Cyclo-oxygenase-2 inhibitors versus non-selective non-steroidal anti-inflammatory drugs and congestive heart failure outcomes in elderly patients: a population-based cohort study

Mamdani, Muhammad; Juurlink, David N.; Lee, Douglas S.; Rochon, Paula A.; Kopp, Alex; Naglie, Gary; Austin, Peter C.; Laupacis, Andreas; Stukel, Thérèse A.

doi:10.1016/s0140-6736(04)16299-5

Cited by 388 publications

(221 citation statements)

References 20 publications

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“…In fact, we observed a significant resistance of HUVE cells to the pSUPER.retro viral infection in comparison with different types of human cancer cells, either CRC cells (HT29 and HCA7) and cervix carcinoma cells (HeLa). This observation indicates that endothelial cells are refractory to retroviral infection and suggests that this kind of virus-based approach might not affect the physiological prostaglandins production in vascular tissues, avoiding some of the well-known side effects coming from therapies based on selective COX-2 inhibitors (coxibs) (Ray et al, 2002;Fitzegerald, 2004;Horton, 2004;Mamdani et al, 2004;Oberholzer and Inamdar, 2004;Mitchell and Warner, 2005).…”

Section: Discussionmentioning

confidence: 99%

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

et al. 2006

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Silencing those genes that are overexpressed in cancer and contribute to the survival and progression of tumour cells is the aim of several researches. Cyclooxygenase-2 (COX-2) is one of the most intensively studied genes since it is overexpressed in most tumours, mainly in colon cancer. The use of specific COX-2 inhibitors to treat colon cancer has generated great enthusiasm. Yet, the side effects of some inhibitors emerging during long-term treatment have caused much concern. Genes silencing by RNA interference (RNAi) has led to new directions in the field of experimental oncology. In this study, we detected sequences directed against COX-2 mRNA, that potently downregulate COX-2 gene expression and inhibit phorbol 12-myristate 13-acetate-induced angiogenesis in vitro in a specific, nontoxic manner. Moreover, we found that the insertion of a specific cassette carrying anti-COX-2 short hairpin RNA sequence into a viral vector (pSUPER.retro) greatly increased silencing potency in a colon cancer cell line (HT29) without activating any interferon response. Phenotypically, COX-2 deficient HT29 cells showed a significant impairment of their in vitro malignant behaviour. Thus, the retroviral approach enhancing COX-2 knockdown, mediated by RNAi, proved to be an useful tool to better understand the role of COX-2 in colon cancer. Furthermore, the higher infection efficiency we observed in tumour cells, if compared to normal endothelial cells, may disclose the possibility to specifically treat tumour cells without impairing endothelial COX-2 activity.

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Section: Discussionmentioning

confidence: 99%

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

et al. 2006

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“…See Table S1 and Figure S1 for more information on the databases used in this study. These databases are routinely used for health services and pharmacoepidemiological research,13, 14, 15 and validation studies have shown them to be of high quality 16, 17, 18, 19. The institutional review boards at St. Michael's Hospital and Sunnybrook Health Science Center approved this study.…”

Section: Methodsmentioning

confidence: 99%

Association Between Statin Use and Cardiovascular Events After Carotid Artery Revascularization

Hussain

Saposnik

Raju

et al. 2018

JAHA

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BackgroundStatins are commonly used for the prevention of cardiovascular events; however, statins are underutilized in patients with noncoronary atherosclerosis. We sought to establish the rates of statin use in patients with carotid artery disease and to examine the association between statin therapy and outcomes after carotid revascularization.Methods and ResultsIn this population‐level retrospective cohort study, we identified all individuals aged ≥66 years who underwent carotid endarterectomy or stenting in Ontario, Canada (2002–2014). The primary outcome was a composite of 1‐year stroke, myocardial infarction, or death (major adverse cardiac and cerebrovascular events). Five‐year risks were also examined. Adjusted hazard ratios were computed using inverse probability of treatment weighting based on propensity scores. A total of 7893 of 10 723 patients (73.6%) who underwent carotid revascularization were on preprocedural statin therapy; moderate‐ or high‐dose therapy was utilized by 7384 patients (68.9%). The composite rate of 1‐year major adverse cardiac and cerebrovascular events was lower among statin users (adjusted hazard ratio: 0.76; 95% confidence interval, 0.70–0.83). Patients who were on persistent long‐term statin therapy after the carotid procedure continued to experience significantly lower risk of major adverse cardiac and cerebrovascular events at 5 years (adjusted hazard ratio: 0.75, 95% confidence interval, 0.71–0.80). The beneficial associations with statin use were observed regardless of type of carotid revascularization procedure, carotid artery symptom status, or statin dose.ConclusionsContinuous statin therapy was associated with a 25% lower risk of long‐term adverse cardiovascular events in patients with significant carotid disease. Along with other supportive evidence, statins should be considered in patients undergoing carotid revascularization, and efforts are required to increase statin use in this undertreated population.

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“…The development of the more specific COX-2 inhibitors was an effort to overcome this problem. Unfortunately, these drugs may increase the risk of cardiovascular diseases (10)(11)(12)(13)(14). Accordingly, there is a major therapeutic need for agents that retain the chemopreventive actions of NSAIDs, but that are devoid of their potential toxicities.…”

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confidence: 99%

Repression of β-catenin function in malignant cells by nonsteroidal antiinflammatory drugs

Cottam

Corr

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Activation of the Wnt͞␤-catenin pathway promotes the development of several cancers and is an attractive target for chemopreventive and chemotherapeutic agents. Nonsteroidal antiinflammatory drugs (NSAIDs) have been reported to antagonize ␤-catenin function, but their mechanism of action is not known. We demonstrate here that interference with ␤-catenin function by NSAIDs does not correlate with cyclooxygenase (COX) inhibition. Instead, NSAID inhibition of ␤-catenin requires the high level expression of peroxisome proliferator-activated receptor ␥ (PPAR-␥) and its coreceptor retinoid-X-receptor ␣ (RXR-␣). Immunoprecipitation experiments show that ␤-catenin interacts with RXR-␣ and PPAR-␥ in some malignant cells. Repression of ␤-catenin-dependent transcription by NSAIDs is thus indirect and depends on the coexpression of other nuclear receptors.peroxisome proliferator-activated receptor ␥ ͉ retinoid X receptor ␣

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Cyclo-oxygenase-2 inhibitors versus non-selective non-steroidal anti-inflammatory drugs and congestive heart failure outcomes in elderly patients: a population-based cohort study

Cited by 388 publications

References 20 publications

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

Association Between Statin Use and Cardiovascular Events After Carotid Artery Revascularization

Repression of β-catenin function in malignant cells by nonsteroidal antiinflammatory drugs

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