Effects of rosuvastatin on postprandial leukocytes in mildly hyperlipidemic patients with premature coronary sclerosis.
We investigated whether pro-inflammatory aspects of the postprandial phase can be modulated by rosuvastatin in premature coronary artery disease (CAD) patients. Herefore standardized 8 h oral fat loading tests were performed off-treatment and after rosuvastatin 40 mg/d in 20 male CAD patients (50 +/- 4 years). The expression of leukocyte activation markers CD11a, CD11b, CD62L and CD66b was studied using flowcytometry. Migration of isolated neutrophils towards chemoattractants was determined in a fluorescence-based assay. Rosuvastatin did not affect baseline leukocyte counts nor the postprandial neutrophil increment (maximum mean increase +10% pre- and +14% post-treatment, P < 0.01 for each). Rosuvastatin reduced baseline platelets (from 266 +/- 78 to 225 +/- 74 x 10(9) cells/L, P < 0.001) and blunted the postprandial platelet count change (maximum mean increase +6%, P = 0.01, and 0%, respectively). The baseline expression of CD11a, CD11b and CD62L increased on most types of leukocytes by rosuvastatin, whereas the postprandial responses were unaffected. Pretreatment, postprandial neutrophil migration increased dose-dependently, but there were no postprandial changes after rosuvastatin. The latter effect was unrelated to changes in lipoprotein concentrations. In conclusion, in CAD patients postprandial pro-inflammatory and pro-coagulant changes can be modified by rosuvastatin. These apparently lipid-lowering independent effects may render protection against atherosclerosis.
van Oostrom
A J H H M
AJ
Department of Internal Medicine, University Medical Center Utrecht, The Netherlands.
Plokker
H W M
HW
van Asbeck
B S
BS
Rabelink
T J
TJ
van Kessel
K P M
KP
Jansen
E H J M
EH
Stehouwer
C D A
CD
Cabezas
M Castro
MC
D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D040881:CD11a Antigen / Q000032:analysis; D039481:CD11b Antigen / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D002634:Chemotaxis, Leukocyte; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications; D004041:Dietary Fats / Q000008:administration & dosage*; D004906:Erythrocyte Count; D005464:Fluorobenzenes / Q000627:therapeutic use*; D058851:GPI-Linked Proteins; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D016209:Interleukin-8 / Q000097:blood; D019041:L-Selectin / Q000032:analysis; D007962:Leukocytes / Q000187:drug effects* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology; D018384:Oxidative Stress; D010976:Platelet Count; D019518:Postprandial Period; D011743:Pyrimidines / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D015703:Antigens, CD; D040881:CD11a Antigen; D039481:CD11b Antigen; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D004041:Dietary Fats; D005464:Fluorobenzenes; D058851:GPI-Linked Proteins; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D016209:Interleukin-8; D011743:Pyrimidines; D013449:Sulfonamides; D019010:Vascular Cell Adhesion Molecule-1; D019041:L-Selectin; D000068718:Rosuvastatin Calcium