Inflammation, atherosclerosis, and stroke

被引:87
作者
Elkind, Mitehell S. V. [1 ]
机构
[1] Columbia Univ, Gertrude H Sergievsky Ctr, Dept Neurol, New York, NY 10027 USA
关键词
atherosclerosis; inflammation; statins; stroke; risk factors;
D O I
10.1097/01.nrl.0000215789.70804.b0
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background: Inflammation has received increasing attention in recent years as a cause of atherosclerosis, coronary artery disease, and stroke. Basic and animal research has implicated inflammatory mechanisms in the pathogenesis and progression of atherosclerosis, as well as in clinical events related to plaque rupture and other atherothrombotic events. Review Summary: The literature on the association of inflammatory markers with risk of stroke was reviewed and a clinical example provided. Several inflammatory biomarkers, and particularly high-sensitivity C-reactive protein (hsCRP), have been identified as likely predictors of the risk of a future stroke. Medications, particularly hydroxymethylglutaryl coenzyme A reductase inhibitors, or statins, have been demonstrated to reduce levels of inflammatory markers independently of effects on cholesterol. Most recently, the ability of these agents to reduce risk of myocardial infarction and other coronary events in patients with acute coronary artery disease has been demonstrated to correlate with their ability to lower levels of hsCRP. Whether reduction of hsCRP would have similar benefits in stroke patients remains unsettled, as does whether other drugs may be similarly used to lower hsCRP levels. Conclusion: Inflammatory biomarkers, especially hsCRP, may allow improved prediction of the risk of stroke in primary and secondary stroke prevention. Modalities to reduce inflammation are becoming available that may help to modify this risk. Further studies, however, are needed before inflammatory markers become a routine part of the evaluation of stroke patients.
引用
收藏
页码:140 / 148
页数:9
相关论文
共 73 条
[31]   WHITE BLOOD-CELL COUNT AND CARDIOVASCULAR-DISEASE - INSIGHTS FROM THE FRAMINGHAM-STUDY [J].
KANNEL, WB ;
ANDERSON, K ;
WILSON, PWF .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1992, 267 (09) :1253-1256
[32]   Conformational rearrangement in C-reactive protein is required for proinflammatory actions on human endothelial cells [J].
Khreiss, T ;
József, L ;
Potempa, LA ;
Filep, JG .
CIRCULATION, 2004, 109 (16) :2016-2022
[33]   Polymerase chain reaction-based method for quantifying recruitment of monocytes to mouse atherosclerotic lesions in vivo -: Enhancement by tumor necrosis factor-α and interleukin-1β [J].
Kim, CJ ;
Khoo, JC ;
Gillotte-Taylor, K ;
Li, A ;
Palinski, W ;
Glass, CK ;
Steinberg, D .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (08) :1976-1982
[34]   Risk factor thresholds: their existence under scrutiny [J].
Law, MR ;
Wald, NJ .
BMJ-BRITISH MEDICAL JOURNAL, 2002, 324 (7353) :1570-1576
[35]   The unstable atheroma [J].
Lee, RT ;
Libby, P .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (10) :1859-1867
[36]   Shear stress induction of the tissue factor gene [J].
Lin, MC ;
AlmusJacobs, F ;
Chen, HH ;
Parry, GCN ;
Mackman, N ;
Shyy, JYJ ;
Chien, S .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (04) :737-744
[37]   Perturbation of the T-cell repertoire in patients with unstable angina [J].
Liuzzo, G ;
Kopecky, SL ;
Frye, RL ;
O'Fallon, WM ;
Maseri, A ;
Goronzy, JJ ;
Weyand, CM .
CIRCULATION, 1999, 100 (21) :2135-2139
[38]   Reduction of atherosclerosis in mice by inhibition of CD40 signalling [J].
Mach, F ;
Schönbeck, U ;
Sukhova, GK ;
Atkinson, E ;
Libby, P .
NATURE, 1998, 394 (6689) :200-203
[39]   C-reactive protein and outcome after ischemic stroke [J].
Muir, KW ;
Weir, CJ ;
Alwan, W ;
Squire, IB ;
Lees, KR .
STROKE, 1999, 30 (05) :981-985
[40]  
MUNRO JM, 1987, HUM PATHOL, V18, P375