Potential Cardiovascular Effects of COX-2 Selective Nonsteroidal Antiinflammatory Drugs

References

• Vane J R, Bakhle Y S, Botting R M. Cyclooxygenases 1 and 2. Annu Rev Pharmacol Toxicol 1998; 38: 97–120
   PubMed Web of Science ®Google Scholar
• Cheng Y, Austin S C, Rocca B, et al. Role of prostacyclin in the cardiovascular response to thromboxane A2. Science 2002; 296: 539–541
   PubMed Web of Science ®Google Scholar
• Fu J Y, Masferrer J L, Seibert K, Raz A, Needleman P. The induction and suppression of prostaglandin H2 synthase (cyclooxygenase) in human monocytes. J Biol Chem 1990; 265: 16737–16740
   PubMed Web of Science ®Google Scholar
• Kujubu D A, Fletcher B S, Varnum B C, Lim R W, Herschman H R. TIS10, a phorbol ester tumor promoter-inducible mRNA from Swiss 3T3 cells, encodes a novel prostaglandin synthase/cyclooxygenase homologue. J Biol Chem 1991; 266: 12866–12872
   PubMed Web of Science ®Google Scholar
• Smith W L, Langenbach R. Why are there two cyclooxygenase isoenzymes?. J Clin Invest 2001; 107: 1491–1495
   PubMed Web of Science ®Google Scholar
• Seibert K, Zhang Y, Leahy K, et al. Pharmacological and biochemical demonstration of the role of cyclooxygenase 2 in inflammation and pain. Proc Natl Acad Sci USA 1994; 91: 12013–12017
   PubMed Web of Science ®Google Scholar
• Iniguez M A, Pablos J L, Carreira P E, et al. Detection of COX-1 and COX-2 isoforms in synovial fluid cells from inflammatory joint diseases. Br J Rheumatol 1998; 37: 773–778
   PubMedGoogle Scholar
• Konno H, Baba M, Shoji M, et al. Cyclooxygenase-2 expression correlates with uPAR levels and is responsible for poor prognosis of colorectal cancer. Clin Exp Metastasis 2002; 19(6)527–534
   Google Scholar
• Fujita H, Koshida K, Keller E T, et al. Cyclooxygenase-2 promotes prostate cancer progression. Prostate Nov 1, 2002; 53(3)232–240
   Google Scholar
• Kim Y B, Kim G E, Cho N H, et al. Overexpression of cyclooxygenase-2 is associated with a poor prognosis in patients with squamous cell carcinoma of the uterine cervix treated with radiation and concurrent chemotherapy. Cancer Aug 1, 2002; 95(3)531–539
   Google Scholar
• Howe L R, Dannenberg A J. A role for cyclooxygenase-2 inhibitors in the prevention and treatment of cancer. Semin Oncol Jun, 2002; 29(3 Suppl 11)111–119
   Google Scholar
• Fitzgerald G A, Patrono C. The coxibs, selective inhibitors of cyclooxygenase-2. New Eng J Med 2001; 345: 433–442
   PubMed Web of Science ®Google Scholar
• Bombardier C, Laine L, Reicin A, et al. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. N Engl J Med 2000; 343: 1520–1528
   PubMed Web of Science ®Google Scholar
• Silverstein F E, Faich G, Goldstein J L, et al. for the Celecoxib Long-term Arthritis Safety Study. Gastrointestinal toxicity with celecoxib vs. nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: a randomized controlled trial. JAMA 2000; 284: 1247–1255
   PubMed Web of Science ®Google Scholar
• Schonbeck U, Sukhova G K, Graber P, Coulter S, Libby P. Augmented expression of cyclooxygenase-2 in human atherosclerotic lesions. Am J Pathol 1999; 155: 1281–1291
   PubMed Web of Science ®Google Scholar
• Fitz Gerald G A, Smith B, Pedersen A K, Brash A R. Increased prostacyclin biosynthesis in patients with severe atherosclerosis and platelet activation. N Engl J Med 1984; 310: 1065–1068
   Google Scholar
• Cullen L, Kelly L, Connor S O, Fitzgerald D J. Selective cyclooxygenase-2 inhibition by nimesulide in man. J Pharmacol Exp Ther 1998; 287: 578–582
   PubMed Web of Science ®Google Scholar
• Fitz Gerald GA, Brash A R, Falardeau P, Oates J A. Estimated rate of prostacyclin secretion into the circulation of normal man. J Clin Invest 1981; 68: 1272–1275
   Google Scholar
• Shinmura K, Tang X L, Wang Y, et al. Cyclooxygenase-2 mediates the cardio-protective effects of the late phase of ischemic preconditioning in conscious rabbits. Proc Natl Acad Sci USA 2000; 97: 10197–10202
