Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels

被引:1084
作者
Ridker, PM
Rifai, N
Pfeffer, MA
Sacks, FM
Moye, LA
Goldman, S
Flaker, GC
Braunwald, E
机构
[1] Brigham & Womens Hosp, Div Cardiovasc Dis, Dept Med, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA USA
[3] Childrens Hosp, Med Ctr, Houston, TX USA
[4] Univ Texas, Sch Publ Hlth, Houston, TX USA
[5] Vet Adm Med Ctr, Tucson, AZ 85723 USA
[6] Univ Missouri, Columbia, MO USA
关键词
C-reactive protein; serum amyloid A; myocardial infarction; atherosclerosis; cholesterol;
D O I
10.1161/01.CIR.98.9.839
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-We studied whether inflammation after myocardial infarction (MI) is a risk factor for recurrent coronary events and whether randomized treatment with pravastatin reduces that risk. Methods and Results-A nested case-control design was used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood samples from 391 participants in the Cholesterol and Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal coronary event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (control subjects). Overall, CRP and SAA were higher among cases than control subjects (for CRP P=0.05; for SAA P=0.006) such that those with levels in the highest quintile had a relative risk (RR) of recurrent events 75% higher than those with levels in the lowest quintile (for CRP RR=1.77, P=0.02; for SAA RR=1.74, P=0.02). The study group with the highest risk was that with consistent evidence of inflammation (elevation of both CRP and SAA) who were randomly assigned to placebo (RR=2.81, P=0.007); this risk estimate was greater than the product of the individual risks associated with inflammation or placebo assignment alone. In stratified analyses, the association between inflammation and risk was significant among those randomized to placebo (RR=2.11, P=0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P=0.5), Conclusions-Evidence of inflammation after MI is associated with increased risk of recurrent coronary events. Therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent.
引用
收藏
页码:839 / 844
页数:6
相关论文
共 34 条
[1]   THE EFFECT OF CHOLESTEROL-LOWERING AND ANTIOXIDANT THERAPY ON ENDOTHELIUM-DEPENDENT CORONARY VASOMOTION [J].
ANDERSON, TJ ;
MEREDITH, IT ;
YEUNG, AC ;
FREI, B ;
SELWYN, AP ;
GANZ, P .
NEW ENGLAND JOURNAL OF MEDICINE, 1995, 332 (08) :488-493
[2]   ELEVATION OF C-REACTIVE PROTEIN IN ACTIVE CORONARY-ARTERY DISEASE [J].
BERK, BC ;
WEINTRAUB, WS ;
ALEXANDER, RW .
AMERICAN JOURNAL OF CARDIOLOGY, 1990, 65 (03) :168-172
[3]   SERUM AMYLOID-A PROTEIN IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION [J].
CASL, MT ;
SURINA, B ;
GLOJNARICSPASIC, I ;
PAPE, E ;
JAGARINEC, N ;
KRANJCEVIC, S .
ANNALS OF CLINICAL BIOCHEMISTRY, 1995, 32 :196-200
[4]   Inhibitor of proliferation of arterial smooth-muscle cells by fluvastatin [J].
Corsini, A ;
Pazzucconi, F ;
Pfister, P ;
Paoletti, R ;
Sirtori, CR .
LANCET, 1996, 348 (9041) :1584-1584
[5]   Non-lipid-related effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors [J].
Corsini, A ;
Bernini, F ;
Quarato, P ;
Donetti, E ;
Bellosta, S ;
Fumagalli, R ;
Paoletti, R ;
Soma, VMR .
CARDIOLOGY, 1996, 87 (06) :458-468
[6]  
DEBEER FC, 1982, BRIT HEART J, V47, P239
[7]   REDUCTION IN SERUM-CHOLESTEROL WITH PRAVASTATIN IMPROVES ENDOTHELIUM-DEPENDENT CORONARY VASOMOTION IN PATIENTS WITH HYPERCHOLESTEROLEMIA [J].
EGASHIRA, K ;
HIROOKA, Y ;
KAI, H ;
SUGIMACHI, M ;
SUZUKI, S ;
INOU, T ;
TAKESHITA, A .
CIRCULATION, 1994, 89 (06) :2519-2524
[8]  
Haverkate F, 1997, LANCET, V349, P462, DOI 10.1016/S0140-6736(96)07591-5
[9]   PRAVASTATIN INHIBITS CELLULAR CHOLESTEROL-SYNTHESIS AND INCREASES LOW-DENSITY-LIPOPROTEIN RECEPTOR ACTIVITY IN MACROPHAGES - IN-VITRO AND IN-VIVO STUDIES [J].
KEIDAR, S ;
AVIRAM, M ;
MAOR, I ;
OIKNINE, J ;
BROOK, JG .
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 1994, 38 (06) :513-519
[10]  
Kraul D, 1997, CLIN CHEM, V43, P199