{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T00:12:10Z","timestamp":1758845530797},"reference-count":31,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2006,5,8]],"date-time":"2006-05-08T00:00:00Z","timestamp":1147046400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brit J Clinical Pharma"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:sec><jats:title>Aims<\/jats:title><jats:p>To investigate the relationship between acute coronary syndrome (ACS) and ingested doses of selective cyclooxygenase\u20102 (COX\u20102) inhibitors and other nonsteroidal anti\u2010inflammatory drugs (NSAIDs).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Case\u2013control study, commenced August 2003. Cases were patients admitted to hospital with ACS (myocardial infarction\/unstable angina). Controls were hospital patients admitted for reasons other than acute vascular ischaemia or conditions that are believed to be complications of treatment with COX\u20102 inhibitors or NSAIDs. Structured interviews were undertaken within 7\u2003days of admission, collecting information on cardiovascular events and risk factors and all ingested drugs, including the doses of COX\u20102 inhibitors and NSAID consumed in the previous week and month.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>An interim analysis of the data was conducted in late 2004 to inform a review of the COX\u20102 inhibitors by the Australian drug regulatory agency. Between August 2003 and October 2004, we recruited 328 ACS cases and 478 controls. With non\u2010use of COX\u20102 inhibitors or NSAIDs as the reference the adjusted odds ratios (OR) for ACS were: celecoxib 1.11 (95% confidence interval 0.59, 2.11), rofecoxib 0.63 (0.31, 1.28) and other NSAIDs 0.67 (0.41, 1.09). Among control subjects, median daily ingested doses of celecoxib and rofecoxib were 200\u2003mg and 13.4\u2003mg, respectively. Using these to stratify risk, adjusted ORs for ACS were: \u2018low\u2019 dose (&lt;\u2003median) 0.44 (0.19, 1.03); \u2018high\u2019 dose (\u2265\u2003median) 1.22 (0.67, 2.21). A test for interaction across doses was statistically significant, OR 2.8 (1.0, 7.7), suggesting that at low doses, COX\u20102 inhibitors may be protective, becoming risk\u2010inducing only at higher doses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The possibility that the gradient of cardiovascular risk with COX\u20102 inhibitors runs from protective to risk\u2010inducing has biological plausibility and merits further investigation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2125.2006.02660.x","type":"journal-article","created":{"date-parts":[[2006,5,8]],"date-time":"2006-05-08T16:34:05Z","timestamp":1147106045000},"page":"358-365","source":"Crossref","is-referenced-by-count":24,"title":["Cyclooxygenase\u20102 inhibitors and coronary occlusion \u2013 exploring dose\u2013response relationships"],"prefix":"10.1111","volume":"62","author":[{"given":"Patricia","family":"McGettigan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pearline","family":"Han","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Henry","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,5,8]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(05)17864-7"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(04)17514-4"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa050493"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa050405"},{"key":"e_1_2_6_6_2","first-page":"85","article-title":"Both selective COX\u20102 inhibitors and non\u2010selective NSAIDs increase the risk of acute myocardial infarction in patients with arthritis: selectivity is with the patient, not the drug class","volume":"64","author":"Singh G","year":"2005","journal-title":"Ann Rheum Dis"},{"key":"e_1_2_6_7_2","first-page":"S57","article-title":"Cardiovascular events during use of COX\u20102 selective and non\u2010selective NSAIDs","volume":"14","author":"Sturkenboom MCJM","year":"2005","journal-title":"Pharmacoepidemiol Drug Saf"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.330.7504.1366"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.165.9.978"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-142-7-200504050-00113"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-142-3-200502010-00005"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000127578.21885.3E"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.163.4.481"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)11131-7"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.165.2.181"},{"key":"e_1_2_6_16_2","doi-asserted-by":"publisher","DOI":"10.5694\/j.1326-5377.2003.tb05616.x"},{"key":"e_1_2_6_17_2","volume-title":"Pharmaceutical Benefits Schedule Item Statistics.","year":"2006"},{"key":"e_1_2_6_18_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2125.2002.01637.x"},{"key":"e_1_2_6_19_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.162.10.1099"},{"key":"e_1_2_6_20_2","first-page":"1488","article-title":"Platelet receptor inhibition in ischaemic syndrome management in patients limited by unstable signs and symptoms. 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