   PubMed Web of Science ®Google Scholar
• Hennan J K, Huang J, Barrett T D, et al. Effects of selective cyclooxygenase-2 inhibition on vascular responses and thrombosis in canine coronary arteries. Circulation 2001; 104: 820–825
   PubMed Web of Science ®Google Scholar
• Hu Z W, Kerb R, Shi X Y, et al. Angiotensin II increases expression of cyclo-oxygenase-2: implications for the function of vascular smooth muscle cells. J Pharmacol Exp Ther Nov, 2002; 303(2)563–573
   Google Scholar
• Wort S J, Woods M, Warner T D, et al. Cyclooxygenase-2 acts as an endogenous brake on endothelin-1 release by human pulmonary artery smooth muscle cells: implications for pulmonary hypertension. Mol Pharmacol Nov, 2002; 62(5)1147–1153
   Google Scholar
• Baker C S, Hall R J, Evans T J, et al. Cyclooxygenase-2 is widely expressed in atherosclerotic lesions affecting native and transplanted human coronary arteries and co-localizes with inducible nitric oxide synthase and nitrotyrosine particularly in macrophages. Arterioscler Thromb Vasc Biol 1999; 19: 646–655
   PubMed Web of Science ®Google Scholar
• Alexander R W. Inflammation and coronary artery disease. N Engl J Med 1994; 331: 468–469
   PubMed Web of Science ®Google Scholar
• Ridker P M, Cushman M, Stampfer M J, Tracy R P, Hennekens C H. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973–979, [Erratum, N Engl J Med 1997;337: 356.]
   PubMed Web of Science ®Google Scholar
• Burleigh M E, Babaev V R, Oates J A, et al. Cyclooxygenase-2 promotes early atherosclerotic lesion formation in LDL receptor-deficient mice. Circulation 2002; 105: 1816–1823
   PubMed Web of Science ®Google Scholar
• Altman R, Luciardi H L, Muntaner J, et al. Efficacy of assessment of meloxicam, a preferential COX-2 inhibitor in acute coronary syndromes without ST-segment elevation: the NUT-2 pilot study. Circulation 2002; 106: 191–195
   PubMed Web of Science ®Google Scholar
• Rocca B, Secchiero P, Ciabattoni G, et al. Cyclooxygenase-2 expression is induced during human megakaryopoiesis and characterizes newly formed platelets. Proc Natl Acad Sci 2002; 99: 7634–7639
   PubMed Web of Science ®Google Scholar
• Cipollone F, Ciabattoni G, Patrignani P, et al. Oxidant stress and aspirin-insensitive thromboxane biosynthesis in severe unstable angina. Circulation 2000; 102: 1007–1013
   PubMed Web of Science ®Google Scholar
• Murata T, Ushikubi F, Matsuoka T, et al. Altered pain perception and inflammatory response in mice lacking prostacyclin receptor. Nature 1997; 388: 678–682
   PubMed Web of Science ®Google Scholar
• Patrono C. Aspirin as an antiplatelet drug. N Engl J Med 1994; 330: 1287–1294
   PubMed Web of Science ®Google Scholar
• Ridker P M, Rifai N, Rose L, Buring J E, Cook N R. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 2002; 347: 1557–1565
   PubMed Web of Science ®Google Scholar
• Marcus A J, Brockman M J, Drosopoulos J HF, et al. The endothelial cell ecto-ADPase responsible for inhibition of platelet function is CD39. J Clin Invest 1997; 99: 1351–1360
   PubMed Web of Science ®Google Scholar
• Lauer M S. Aspirin for primary prevention of coronary events. New Eng J Med 2002; 346: 1468–1474
   Google Scholar
• Gaspoz J-M, Coxson P G, Goldman P A, et al. Cost effectiveness of aspirin, clopidogrel, or both for secondary prevention of coronary heart disease. N Engl J Med 2002; 346: 1800–1806
   PubMed Web of Science ®Google Scholar
• Chesebro J H, Badimon J J. Platelet glycoprotein IIb/IIIa receptor blockade in unstable coronary disease. N Engl J Med 1998; 338: 1538–1541
   Google Scholar
• Pope J E, Anderson J J, Felson D T. A meta-analysis of the effects of nonsteroidal anti-inflammatory drugs on blood pressure. Arch Int Med 1993; 153: 477–484
   PubMed Web of Science ®Google Scholar
• Whelton A. Renal and related cardiovascular effects of conventional and COX-2-specific NSAIDs and non-NSAID analgesics. Am J Ther 2000; 7: 63–74
