Lipid-lowering therapies in the management of acute coronary syndromes

被引：13

作者：

Mosca L. ^{[1
]}

Biviano A. ^{[1
]}

机构：

[1] Preventive Cardiology Program, New York-Presbyterian Hospital, Columbia University, New York, NY 10032

来源：

Current Cardiology Reports | 2002年 / 4卷 / 4期

关键词：

Statin; Acute Coronary Syndrome; Simvastatin; Atorvastatin; Pravastatin;

D O I：

10.1007/s11886-002-0068-7

中图分类号：

学科分类号：

摘要：

Despite the significant advances made in the treatment of acute coronary syndromes (ACS) with antiplatelet and antithrombotic therapy, the risk of serious complications remains high, especially in the first few months following an acute coronary event. Although lipid-lowering therapy in patients with significant risk factors (primary prevention) or stable coronary disease (secondary prevention) is known to improve long-term survival, patients with a recent ACS were specifically excluded from the early statin trials. However, the use of lipid-lowering agents (principally statins) during hospitalization or in the period immediately following an acute coronary event has recently been studied. Statin therapy in this setting has been shown to reduce angina, rehospitalization, and mortality. Improved outcomes associated with lipid-lowering therapy in ACS may be mediated through beneficial effects on plaque stabilization, endothelial function, inflammation, and thrombus formation. This paper reviews the evidence supporting the potential benefits and mechanisms of statin therapy in the management of ACS. Clinical guidelines to achieve optimal lipid management are also discussed. Copyright © 2002 by Current Science Inc.

引用

页码：320 / 326

页数：6

共 53 条

[21] Marchesi S., Lupattelli G., Siepi D., Et al., Short-term atorvastatin treatment improves endothelial function in hypercholesterolemic women, J Cardiovasc Pharmacol, 36, pp. 617-621, (2000)
[22] Tannous M., Chenung R., Vignini A., Mutus B., Atorvastatin increases ecNOS levels in human platelets of hyperlipidemic subjects, Thromb Haemost, 82, pp. 1390-1394, (1999)
[23] Davis M.E., Harrison D.G., Cracking down on caveolin. role of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors in modulating endothelial cell nitric oxide production, Circulation, 103, pp. 2-4, (2001)
[24] Bustos C., Hernandez-Presa A., Ortego M., Et al., HMG-CoA reductase inhibition by atorvastatin reduces neointimal inflammation in a rabbit model of atherosclerosis, J Am Coll Cardiol, 32, pp. 2057-2064, (1998)
[25] Bickel C., Rupprecht H.J., Blankenberg S., Et al., Influence of HMG-CoA reductase inhibitors on markers of coagulation, systemic inflammation and soluble cell adhesion, Int J Cardiol, 82, pp. 25-31, (2002)
[26] Inoue I., Goto S., Mizotani K., Et al., Lipophilic HMG-CoA reductase inhibitor has an anti-inflammatory effect. reduction of MRNA levels for interleukin-1beta, interleukin-6, cyclooxygenase-2, and p22phox by regulation of peroxisome proliferator-activated receptor alpha (PPARalpha) in primary endothelial cells, Life Sci, 67, pp. 863-876, (2000)
[27] Brull D.J., Sanders J., Rumley A., Et al., Statin therapy and the acute inflammatory response after coronary artery bypass grafting, Am J Cardiol, 88, pp. 431-433, (2001)
[28] Ridker P.M., Rifai N., Lewenthal S.P., Rapid reduction in C-reactive protein with cerivastatin among 785 patients with primary hypercholesterolemia, Circulation, 102, pp. 1191-1193, (2001)
[29] Jilial I., Stein D., Balis D., Et al., Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive Creactive protein levels, Circulation, 103, pp. 1933-1935, (2001)
[30] Koh K.K., Effects of HMG-CoA reductase inhibitor on hemostatis, Int J Cardiol, 76, pp. 23-32, (2000)

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