Low-dose and high-dose acetylsalicylic acid for patients undergoing carotid endarterectomy: a randomised controlled trial

Taylor, D. Wayne; Barnett, H. J. M.; Haynes, R. Brian; Ferguson, Gary G.; Sackett, David L.; Thorpe, Kevin E.; Simard, Denis; Silver, Frank L.; Hachinski, Vladimir; Clagett, G. Patrick; Barnes, Robert W.; Spence, J. David

doi:10.1016/s0140-6736(99)05388-x

Cited by 507 publications

(272 citation statements)

References 18 publications

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“…42 Moreover, a recent study that showed greater efficacy in stroke prevention with a lower dose of aspirin suggests a role for endogenous PGI 2 . 43 Thus, the reduction in PGI2 formation seen with a COX-2 inhibitor in the presence of normal TXA 2 formation may place patients at an increased risk of thrombosis. However, it should be emphasized that the findings for the present study group of severely diseased patients may not be applicable to patients with in more modest disease state.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-1 and -2–Dependent Prostacyclin Formation in Patients With Atherosclerosis

et al. 2000

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Background-The formation of prostacyclin (PGI 2 ), thromboxane (TX) A 2 , and isoprostanes is markedly enhanced in atherosclerosis. We examined the relative contribution of cyclooxygenase (COX)-1 and -2 to the generation of these eicosanoids in patients with atherosclerosis. Methods and Results-The study population consisted of 42 patients with atherosclerosis who were undergoing surgical revascularization. COX-2 mRNA was detected in areas of atherosclerosis but not in normal blood vessel walls, and there was evidence of COX-1 induction. The use of immunohistochemical studies localized the COX-2 to proliferating vascular smooth muscle cells and macrophages. Twenty-four patients who did not previously receive aspirin were randomized to receive either no treatment or nimesulide at 24 hours before surgery and then for 3 days. Eighteen patients who were receiving aspirin were continued on a protocol of either aspirin alone or a combination of aspirin and nimesulide. Urinary levels of 11-dehydro-TXB 2 and 2,3-dinor-6-keto-PGF 1␣ , metabolites of TXA 2 and PGI 2 , respectively, were elevated in patients with atherosclerosis compared with normal subjects (3211Ϯ533 versus 679Ϯ63 pg/mg creatinine, PϽ0.001; 594Ϯ156 versus 130Ϯ22 pg/mg creatinine, PϽ0.05, respectively), as was the level of the isoprostane 8-iso-PGF 2␣ . Nimesulide reduced 2,3-dinor-6-keto-PGF 1␣ excretion by 46Ϯ5% (378.3Ϯ103 to 167Ϯ37 pg/mg creatinine, PϽ0.01) preoperatively and blunted the increase after surgery. Nimesulide had no significant effect on 11-dehydro-TXB 2 before (2678Ϯ694 to 2110Ϯ282 pg/mg creatinine) or after surgery. The levels of both products were lower in patients who were taking aspirin, and no further reduction was seen with the addition of nimesulide. None of the treatments influenced urinary 8-iso-PGF 2␣ excretion. Conclusions-Both COX-1 and -2 are expressed and contribute to the increase in PGI 2 in patients with atherosclerosis, whereas TXA 2 is generated by COX-1. (Circulation. 2000;102:840-845.)

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Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-1 and -2–Dependent Prostacyclin Formation in Patients With Atherosclerosis

et al. 2000

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“…Ponieważ endarterektomia minimalizuje potrzebę łączenia OAC z leczeniem przeciwpłytkowym [1030], to takie podejście mogłoby być korzystne u pacjentów z AF w celu obniżenia ryzyka krwawienia. Pacjentów z AF włączano jednak do niewielu z tych badań.…”

Section: Konkurencyjne Przyczyny Udaruunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

2,399

4,206

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“…17 Because 75 mg daily is at least twice as high as the lowest dose necessary and sufficient to fully inhibit platelet COX-1 activity, there are no significant differences in the antiplatelet effects of doses ranging between 75 and 100 mg. 17 Randomized comparisons of higher vs lower aspirin doses in patients with ACS 30 and cerebrovascular disease 31,32 showed no evidence of superiority of higher vs lower doses of aspirin. 17 Although aspirin 325 mg can be used as a loading dose in the setting of ACS or acute ischemic stroke, prescribing aspirin 325 mg daily for long-term treatment does not produce any additional benefit, while exposing the patient to unnecessary possible side effects: gastrointestinal damage, bleeding complications, and possibly negative interactions with ticagrelor.…”

Section: Casementioning

confidence: 99%

How I use laboratory monitoring of antiplatelet therapy

Michelson

Bhatt

2017

Blood

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Antiplatelet therapy is of proven benefit in coronary artery disease and a number of other clinical settings. This article reviews platelet function, molecular targets of antiplatelet agents, and clinical indications for antiplatelet therapy before focusing on a frequent question to hematologists about the 2 most commonly used antiplatelet therapies: Could the patient be aspirin “resistant” or clopidogrel “resistant”? If so, should results of a platelet function test be used to guide the dose or type of antiplatelet therapy? Whether such guided therapy is of clinical benefit to patients has been a source of controversy. The present article reviews this subject in the context of 2 prototypical clinical cases. Available evidence does not support the use of laboratory tests to guide the dose of aspirin or clopidogrel in patients with so-called aspirin or clopidogrel “resistance.”

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Low-dose and high-dose acetylsalicylic acid for patients undergoing carotid endarterectomy: a randomised controlled trial

Cited by 507 publications

References 18 publications

Cyclooxygenase-1 and -2–Dependent Prostacyclin Formation in Patients With Atherosclerosis

Cyclooxygenase-1 and -2–Dependent Prostacyclin Formation in Patients With Atherosclerosis

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

How I use laboratory monitoring of antiplatelet therapy

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