   PubMedGoogle Scholar
• Perazella M A, Tray K. Selective cyclooxygenase-2 inhibitors: a pattern of nephrotoxicity similar to traditional nonsteroidal anti-inflammatory drugs. Am J Med 2001; 111: 64–67
   PubMed Web of Science ®Google Scholar
• Brater D C, Harris C, Redfern J S, Gertz B J. Renal effects of COX-2-selective inhibitors. Am J Nephrol 2001; 21: 1–15
   PubMed Web of Science ®Google Scholar
• Whelton A, White W B, Bello A E, et al. Effects of celecoxib and rofecoxib on blood pressure and edema in patients 65 years of age with systemic hypertension and osteoarthritis. Am J Cardiol 2002; 90: 959–963
   PubMed Web of Science ®Google Scholar
• Geba G P, Weaver A L, Polis A B, et al. Efficacy of rofecoxib, celecoxib, and acetaminophen in osteoarthritis of the knee. A randomized trial. JAMA 2002; 287: 64–71
   PubMed Web of Science ®Google Scholar
• White W B, Kent J, Taylor A, et al. Effects of celecoxib on ambulatory blood pressure in hypertensive patients on ACE inhibitors. Hypertension 2002; 39: 929–934
   PubMed Web of Science ®Google Scholar
• Mukherjee D, Nissen S E, Topol E J. Risk of cardiovascular events associated with COX-2 inhibitors. JAMA 2001; 286: 954–959
   PubMed Web of Science ®Google Scholar
• Konstam M A, Weir M R, Reicin A, et al. Cardiovascular thrombotic events in controlled, clinical trials, of rofecoxib. Circulation 2001; 104: 2280–2288
   PubMed Web of Science ®Google Scholar
• Ray W A, Stein C M, Hall K. Non-steroidal anti-inflammatory drugs and risk of serious coronary heart disease: an observational cohort study. Lancet 2002; 359: 118–123
   PubMed Web of Science ®Google Scholar
• Solomon D H, Glynn R J, Levin R, Avorn J. Nonsteroidal anti-inflammatory drug use and acute myocardial infarction. Arch Intern Med 2002; 162: 1099–1104
   PubMed Web of Science ®Google Scholar
• Watson D J, Rhodes T, Cai B, Guess H A. Lower risk of thromboembolic cardiovascular events with naproxen among patients with rheumatoid arthritis. Arch Intern Med 2002; 162: 1105–1110
   PubMed Web of Science ®Google Scholar
• Rahme E, Pilote L, LeLorier J. Association between naproxen use and protection against acute myocardial infarction. Arch Intern Med 2002; 162: 1111–1115
   PubMed Web of Science ®Google Scholar
• Van Hecken A, Schwartz J I, Depre M, et al. Comparative inhibitory activity of rofecoxib, meloxicam, diclofenac, ibuprofen, and naproxen on COX-2 versus COX-1 in healthy volunteers. J Clin Pharmacol 2000; 40: 1109–1120
   PubMed Web of Science ®Google Scholar
• Reicin A S, Shapiro D, Sperling R S, et al. Comparison of cardiovascular thrombotic events in patients with osteroarthritis treated with rofecoxib versus nonselective nonsteroidal anti-inflammatory drugs (ibuprofen, diclofenac, and nabumetone). Am J Cardiol 2002; 89: 204–209
   PubMed Web of Science ®Google Scholar
• White W B, Faich G, Whelton A, et al. Comparison of thromboembolic events in patients treated with celecoxib, a cyclooxygenase-2 specific inhibitor, versus ibuprofen or diclofenac. Am J Cardiol 2002; 89: 425–430
   PubMed Web of Science ®Google Scholar
• Gabriel S E, Crowson C S, O'Fallon K P. Comorbidity in rheumatoid arthritis. J Rheumatol 1999; 26: 2475–2479
   PubMed Web of Science ®Google Scholar
• Riise T, Jacobsen B K, Gran J T, et al. Total mortality is increased in rheumatoid arthritis. A 17-year prospective study. Clin Rheumatol 2001; 20: 123–127
   PubMed Web of Science ®Google Scholar
• Watson D J, Rhodes T. Higher incidence of cardiovascular disease (CVD) with rheumatoid arthritis (RA) than osteoarthritis (OA) in the UK general practice research database (GPRD). [abstract]. Arthritis Rheum 2001; 449(suppl 90)5106
   Google Scholar
• McEntegart A, Capell H A, Creran C, et al. Cardiovascular risk factors, including thrombotic variables, in a population with rheumatoid arthritis. Rheumatol (Oxford) 2001; 40: 640–644
   PubMed Web of Science ®Google Scholar
