title: Elevation of HDL-C in response to statin treatment is involved in the regression of carotid atherosclerosis.
abstract: OBJECTIVE
  Atherosclerosis is strongly associated with an increased mortality in subjects with diabetes. The carotid intima-media thickness (IMT) is commonly measured as a surrogate marker for cardiovascular risk. Statins are well-established protective agents against atherosclerosis and reportedly suppress IMT progression in subjects with diabetes. To clarify the effects of statins on subclinical atherosclerosis, we herein investigated changes in the carotid IMT and lipid profiles in a multi-center, prospective, randomized trial.
  
  
  METHODS
  Hypercholesterolemic subjects with type 2 diabetes were randomly assigned to open-label treatment with either pravastatin or pitavastatin. The primary endpoint of this study was the IMT change after 36 months of statin treatment.
  
  
  RESULTS
  A total of 97 subjects (51 pitavastatin; 46 pravastatin) completed this 36-month study. The LDL-C decreased significantly from 163.4 ± 27.9 mg/dl at baseline to 100.4 ± 19.6 mg/dl at 36 months in the pitavastatin group and from 159.7 ± 25.6 mg/dl to 118.5 ± 22.1 mg/dl in the pravastatin group. The mean IMT showed moderate regression in both the pitavastatin (-0.070 ± 0.215 mm, P<0.05) and the pravastatin (-0.067 ± 0.260 mm) group. However, there was no significant difference in the IMT change between the two groups. When the two groups were combined, the 36-month change in the mean IMT was significantly associated with HDL-C change (r=-0.24, P= 0.03). Multiple linear regression analysis revealed the change in HDL-C to be an independent variable showing a positive correlation with the carotid IMT reduction.
  
  
  CONCLUSIONS
  The administration of statins for 3 years to subjects with type 2 diabetes resulted in a significant regression of the carotid IMT. An elevation of the plasma HDL-C with statin treatment was closely related to a regression of atherosclerosis.
authors.affiliation: Division of Metabolism and Diabetes, Tohoku University, Graduate School of Medicine.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Ishigaki
authors.forename: Suminori
authors.initials: S
authors.lastname: Kono
authors.forename: Hideki
authors.initials: H
authors.lastname: Katagiri
authors.forename: Yoshitomo
authors.initials: Y
authors.lastname: Oka
authors.forename: Shinichi
authors.initials: S
authors.lastname: Oikawa
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D002340:Carotid Artery Diseases / Q000097:blood / Q000188:drug therapy*; D008076:Cholesterol, HDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000150:complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D055815:Young Adult
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors