Statin use in acute coronary syndromes: cellular mechanisms and clinical evidence

被引:25
作者
Rosenson, RS
Brown, AS
机构
[1] Northwestern Univ, Dept Med, Prevent Cardiol Ctr, Div Cardiol,Feinberg Sch Med, Chicago, IL 60611 USA
[2] Midw Heart Res Fdn, Naperville, IL USA
[3] Midw Heart Dis Prevent Ctr, Naperville, IL USA
[4] Northwestern Univ, Prevent Cardiol Ctr, Div Cardiol, Dept Prevent Med,Feinberg Sch Med, Chicago, IL 60611 USA
关键词
statins; acute coronary syndromes; unstable atherosclerotic plaque; endothelial function; inflammatory mediators;
D O I
10.1097/00041433-200212000-00005
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Purpose of review Review the cellular mechanisms and clinical evidence for the use of statins in patients with unstable coronary syndromes. Recent findings Clinical trials of statin therapy in acute coronary syndromes demonstrate a rapid improvement in endothelial function, improved perfusion to ischemic myocardium, and an early reduction in cardiovascular events. The early benefit of statin therapy is related to a combination of molecular mechanisms that involve the oxidized LDL receptor (LOX-1), endothelial localized nitric oxide synthase, inflammatory cytokines, interstitial collagenases, and tissue factor expression. In human atheroma, 3 months' use of statin (pravastatin) therapy reduced the content of oxidized LDL, inflammatory cells (macrophage, T cells) infiltrates, and improved plaque stability by increasing the Collagen content of the fibrous cap. Summary The antiatherothrombotic effects of statin therapy appear to have important clinical relevance to patients with impaired myocardial perfusion and acute coronary syndrome.
引用
收藏
页码:625 / 630
页数:6
相关论文
共 52 条
[31]   Atorvastatin reduces NF-κB activation and chemokine expression in vascular smooth muscle cells and mononuclear cells [J].
Ortego, M ;
Bustos, C ;
Hernández-Presa, MA ;
Tuñón, J ;
Díaz, C ;
Hernández, G ;
Egido, J .
ATHEROSCLEROSIS, 1999, 147 (02) :253-261
[32]  
Ridker PM, 2001, CIRCULATION, V103, P1191
[33]   Long-term effects of pravastatin on plasma concentration of C-reactive protein [J].
Ridker, PM ;
Rifai, N ;
Pfeffer, MA ;
Sacks, F ;
Braunwald, E .
CIRCULATION, 1999, 100 (03) :230-235
[34]   Pluripotential mechanisms of cardioprotection with hmg-coa reductase inhibitor therapy [J].
Rosenson R.S. .
American Journal of Cardiovascular Drugs, 2001, 1 (6) :411-420
[35]   Antiatherothrombotic properties of statins - Implications for cardiovascular event reduction [J].
Rosenson, RS ;
Tangney, CC .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1998, 279 (20) :1643-1650
[36]   Inhibition of proinflammatory cytokine production by pravastatin [J].
Rosenson, RS ;
Tangney, CC ;
Casey, LC .
LANCET, 1999, 353 (9157) :983-984
[37]   Comparative study of HMG-CoA reductase inhibitors on fibrinogen [J].
Rosenson, RS ;
Tangney, CC ;
Schaefer, EJ .
ATHEROSCLEROSIS, 2001, 155 (02) :463-466
[38]   High-sensitivity C-reactive protein and cardiovascular risk in patients with coronary heart disease [J].
Rosenson, RS ;
Koenig, W .
CURRENT OPINION IN CARDIOLOGY, 2002, 17 (04) :325-331
[39]   Effects of lipids and lipoproteins on thrombosis and rheology [J].
Rosenson, RS ;
Lowe, GDO .
ATHEROSCLEROSIS, 1998, 140 (02) :271-280
[40]  
ROSENSON RS, 2002, LIPIDS ATHEROSCLEROS