Can statins reduce the inflammatory response to cardiopulmonary bypass?: A clinical study

被引:31
作者
Florens, E
Salvi, S
Peynet, J
Elbim, C
Mallat, Z
Bel, A
Nguyen, A
Tedgui, A
Pasquier, C
Menasché, P
机构
[1] Grp Hosp Bichat Claude Bernard, Dept Cardiovasc Surg, F-75018 Paris, France
[2] Hop Lariboisiere, Dept Biochem, F-75475 Paris, France
关键词
D O I
10.1111/j.1540-8191.2001.tb00513.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: In addition to lowering lipid levels, statins might reduce leukocyte-endothelial cell interactions. Therefore, we assessed whether this effect could limit the inflammatory response to cardiopulmonary bypass (CPB) in cardiac surgical patients. Methods: Twenty patients undergoing valve or coronary operations with tepid (34 C) CPB were randomized to receive an oral dose of atorvastatine (40 mg the evening before and 40 mg the morning of surgery) or to serve as controls. Pre- and post-CPB blood samples were assayed for neutrophil CD11b surface adhesion molecule and oxidative burst. Plasma levels of interleukins 6 and 8, P-selectin, soluble intercellular adhesion molecule-1, and lactoferrin were measured by enzyme-linked immunosorbent assay (ELISA). In addition, right atrial biopsies were taken before and at the end of CPB, and processed for the expression of the transcription nuclear factor-kappa B (NF-kappaB). Results: The two groups did not differ with regard to pre- and intraoperative data. Except for P-selectin, postbypass values of all markers significantly increased over baseline values, but atorvastatin therapy failed to attenuate the magnitude of this increase. In the two groups, the expression of NF-kappaB significantly (p = 0.004) increased over baseline without group effect. Postoperative clinical outcomes did not differ either between the two groups. Conclusion: These data show that acute preoperative statin therapy fails to limit the inflammatory response to CPB; however, the data also document a major upregulation of NF-kappaB during cardiac operations, thereby providing a sound rationale for interventions targeted at inactivating this key component of the inflammatory cascade.
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页码:232 / 239
页数:8
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