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Journal ArticleDOI

Failure of antiplatelet and anticoagulant therapy to improve patency of grafts after coronary-artery bypass: a controlled, randomized study.

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TLDR
Postoperative treatment either with aspirin and dipyridamole or with warfarin failed to improve the patency of the grafts and no statistically significant differences were found in various clinical, hemodynamic and angios.
Abstract
Fifty patients who underwent aortocoronary saphenous-vein bypass-graft surgery were randomly assigned to one of three groups to determine the effects of antiplatelet or anticoagulant therapy on graft patency. Twenty-four patients served as controls; 13 patients received aspirin (325 mg three times a day) and dipyridamole (75 mg three times a day); and 13 patients received closely regulated warfarin therapy. Medications were begun on the third post-operative day. Six months after surgery, all patients underwent coronary angiography to assess graft patency. There were no statistically significant differences between groups in various clinical, hemodynamic and angios, 27 of 33 grafts (82 per cent) with aspirin and dipyridamole and 29 of 37 grafts (78 per cent) with warfarin (P less than 0.5), all patients had at least one patent graft. Postoperative treatment either with aspirin and dipyridamole or with warfarin failed to improve the patency of the grafts.

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Collaborative overview of randomized trials of antiplatelet therapy .1. prevention of death, myocardial-infarction, and stroke by prolonged antiplatelet therapy in various categories of patients

R Altman, +418 more
- 08 Jan 1994 - 
TL;DR: There was no appreciable evidence that either a higher aspirin dose or any other antiplatelet regimen was more effective than medium dose aspirin in preventing vascular events, so in each of the four main high risk categories overall mortality was significantly reduced.
Journal ArticleDOI

Comparing the Means of Several Groups

TL;DR: Investigators need to become better acquainted with statistical techniques for making multiple comparisons and use inappropriate statistical methods to analyze the differences between group means.
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Differential Inhibition by Aspirin of Vascular and Platelet Prostaglandin Synthesis in Atherosclerotic Patients

TL;DR: It is indicated that a low dose of aspirin (40 to 80 mg) can largely inhibit platelet aggregation and thromboxane synthesis but has much less effect on prostacyclin production in arterial and venous endothelium.
Journal ArticleDOI

Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study.

TL;DR: Coumadin was not show to be more effective than aspirin as adjunctive treatment after PTCA, while aspirin was shown to be superior to coumadin in patients with a longer history of angina.
References
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Journal ArticleDOI

Acetylation of prostaglandin synthase by aspirin

TL;DR: The results suggest that aspirin acts as an active-site acetylating agent for the enzyme cyclo-oxygenase, which may account for its anti-inflammatory and anti-platelet action.
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Modulation of human platelet adenylate cyclase by prostacyclin (PGX).

TL;DR: A model of platelet homeostasis is proposed that suggests platelet aggregation is controlled by a balance between the adenylate cyclase stimulating activity of prostacyclin, and the cAMP lowering activity of PGH2.
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Effects of prostacyclin (PGX) on cyclic AMP concentrations in human platelets

TL;DR: Prostacyclin (PGX) strikingly increases cyclic AMP concentrations in human platelets, and these results correlate well with the anti-aggregating activity of prostacyClin, compared with PGE1 and PGD2.
Journal ArticleDOI

Inhibition of platelet prostaglandin synthetase by oral aspirin.

TL;DR: Platelet cyclooxygenase is more sensitive to inactivation by aspirin than enzyme in sheep seminal vesicles, which suggests that oral aspirin also inactivated megakaryocyte cyclo oxygengenase.
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