Coxibs and cardiovascular disease.
By G. FitzGerald. New England Journal of Medicine, 2004
926 citations recorded by the source corpus.
Subfields: Biochemistry, Organic Chemistry, Pharmacology
View Paper: https://www.semanticscholar.org/paper/e337ccc320b605457a65c7f6d517c0d084598d1e
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In Biochemistry
In Organic Chemistry
In Pharmacology
Citations in the corpus
- [Guidelines on the management of stable angina pectoris: executive summary]. (2006, background): “Attenuation of prostacyclin formation may predispose to elevated blood pressure, accelerated atherogenesis, and thrombosis upon plaque rupture.(145) The recent withdrawal of rofecoxib (Vioxx), a highly selective COX-2 inhibitor, was caused by findings of an increased risk of serious coronary events ”
- The immune response in atherosclerosis: a double-edged sword (2006, background): “Indeed, treatment with NSAIDs selective for cyclooxygenase-2 seems to increase the risk of thrombotic complication”
- Soluble Epoxide Hydrolase as a Therapeutic Target for Cardiovascular Diseases (2009, background): “Indeed, aspirin and non-steroidal anti-inflammatory drugs (NSAIDs), including inhibitors of COX2 (also known as PTGS2), are effective drugs that treat pain and inflammatio”
- Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2–dependent mechanisms (2005, background): “The adverse effects of COX-2 inhibitors on cardiovascular events are thought to result from a perturbation of vascular homeostasis due to reduced synthesis of prostacycli”
- Effects of Nonsteroidal Antiinflammatory Drugs on Patient-controlled Analgesia Morphine Side Effects: Meta-analysis of Randomized Controlled Trials (2005, background): “Rofecoxib has been recently withdrawn from the market because of an increase in cardiovascular risk.(50) This risk was documented for long-term use of the drug.”
- Prostaglandins, NSAIDs, and gastric mucosal protection: why doesn't the stomach digest itself? (2008, background): “The cardiovascular toxicity of selective COX-2 inhibitors and possibly other NSAIDs has been suggested to be a consequence of the inhibition of the synthesis of prostacyclin (PGI2), which has antithrombotic properties, to an extent greater than inhibition of thromboxane (TxA2), which has prothrombot”