title: Metabolic syndrome abating the beneficial effect of pravastatin treatment on adhesion of endothelium by monocytes in subjects with hypercholesterolemia.
abstract: Statin, a potent lipid-lowering agent, ameliorates the interaction of monocytes and endothelium, a critical step in the atherosclerotic process. However, it remains unclear whether this effect of statin depends on different doses or the presence of metabolic syndrome. In this prospectively double-blind study, 21 hypercholesterolemia subjects, with low-density lipoprotein cholesterol between 130 and 170 mg/dL, received low-dose (10 mg/d) or high-dose (40 mg/d) pravastatin treatment for 8 weeks. We assessed the reduction of monocyte adhesion to cultured endothelium between different-dose groups and the relationship to metabolic syndrome. Total cholesterol and low-density lipoprotein cholesterol were significantly decreased after 40-mg pravastatin treatment (-23.3% +/- 3.7%, P < .001 and -28.8% +/- 3.0%, P < .001), and the reductions were greater than those in the 10-mg group (P = .041 and P = .045, respectively). There was no significant difference in monocyte adhesion between high-dose and low-dose pravastatin treatment. When all subjects were divided into an improvement group and a no improvement group, according to the median of change percentage of monocyte adhesion after pravastatin treatment, there were significantly more subjects with metabolic syndrome in the no improvement than the improvement group (6 vs 1 person, P =.024). Using logistic regression analysis, metabolic syndrome, rather than dose effect of pravastatin, was an independent predictor of interaction between monocytes and endothelium (95% confidence interval = 0.001-0.865, P = .041). Attenuating adhesion between monocytes and endothelium is altered by the presence of metabolic syndrome when hypercholesterolemia subjects receive pravastatin treatment.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung 407, Taiwan.
authors.forename: I-Te
authors.initials: IT
authors.lastname: Lee
authors.forename: Wen-Jane
authors.initials: WJ
authors.lastname: Lee
authors.forename: Hsiu-Chung
authors.initials: HC
authors.lastname: Ou
authors.forename: Chien-Ning
authors.initials: CN
authors.lastname: Huang
authors.forename: Wayne Huey-Herng
authors.initials: WH
authors.lastname: Sheu
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy* / Q000503:physiopathology*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology*; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology*; D018579:Patient Selection; D017035:Pravastatin / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood; D055815:Young Adult
chemical_list: D000924:Anticholesteremic Agents; D001786:Blood Glucose; D008055:Lipids; D014280:Triglycerides; D002097:C-Reactive Protein; D017035:Pravastatin