Are there potential non-lipid-lowering uses of statins?

被引:42
作者
Wheeler, DC [1 ]
机构
[1] Univ Hosp NHS Trust, Dept Nephrol, Birmingham, W Midlands, England
关键词
D O I
10.2165/00003495-199856040-00001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Recent clinical trials have demonstrated beyond doubt that statins are effective in the prevention of acute coronary events. Critical analysis of these studies suggests that the benefits of statin therapy cannot be fully explained on the basis of reductions in plasma cholesterol levels. Accumulating knowledge of the actions of these drugs shows that they may prevent several processes that eventually lead to plaque rupture and the development of occlusive thrombosis, the basis of acute coronary events. Hence, statins may correct endothelial dysfunction (thus protecting against ischaemic injury), stabilise existing plaques and modify the coagulation pathway, thereby reducing the likelihood of a sudden vascular event. At a cellular level, these drugs inhibit the synthesis not just of cholesterol, but of other compounds important in cell proliferation. Antiproliferative effects have been demonstrated in vitro and may broaden the applications of statins to the treatment of noncardiovascular diseases. Finally, preliminary clinical studies indicate that as a result of immunosuppressive actions, statins may reduce the incidence of rejection following organ transplantation.
引用
收藏
页码:517 / 522
页数:6
相关论文
共 50 条
[1]  
Andrews TC, 1997, CIRCULATION, V95, P324
[2]  
[Anonymous], 1993, Am J Cardiol, V72, P1031
[3]   CHANGES INDUCED BY PRAVASTATIN TREATMENT ON HEMOSTATIC AND FIBRINOLYTIC PATTERNS IN PATIENTS WITH TYPE IIB HYPERLIPOPROTEINEMIA [J].
AVELLONE, G ;
DIGARBO, V ;
CORDOVA, R ;
RANELI, G ;
DESIMONE, R ;
BOMPIANI, G .
CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL, 1994, 55 (11) :1335-1344
[4]   LOVASTATIN INHIBITS LOW-DENSITY-LIPOPROTEIN OXIDATION AND ALTERS ITS FLUIDITY AND UPTAKE BY MACROPHAGES - INVITRO AND INVIVO STUDIES [J].
AVIRAM, M ;
DANKNER, G ;
COGAN, U ;
HOCHGRAF, E ;
BROOK, JG .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1992, 41 (03) :229-235
[5]   Effect of pravastatin on angiographic restenosis after coronary balloon angioplasty [J].
Bertrand, ME ;
McFadden, EP ;
Fruchart, JC ;
VanBelle, E ;
Commeau, P ;
Grollier, G ;
Bassand, JP ;
Machecourt, J ;
Cassagnes, J ;
Mossard, JM ;
Vacheron, A ;
Castaigne, A ;
Danchin, N ;
Lablanche, JM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1997, 30 (04) :863-869
[6]   DISEASE-FREE INTERVALS AFTER PARTIAL ILEAL BYPASS IN PATIENTS WITH CORONARY HEART-DISEASE AND HYPERCHOLESTEROLEMIA - REPORT FROM THE PROGRAM ON THE SURGICAL CONTROL OF THE HYPERLIPIDEMIAS (POSCH) [J].
BUCHWALD, H ;
CAMPOS, CT ;
BOEN, JR ;
NGUYEN, PA ;
WILLIAMS, SE .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 26 (02) :351-357
[7]   REDUCTION IN CARDIOVASCULAR EVENTS DURING PRAVASTATIN THERAPY - POOLED ANALYSIS OF CLINICAL EVENTS OF THE PRAVASTATIN ATHEROSCLEROSIS INTERVENTION PROGRAM [J].
BYINGTON, RP ;
JUKEMA, JW ;
SALONEN, JT ;
PITT, B ;
BRUSCHKE, AV ;
HOEN, H ;
FURBERG, CD ;
MANCINI, J .
CIRCULATION, 1995, 92 (09) :2419-2425
[8]   P21RAS IS MODIFIED BY A FARNESYL ISOPRENOID [J].
CASEY, PJ ;
SOLSKI, PA ;
DER, CJ ;
BUSS, JE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (21) :8323-8327
[9]   RELATIONSHIP BETWEEN MEVALONATE PATHWAY AND ARTERIAL MYOCYTE PROLIFERATION - IN-VITRO STUDIES WITH INHIBITORS OF HMG-COA REDUCTASE [J].
CORSINI, A ;
MAZZOTTI, M ;
RAITERI, M ;
SOMA, MR ;
GABBIANI, G ;
FUMAGALLI, R ;
PAOLETTI, R .
ATHEROSCLEROSIS, 1993, 101 (01) :117-125
[10]   SUPPRESSION OF LYMPHOID-CELL FUNCTION-INVITRO BY INHIBITION OF 3-HYDROXY-3-METHYLGLUTARYL COENZYME-A REDUCTASE BY LOVASTATIN [J].
CUTTS, JL ;
BANKHURST, AD .
INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY, 1989, 11 (08) :863-869