Aspirin Selectively Inhibits Prostaglandin Production in Human Platelets

Smith, J B; Willis, A.L.

doi:10.1038/newbio231235a0

Cited by 1,266 publications

(453 citation statements)

References 21 publications

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“…[1][2][3][4][5][6] Thromboxane A 2 stimulates platelet recruitment, activation, aggregation and vasoconstriction. The ASA-induced inhibition lasts for the life of the platelet, or about 7-10 days.…”

Section: Introductionmentioning

confidence: 99%

A Randomized, Quadruple Crossover Single-Blind Study on Immediate Action of Chewed and Unchewed Low-Dose Acetylsalicylic Acid Tablets in Healthy Volunteers

Sai

Kusaka

Imanishi

et al. 2011

Journal of Pharmaceutical Sciences

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Section: Introductionmentioning

confidence: 99%

A Randomized, Quadruple Crossover Single-Blind Study on Immediate Action of Chewed and Unchewed Low-Dose Acetylsalicylic Acid Tablets in Healthy Volunteers

Sai

Kusaka

Imanishi

et al. 2011

Journal of Pharmaceutical Sciences

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“…Aspirin alters prostaglandin metabolism and irreversibly inhibits cyclooxygenase-1, suppressing thromboxane A 2 synthesis, and thus platelet function [7,8]. It is an effective antithrombotic agent even at low doses (50-100 mg/day and possibly lower) [9].…”

Section: Pharmacologymentioning

confidence: 99%

Modified-Release Dipyridamole Combined with Aspirin for Secondary Stroke Prevention

Diener

2005

Aging Health

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Patients suffering from transient ischemic attack (TIA) or ischemic stroke have a high risk of suffering a first or recurrent stroke, with an annual risk of between 5 and 15%. The European Stroke Prevention Study (ESPS)2 was a randomized, double-blind, placebocontrolled trial involving 6602 patients with TIA or stroke comparing aspirin alone (50 mg daily), modified-release (MR) dipyridamole alone (200 mg twice daily), aspirin plus dipyridamole, and placebo. The 2-year relative risk reduction of stroke in the aspirin plus MR-dipyridamole group (37.0%) was significantly higher than in either the aspirin group (18.1%) or the MR-dipyridamole group (16.3%). The results of the comparison between aspirin plus MR-dipyridamole versus placebo confirmed the findings of ESPS1. The results of ESPS2 were at odds with all prior trials with dipyridamole alone or in association with aspirin, but it was also the only trial sufficiently powered to show a significant difference. For this reason, a meta-analysis was performed based on a systematic review of individual patient data from randomized controlled trials involving dipyridamole in patients with prior ischemic stroke or TIA. Recurrent stroke was reduced by dipyridamole compared with placebo, and by combined aspirin and dipyridamole versus aspirin alone, dipyridamole alone or placebo. In two post hoc analyses the efficacy of aspirin plus extended-release dipyridamole was compared with aspirin alone for the prevention of recurrent stroke among high-risk groups. Stroke models from the Framingham Study and the Stroke Prognostic Instrument II were applied to subjects in ESPS2 to assign patients to risk groups. Compared with aspirin alone, aspirin plus MR-dipyridamole demonstrated a more pronounced efficacy in reducing the risk for stroke and vascular events among patients younger than 70 years of age, with hypertension, or prior stroke; current smokers; and those with any prior cardiovascular disease. Another model (Essen risk score) showed that patients with a high risk of recurrent stroke show a much greater benefit from aspirin plus MR-dipyridamole compared with aspirin monotherapy than patients with a low risk.Annually, 15 million people worldwide suffer a stroke, of whom 5 million die and 5 million are permanently disabled [1]. The age-related incidence of stroke is declining in many developed countries, largely as a result of the control of risk factors such as high blood pressure and smoking. The absolute number of strokes continue to increase because of the aging population. For example, stroke is the biggest single cause of disability in the UK. People who have an ischemic stroke or transient ischemic attack (TIA) are at high risk of a second stroke [2], although this risk ranges from approximately 5% to around 20% per year [3,4]. The recurrence risk is highest in the first few days after a TIA or stroke and declines with time. Such second strokes often cause substantial disability and greatly reduce quality of life.Evidence-based improvements to the prevention of second...

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“…Agents that inhibit signaling via the thromboxane and ADP receptors are effective antithrombotic drugs (33,34). Given thrombin's remarkable potency as a platelet activator and its ability to activate even aspirin-treated platelets (35,36), blockade of thrombin signaling in platelets might also prove to be a useful strategy for preventing thrombosis. Because inhibition of PAR1 alone markedly attenuated platelet responses at low concentrations of thrombin, PAR1 antagonism might be sufficient for an antithrombotic effect.…”

Section: Figurementioning

confidence: 99%

Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin

Kahn

Nakanishi‐Matsui²,

Shapiro³

et al. 1999

J. Clin. Invest.

754

628

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Aspirin Selectively Inhibits Prostaglandin Production in Human Platelets

Cited by 1,266 publications

References 21 publications

A Randomized, Quadruple Crossover Single-Blind Study on Immediate Action of Chewed and Unchewed Low-Dose Acetylsalicylic Acid Tablets in Healthy Volunteers

A Randomized, Quadruple Crossover Single-Blind Study on Immediate Action of Chewed and Unchewed Low-Dose Acetylsalicylic Acid Tablets in Healthy Volunteers

Modified-Release Dipyridamole Combined with Aspirin for Secondary Stroke Prevention

Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin

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