Results 21 to 30 of about 47,972 (292)

Is clopidogrel better than aspirin following breakthrough strokes while on aspirin? A retrospective cohort study. [PDF]

open access: yes, 2014
ObjectiveThere is insufficient evidence on which to base a recommendation for optimal antiplatelet therapy following a stroke while on aspirin. The objective was to compare clopidogrel initiation vs aspirin reinitiation for vascular risk reduction among ...
Chang, Ku-Chou   +10 more
core   +1 more source

'Aspirin resistance' or treatment non-compliance: Which is to blame for cardiovascular complications?

open access: yesJournal of Translational Medicine, 2008
Aspirin is one of the 'cornerstone' drugs in our current management of cardiovascular disorders. However, despite the prescription of aspirin recurrent vascular events still occur in 10–20% of patients.
Shantsila Eduard, Lip Gregory YH
doaj   +1 more source

Potentiation of thrombus instability: a contributory mechanism to the effectiveness of antithrombotic medications [PDF]

open access: yes, 2018
© The Author(s) 2018The stability of an arterial thrombus, determined by its structure and ability to resist endogenous fibrinolysis, is a major determinant of the extent of infarction that results from coronary or cerebrovascular thrombosis.
A Gast   +66 more
core   +2 more sources

Aspirin resistance and ischemic heart disease on Iranian experience

open access: yesAdvanced Biomedical Research, 2012
Background: Coronary artery disease (CAD) and myocardial infarction are the most common causes of mortality and morbidity all over the world.
Masoumeh Sadeghi   +5 more
doaj   +1 more source

The association of four common polymorphisms from four candidate genes (COX-1, COX-2, ITGA2B, ITGA2) with aspirin insensitivity: a meta-analysis. [PDF]

open access: yesPLoS ONE, 2013
OBJECTIVE: Evidence is mounting suggesting that a strong genetic component underlies aspirin insensitivity. To generate more information, we aimed to evaluate the association of four common polymorphisms (rs3842787, rs20417, rs201184269, rs1126643) from ...
Zhiyuan Weng   +5 more
doaj   +1 more source

Aspirin resistance: causes, clinical significance, correction

open access: yesMìžnarodnij Endokrinologìčnij Žurnal, 2022
Aspirin is the most frequently prescribed antiplatelet agent today. It exerts its antiplatelet effect by irreversible inactivation of the platelet cyclooxygenase-1, resulting in an irreversible inhibition of thromboxane-A2 formation. The clinical benefit
G.F. Gendeleka, A.N. Gendeleka
doaj   +1 more source

Aspirin resistance in patients with ischemic stroke

open access: yesSouthern Clinics of Istanbul Eurasia, 2019
INTRODUCTION[|]Aspirin is the basic agent of antithrombotic treatment in ischemic cerebrovascular disease (CVD) patients. However several patients don't respond to treatment and therefore aspirin resistance term has been used lately.
Anıl Bulut   +4 more
doaj   +1 more source

Influence of low‐dose aspirin, resistance exercise, and sex on human skeletal muscle PGE2/COX pathway activity

open access: yesPhysiological Reports, 2021
Prostaglandin (PG) E2 has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects.
Masatoshi Naruse   +10 more
doaj   +1 more source

Assessing a 600-mg Loading Dose of Clopidogrel 24 Hours Prior to Pipeline Embolization Device Treatment [PDF]

open access: yes, 2018
Background: Clopidogrel/aspirin antiplatelet therapy routinely is administered 7-10 days before pipeline aneurysm treatment. Our study assessed the safety and efficacy of a 600-mg loading dose of clopidogrel 24 hours before Pipeline Embolization Device ...
Atallah, MD, Elias   +9 more
core   +2 more sources

Aspirin resistance: position paper of the Working Group on Aspirin Resistance [PDF]

open access: yesJournal of Thrombosis and Haemostasis, 2005
Aspirin irreversibly acetylates serine 529 of cyclooxygenase (COX)-1, resulting in inhibition of thromboxane A2 generation by platelets and prostacyclin by endothelial cells [1]. Because platelets lack the synthetic machinery to generate significant amounts of new COX, aspirin-induced COX-1 inhibition lasts for the lifetime of the platelet. In contrast,
MICHELSON AD   +10 more
openaire   +6 more sources

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