (CD154) IS A TRIMERIC TRANSMEMBRANE PROTEIN of the tumor necrosis factor family expressed on several cell types, including activated CD4 ϩ T cells, mast cells, basophils, eosinophils, smooth muscle cells, and activated platelets. CD40L and its membrane receptor, CD40, represent a system involved in cell communication, with CD40L inducing activation of CD40-expressing cells. This interaction mediates signals leading to responses that have a key role in immune activation, inflammation, atherosclerosis, and thrombosis.Platelets constitutively express CD40 on their plasma membrane, whereas CD40L, cryptic in resting platelets, is exposed at their surface upon activation (1) from where it is then cleaved, producing a soluble fragment released in the circulation, sCD40L (20).Platelet surface CD40L is proinflammatory and procoagulant and can induce the activation of normal endothelium by ligation of CD40 o...

show abstract

“…Klopidogrel v odmerku 75 mg/dan je bolnike s PAB v raziskavi CAPRIE bolje varoval pred srčno-žilnimi zapleti in srč-no-žilno smrtjo kot acetilsalicilna kislina (25). Manj podatkov imamo o učinku antiagregacijskega zdravljenja na napredovanje PAB, vendar je obsežna študi-ja primarne preventive pri ameriških zdravnikih pokazala, da je skupina, ki je jemala acetilsalicilno kislino, po petih letih potrebovala pol manj revaskularizacijskih posegov na perifernih arterijah kot skupina, ki je jemala placebo (26).…”

Section: Preprečevanje Srčno-žilnih Ishemičnih Dogodkovunclassified

Priporočila za odkrivanje in zdravljenje periferne arterijske bolezni

et al. 2017

View full text Add to dashboard Cite

show abstract

Low-dose aspirin and subsequent peripheral arterial surgery in the Physicians' Health Study

Cited by 149 publications

References 10 publications

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

Interaction with damaged vessel wall in vivo in humans induces platelets to express CD40L resulting in endothelial activation with no effect of aspirin intake

Priporočila za odkrivanje in zdravljenje periferne arterijske bolezni

Contact Info

Product

Resources

About