Cardiovascular risk, hypertension, and NSAIDs

被引:33
作者
White W.B. [1 ]
机构
[1] Division of Hypertension and Clinical Pharmacology, Pat and Jim Calhoun Cardiology Center, University of Connecticut School of Medicine, Farmington, CT 06030-3940
关键词
Celecoxib; Naproxen; Angiotensin Converting Enzyme Inhibitor; Rofecoxib; Parecoxib;
D O I
10.1007/s11926-007-0020-3
中图分类号
学科分类号
摘要
During the past 2 years, a great deal of evaluation has been conducted on the cardiovascular (CV) effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase (COX)-2 inhibitors. This review focuses on the effects of the NSAIDs and COX-2 inhibitors on blood pressure and CV events. Clinical trial databases for NSAIDs and COX-2 inhibitors have shown varying levels of destabilization of blood pressure control in treated hypertensive patients as well as variable incident rates of the development of arrhythmias, congestive heart failure, myocardial infarction, and stroke. Nonselective and COX-2 selective NSAIDs can be used carefully in arthritis patients with hypertension and stable CV disorders (excluding congestive heart failure and moderate to severe kidney dysfunction) when the individual clinical benefit of anti-inflammatory therapy outweighs the CV and gastrointestinal risk. Copyright © 2007 by Current Medicine Group LLC.
引用
收藏
页码:36 / 43
页数:7
相关论文
共 48 条
[31]  
Whelton A., Schulman G., Wallemark C., Et al., Effects of celecoxib and naproxen on renal function in the elderly, Arch Intern Med, 160, pp. 1465-1470, (2000)
[32]  
Whelton A., White W.B., Bello A.E., Et al., Effects of celecoxib and rofecoxib on blood pressure and edema in patients > or = 65 years of age with systemic hypertension and osteoarthritis, Am J Cardiol, 90, pp. 959-963, (2002)
[33]  
Qi Z., Hao C.M., Langenbach R.I., Et al., Opposite effects of cyclooxygenase-1 and -2 activity on the pressor response to angiotensin II, J Clin Invest, 110, pp. 61-69, (2002)
[34]  
Hermann M., Camici G., Fratton A., Et al., Differential effects of selecctive cyclooxygenase-2 inhibitors on endothelial function in salt-induced hypertension, Circulation, 108, pp. 2308-2311, (2003)
[35]  
Hermann M., Shaw S., Kiss E., Et al., Selective COX-2 inhibitors and renal injury in salt-sensitive hypertension, Hypertension, 45, pp. 193-197, (2005)
[36]  
Hinz B., Dormann H., Brune K., More pronounced inhibition of cyclooxygenase 2, increase in blood pressure, and reduction of heart rate by treatment with diclofenac compared with celecoxib and rofecoxib, Arthritis Rheum, 54, pp. 282-291, (2006)
[37]  
Winner L.K., Elliot D.J., Miners J.O., Knights K.M., In vitro glucoronidation of aldosterone by human liver and kidney cortical microsomes and recombinant UDP-glucuronosyltransferase (UCT) 287: Inhibition by non-steroidal anti-inflammatory drugs (NSAIDs), Proc Aust Soc Clin Exp Pharmacol Toxicol, 11, (2005)
[38]  
Knights K.M., Mangoni A.A., Minors J.O., Non-selective nonsteroidal anti-inflammatory drugs and cardiovascular events: Is aldosterone the silent partner in crime?, Br J Clin Pharmacol, 61, pp. 738-740, (2006)
[39]  
White W.B., Kent J., Taylor A., Et al., Effects of celecoxib on ambulatory blood pressure in hypertensive patients on ACE inhibitors, Hypertension, 39, pp. 929-934, (2002)
[40]  
Izhar M., Alausa T., Folker A., Et al., Effects of COX-inhibition on blood pressure and kidney function in ACE inhibitor-treated blacks and hispanics, Hypertension, 43, pp. 574-577, (2004)