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DOI: 10.4103/1947-489X.210880
Impact of selective cyclooxygenase-2 inhibition on the pathophysiology of atherosclerosis and unstable angina

Background: Selective COX-2 inhibitors (celecoxib) are effective anti-inflammatory drugs, though they may increase cardiovascular risk. Objectives: To verify the possible pathophysiological role of COX-2 inhibitors on experimental atherosclerosis and its clinical outcomes in patients with unstable angina (UA). Methods: Atherosclerosis was induced in twenty four Boscat rabbits and celecoxib was administered as a prophylactic and therapeutic agent. At the end of experiment, the animals were killed and their serum and aortic tissues were evaluated for lipid profile and histopathological examination. In the human study, forty UA patients (group I: received the usual regimen of UA and aspirin for 30 days and group II: additionally received celecoxib and ten controls were incorporated into the study. Estimation of CRP, IL-6 and lipid profiles was carried out at the baseline and 30 days after. Results: Celecoxib administration attenuated the progression of atherosclerosis. Also, after 30-days, group II of UA patients showed a significant reduction of inflammatory markers, risky lipids and CV events with a raise in HDL levels when compared to group I. Conclusion: Celecoxib has beneficial lowering effect on the levels of inflammatory markers, risky lipids and on the size of atheromatous patches. This may explain its potential role in decreasing CV events in UA patients.
Publikationsverlauf
Eingereicht: 07. Oktober 2010
Angenommen: 21. Januar 2011
Artikel online veröffentlicht:
23. Mai 2022
© 2011. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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