Relation of markers of inflammation (C-reactive protein, fibrinogen, von Willebrand factor, and leukocyte count) and statin therapy to long-term mortality in patients with angiographically proven coronary artery disease

被引:111
作者
Bickel, C
Rupprecht, HJ
Blankenberg, S
Espiniola-Klein, C
Schlitt, A
Rippin, G
Hafner, G
Treude, R
Othman, H
Hofmann, KP
Meyer, J
机构
[1] Bundeswehrzent Krankenhaus Koblenz, Dept Med, D-56064 Koblenz, Germany
[2] Bundeswehrzent Krankenhaus Koblenz, Dept Clin Chem, D-56064 Koblenz, Germany
[3] Johannes Gutenberg Univ Mainz, Dept Med 2, D-6500 Mainz, Germany
[4] Johannes Gutenberg Univ Mainz, Dept Med Stat & Documentat, D-6500 Mainz, Germany
[5] Johannes Gutenberg Univ Mainz, Dept Clin Chem, D-6500 Mainz, Germany
关键词
D O I
10.1016/S0002-9149(02)02236-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We evaluated a possible interaction between statins and inflammation in 1,246 patients with angiographically diagnosed coronary artery disease. Four different inflammatory markers were determined: high, sensitive C-reactive protein (hs-CRP) (p = 0.001), fibrinogen (p = 0.006), von Willebrand factor (p = 0.006), and leukcocyte count (p = 0.03); these levels were significantly higher among the 88 patients who died of cardiac causes during follow-up (median 2.9 years) than among survivors. In a multivariate backward stepwise Cox regression mode, only hs-CRP was evaluated to be a a significant predictor of death from coronary artery disease. This prediction was lost in statin-treated patients. Compared with patients receiving statin medication, patients without statins did not have increased cardiac mortality (even when low-density lipoprotein [LDL] levels were > 125 mg/dl) when hs-CRP levels were not elevated. In contrast, patients without statins and elevated hs-CRP (top quartile) had a 2.3-fold increase in risk for fatal coronary events, independent of LDL levels. In conclusion, only elevated hs-CRP was selected as an independent predictor of death. Statin therapy is associated with elevated hs-CRP, with a risk reduction for fatal coronary events, independent of LDL levels; this, in part, may be explained by the anti-inflammatory effects on atherosclerosis. (C) 2002 by Excerpta Medica, Inc.
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页码:901 / 908
页数:8
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