C-reactive protein as a cardiovascular risk factor - More than an epiphenomenon?

被引:725
作者
Lagrand, WK
Visser, CA
Hermens, WT
Niessen, HWM
Verheugt, FWA
Wolbink, GJ
Hack, CE
机构
[1] Free Univ Amsterdam Hosp, Dept Cardiol, NL-1007 MB Amsterdam, Netherlands
[2] Free Univ Amsterdam Hosp, Dept Pathol, NL-1007 MB Amsterdam, Netherlands
[3] Free Univ Amsterdam Hosp, Dept Internal Med, NL-1007 MB Amsterdam, Netherlands
[4] Univ Maastricht, Inst Cardiovasc Res, Maastricht, Netherlands
[5] Univ Hosp Sint Radboud, Dept Cardiol, Nijmegen, Netherlands
[6] Sanquin Blood Supply Fdn, CLB, Amsterdam, Netherlands
关键词
cardiovascular diseases; myocardial infarction; inflammation; risk factors; physiology;
D O I
10.1161/01.CIR.100.1.96
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background-Circulating levels of C-reactive protein (CRP) may constitute an independent risk factor for cardiovascular disease. How CRP as a risk factor is involved in cardiovascular disease is still unclear. Methods ann Results-By reviewing available studies, we discuss explanations for the associations between CRP and cardiovascular disease. CRP levels within the upper quartile/quintile of the normal range constitute an increased risk for cardiovascular events, both in apparently healthy persons and in persons with preexisting angina pectoris. High CRP responses after acute myocardial infarction indicate an unfavorable outcome, even after correction for other risk factors. This link between CRP and cardiovascular disease has been considered to reflect the response of the body to the inflammatory reactions in the atherosclerotic (coronary) vessels and adjacent myocardium. However, because CRP localizes in infarcted myocardium (with colocalization of activated complement), we hypothesize that CRP may directly interact with atherosclerotic vessels or ischemic myocardium by activation of the complement system, thereby promoting inflammation and thrombosis. Conclusions-CRP constitutes an independent cardiovascular risk factor. Unraveling the molecular background of this association may provide new directions for prevention of cardiovascular events.
引用
收藏
页码:96 / 102
页数:7
相关论文
共 70 条
  • [21] PHOSPHOLIPASE-A2 ENZYMES - REGULATION AND INHIBITION
    GLASER, KB
    MOBILIO, D
    CHANG, JY
    SENKO, N
    [J]. TRENDS IN PHARMACOLOGICAL SCIENCES, 1993, 14 (03) : 92 - 98
  • [22] A role for secretory phospholipase A(2) and C-reactive protein in the removal of injured cells
    Hack, CE
    Wolbink, GJ
    Schalkwijk, C
    Speijer, H
    Hermens, WT
    vandenBosch, H
    [J]. IMMUNOLOGY TODAY, 1997, 18 (03): : 111 - 115
  • [23] HAMILTON KK, 1990, J BIOL CHEM, V265, P3809
  • [24] HANSSON GK, 1993, BRIT HEART J, V69, pS38
  • [25] IMMUNOHISTOCHEMICAL LOCALIZATION OF C-REACTIVE PROTEIN-BINDING SITES IN HUMAN ATHEROSCLEROTIC AORTIC LESIONS BY A MODIFIED STREPTAVIDIN-BIOTIN-STAINING METHOD
    HATANAKA, K
    LI, XA
    MASUDA, K
    YUTANI, C
    YAMAMOTO, A
    [J]. PATHOLOGY INTERNATIONAL, 1995, 45 (09) : 635 - 641
  • [26] Haverkate F, 1997, LANCET, V349, P462, DOI 10.1016/S0140-6736(96)07591-5
  • [27] HEINRICH J, 1995, THROMB HAEMOSTASIS, V73, P374
  • [28] HEUERTZ RM, 1993, AM J PATHOL, V142, P319
  • [29] FLIP-FLOP - THE TRANSMEMBRANE TRANSLOCATION OF LIPIDS
    HIGGINS, CF
    [J]. CELL, 1994, 79 (03) : 393 - 395
  • [30] EFFECTS OF COMPLEMENT ACTIVATION IN THE ISOLATED HEART - ROLE OF THE TERMINAL COMPLEMENT COMPONENTS
    HOMEISTER, JW
    SATOH, P
    LUCCHESI, BR
    [J]. CIRCULATION RESEARCH, 1992, 71 (02) : 303 - 319