title: Atorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus.
abstract: Endothelial dysfunction is frequently found in diabetic subjects. This study was performed to investigate whether atorvastatin therapy was able to reverse endothelial dysfunction in type 2 diabetes and, if so, whether the effect was due to its antiinflammatory action. Eighty patients (baseline low density lipoprotein, 4.37 +/- 0.71 mmol/liter) were randomized to atorvastatin (10 mg daily for 3 months, followed by 20 mg daily for 3 months) or placebo in a double blind study. Endothelial function was assessed by high resolution vascular ultrasound, and high sensitivity C-reactive protein (CRP) was assessed by immunoturbidimetric assay. Diabetic patients had higher CRP (P < 0.01) than matched nondiabetic controls, and both endothelium-dependent and independent vasodilation were impaired (P < 0.01). Atorvastatin (10 and 20 mg) lowered plasma cholesterol by 32.9% and 38.0%, triglyceride by 15.4% and 23.1%, and low density lipoprotein by 43.4% and 50.1%, respectively. At 6 months, plasma CRP decreased in the atorvastatin group compared with baseline (P < 0.05). Endothelium-dependent vasodilation improved in the atorvastatin group compared with the placebo group (P < 0.05). The percent change in endothelium-dependent vasodilation at 6 months correlated with the percent change in CRP (r = -0.44; P < 0.05), but not with changes in plasma lipids. In conclusion, treatment with atorvastatin in type 2 diabetes led to a significant improvement in endothelium-dependent vasodilation, which might be partly related to its anti-inflammatory effect.
authors.affiliation: Department of Medicine, University of Hong Kong, Hong Kong. kcbtan@hkucc.hku.hk
authors.forename: K C B
authors.initials: KC
authors.lastname: Tan
authors.forename: W S
authors.initials: WS
authors.lastname: Chow
authors.forename: S C F
authors.initials: SC
authors.lastname: Tam
authors.forename: V H G
authors.initials: VH
authors.lastname: Ai
authors.forename: C H L
authors.initials: CH
authors.lastname: Lam
authors.forename: K S L
authors.initials: KS
authors.lastname: Lam
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis / Q000037:antagonists & inhibitors*; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*; D012016:Reference Values; D014280:Triglycerides / Q000037:antagonists & inhibitors / Q000097:blood; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin