Disease | artery disease |
Phenotype | C0040053|thrombosis |
Sentences | 5 |
PubMedID- 20728084 | Impact of inflammatory markers on platelet inhibition and cardiovascular outcome including stent thrombosis in patients with symptomatic coronary artery disease. |
PubMedID- 25728646 | The sponsor sought approval for 2 indications: (1) in the setting of percutaneous coronary intervention for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with coronary artery disease and (2) in the setting of bridging therapy in patients with acute coronary syndrome or with stents who are at increased risk for thrombotic events (such as stent thrombosis) when oral p2y12 therapy is interrupted because of surgery. |
PubMedID- 24806382 | Stent thrombosis in patients with coronary artery disease treated with biodegradable polymer drug-eluting stents: an update meta-analysis. |
PubMedID- 21816733 | Fig 3 association between gain of function cyp2c19*17 polymorphisms with major adverse cardiovascular events (mace) or stent thrombosis in patients with coronary artery disease receiving clopidogrel treatment. |
PubMedID- 23170144 | The mainstay of such antithrombotic therapy (at) is low dose aspirin (lda).1 however, lda is an ulcerogenic agent that inhibits cyclooxygenase, thus increasing the risk of peptic ulcers and upper gastrointestinal bleeding (ugib).2-5 in addition, antithrombotic therapies are becoming more aggressive, and dual antiplatelet therapies, mainly combinations of lda with clopidogrel, have become standard treatment for preventing stent thrombosis in patients with coronary artery diseases who undergo coronary stenting with drug-eluting stents.6 importantly, combined antithrombotic therapies further increase the threat of ugib, compared with antiplatelet monotherapies.7-9 much attention has been paid to the gastrointestinal risks of antithrombotic therapies, and a statement regarding the prevention of upper gastrointestinal complications during at has recently been published.10 in addition, use of nonsteroidal antiinflammatory drugs (nsaids) is also known to increase the risk of ugib.3,8 although an increase in the incidence of ugib during antithrombotic/nsaid therapies has been extensively described, comparisons between the characteristics of hemorrhagic peptic ulcers in patients with and without such therapies are scarce, in particular regarding whether they are associated with an increased risk of massive bleeding and whether they can be treated endoscopically. |
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