• del Rincon I, Williams K, Stern P, et al. High incidence of cardiovascular events in a rheumatoid arthritis cohort not explained by traditional risk factors. Arthritis Rheum 2001; 44: 2737–2745
   PubMed Web of Science ®Google Scholar
• Bolten W W Scientific rationale for specific inhibition of COX-2. J Rheumatol 1998; 25(suppl 51)2–7
   Google Scholar
• Smalley W E, Griffin M R. The risks and costs of upper gastrointestinal disease attributable to NSAIDs. Gastroenterology Clin North Am 1996; 25: 373–398
   PubMed Web of Science ®Google Scholar
• Scheiman J M. NSAIDs, gastrointestinal injury, and cytoprotection. Gastroenterology Clin North Am 1996; 25: 279–298
   PubMed Web of Science ®Google Scholar
• Winzeler S, Rosenstein B D. Nonsteroidal anti-inflammatory drugs. AAOHN J 1998; 46: 253–259
   PubMedGoogle Scholar
• Singh G, Miller J D, Lee F H, et al. Prevalence of cardiovascular disease risk factors among US adults with self-reported osteoarthritis: data from the Third National Health and Nutrition Examination Survey (NHANES). Am J Manag Care 2002; 8(15 Suppl)S428–430
   Google Scholar
• Zhao S Z, Burke T A, Whelton A, et al. Comparison of the baseline cardiovascular risk profile among hypertensive patients prescribed COX-2-specific inhibitors or nonspecific NSAIDs: data from real-life practice. Am J Manag Care 2002; 8(15 Suppl)392–400
   Google Scholar
• Grundy S M, Pasternak R, Greenland P, et al. Assessment of cardiovascular risk by use of multiple-risk-factor assessment equations: a statement for healthcare professionals from the American Heart Association and the American College of Cardiology. Circulation 1999; 100: 1481–1492
   PubMed Web of Science ®Google Scholar
• Pearson T A, Blair S N, Daniels S R, et al. AHA Guidelines for Primary Prevention of Cardiovascular Disease and Stroke: 2002 Update: Consensus Panel Guide to Comprehensive Risk Reduction for Adult Patients Without Coronary or Other Atherosclerotic Vascular Diseases. American Heart Association Science Advisory and Coordinating Committee. Circulation Jul 16, 2002; 106(3)388–391
   PubMed Web of Science ®Google Scholar
• Hayden M, Pignone M, Phillips C, et al. Aspirin for the primary prevention of cardiovascular events: a summary of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2002; 136: 161–172
   PubMed Web of Science ®Google Scholar
• Stafford R S. Aspirin use is low among United States outpatients with coronary disease. Circulation 2000; 101: 1097–1101
   PubMed Web of Science ®Google Scholar
• Weil J, Colin-Jones D, Langman M, et al. Prophylactic aspirin and risk of peptic ulcer bleeding. BMJ 1995; 310: 827–830
   PubMed Web of Science ®Google Scholar
• De Abajo F J, Garcia R, Odriguez L A. Risk of upper gastrointestinal bleeding and perforation associated with low-dose aspirin as plain and enteric formulations. BMC Clinical Pharmacology 2001; 1: 1–8, accessed by internet Dec 2002 at www.biomedcentral.com/1472–6904/1/1)
   PubMedGoogle Scholar
• Catella-Lawson F, Reilly M P, Kapoor S C, et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med 2001; 345: 1809–1817
   PubMed Web of Science ®Google Scholar
• The National Institute for Clinical Excellence. “Guidance on the use of cyclo-oxygenase (Cox) II selective inhibitors, celecoxib, rofecoxib, meloxicam and etodolac for osteoarthritis and rheumatoid arthritis”. 2001, Accessed by internet Dec 2002 at www.nice.org.ukAppraisal No. 27
   Google Scholar
• The Australian CSI Working Group. Considerations for the safe prescribing and use of COX-2-specific inhibitors. The Medical Journal of Australia 2002; 176: 328–331
   Google Scholar
• Consensus Conference Report, Controversies in COX-2 Selective Inhibition. 2002. 29: 1501–1510, J Rheumatol
   Google Scholar
• Chan F KL, Chung S CS, Suen B Y, et al. Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen. New Eng J Med 2001; 344: 967–973
   PubMed Web of Science ®Google Scholar