Neutrophil superoxide anion generation during atorvastatin and fluvastatin therapy used in coronary heart disease primary prevention

被引:43
作者
Kowalski, Jan
Barylski, Marcin
Banach, Maciej
Grycewicz, Joanna
Irzmanski, Robert
Pawlicki, Lucjan
机构
[1] Med Univ Lodz, Univ Hosp Lodz 5, Dept Internal Med & Cardiol Rehabil, PL-91425 Lodz, Poland
[2] Med Univ Lodz, Univ Hosp Lodz 3, Chair Cardiol & Cardiac Surg 1, Dept Cardiol, PL-91425 Lodz, Poland
关键词
atorvastatin; coronary heart disease; fluvastatin; neutrophil superoxide anion generation; prevention;
D O I
10.1097/01.fjc.0000246150.52382.07
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Neutrophil superoxide anion generation was measured during atorvastatin and fluvastatin therapy in patients with coronary heart disease (CHD) risk. The patients were randomly allotted into three groups. The atorvastatin group comprised 17 patients who were administered the drug orally 10 mg a day at bed time. The fluvastatin group consisted of 18 patients on an oral dose of 40 mg once daily at bed time. The control group comprised 12 healthy subjects with no drug administration. Blood samples were collected from cubital vein before and after 6-week therapy with these drugs and once in the control group. Neutrophil superoxide anion generation in whole blood without and with opsonized zymosan (OZ) stimulation was determined using superoxide dismutase from bovine erythrocytes. In the atorvastatin group, statistically significant (P < 0.05) decrease in superoxide anion generation by nonstimulated and OZ-stimulated neutrophils was observed after 6 weeks of therapy. In fluvastatin group, no changes in neutrophil superoxide anion generation were observed after the 6-week treatment period. Our study has shown an additional nonlipid mechanism of atorvastatin used in CHD primary prevention.
引用
收藏
页码:143 / 147
页数:5
相关论文
共 33 条
[1]   Atorvastatin and gemfibrozil metabolites, but not the parent drugs, are potent antioxidants against lipoprotein oxidation [J].
Aviram, M ;
Rosenblat, M ;
Bisgaier, CL ;
Newton, RS .
ATHEROSCLEROSIS, 1998, 138 (02) :271-280
[2]  
BANACH M, 2005, GERIATR POL, V1, P45
[3]  
Banach M, 2005, CELL MOL IMMUNOL, V2, P433
[4]  
BELLAVITE P, 1983, EUR J CLIN INVEST, V13, P363
[5]   AN INTRODUCTION TO FREE-RADICAL BIOCHEMISTRY [J].
CHEESEMAN, KH ;
SLATER, TF .
BRITISH MEDICAL BULLETIN, 1993, 49 (03) :481-493
[6]   GRANULOCYTE FUNCTION IN CORONARY-ARTERY DISEASE [J].
DESERVI, S ;
RICEVUTI, G ;
MAZZONE, A ;
GHIO, S ;
ZITO, A ;
RAFFAGHELLO, S ;
SPECCHIA, G .
AMERICAN JOURNAL OF CARDIOLOGY, 1991, 68 (07) :B64-B68
[7]   Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels - Results of AFCAPS/TexCAPS [J].
Downs, JR ;
Clearfield, M ;
Weis, S ;
Whitney, E ;
Shapiro, DR ;
Beere, PA ;
Langendorfer, A ;
Stein, EA ;
Kruyer, W ;
Gotto, AM .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1998, 279 (20) :1615-1622
[8]   SIMVASTATIN INHIBITS THE OXIDATION OF LOW-DENSITY LIPOPROTEINS BY ACTIVATED HUMAN MONOCYTE-DERIVED MACROPHAGES [J].
GIROUX, LM ;
DAVIGNON, J ;
NARUSZEWICZ, M .
BIOCHIMICA ET BIOPHYSICA ACTA, 1993, 1165 (03) :335-338
[9]  
HAWLEY HP, 1976, LAB INVEST, V34, P216
[10]   Reduced susceptibility of low density lipoprotein (LDL) to lipid peroxidation after fluvastatin therapy is associated with the hypocholesterolemic effect of the drug and its binding to the LDL [J].
Hussein, O ;
Schlezinger, S ;
Rosenblat, M ;
Keidar, S ;
Aviram, M .
ATHEROSCLEROSIS, 1997, 128 (01) :11-18