title: High HbA1c levels correlate with reduced plaque regression during statin treatment in patients with stable coronary artery disease: results of the coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS).
abstract: BACKGROUND
  The incidence of cardiac events is higher in patients with diabetes than in people without diabetes. The Coronary Atherosclerosis Study Measuring Effects of Rosuvastatin Using Intravascular Ultrasound in Japanese Subjects (COSMOS) demonstrated significant plaque regression in Japanese patients with chronic coronary disease after 76 weeks of rosuvastatin (2.5 mg once daily, up-titrated to a maximum of 20 mg/day to achieve LDL cholesterol <80 mg/dl).
  
  
  METHODS
  In this subanalysis of COSMOS, we examined the association between HbA1c and plaque regression in 40 patients with HbA1c ≥6.5% (high group) and 86 patients with HbA1c <6.5% (low group).
  
  
  RESULTS
  In multivariate analyses, HbA1c and plaque volume at baseline were major determinants of plaque regression. LDL cholesterol decreased by 37% and 39% in the high and low groups, respectively, while HDL cholesterol increased by 16% and 22%, respectively. The reduction in plaque volume was significantly (p = 0.04) greater in the low group (from 71.0 ± 39.9 to 64.7 ± 34.7 mm(3)) than in the high group (from 74.3 ± 34.2 to 71.4 ± 32.3 mm(3)). Vessel volume increased in the high group but not in the low group (change from baseline: +4.2% vs -0.8%, p = 0.02). Change in plaque volume was significantly correlated with baseline HbA1c.
  
  
  CONCLUSIONS
  Despite similar improvements in lipid levels, plaque regression was less pronounced in patients with high HbA1c levels compared with those with low levels. Tight glucose control during statin therapy may enhance plaque regression in patients with stable coronary disease.
  
  
  BACKGROUND
  ClinicalTrials.gov, Identifier NCT00329160.
authors: Department of Cardiology, Juntendo University School of Medicine, 2-1-1 Hongo, Tokyo 113-8421, Japan. daida@med.juntendo.ac.jp
authors: Hiroyuki
authors: H
authors: Daida
authors: Tadateru
authors: T
authors: Takayama
authors: Takafumi
authors: T
authors: Hiro
authors: Masakazu
authors: M
authors: Yamagishi
authors: Atsushi
authors: A
authors: Hirayama
authors: Satoshi
authors: S
authors: Saito
authors: Tetsu
authors: T
authors: Yamaguchi
authors: Masunori
authors: M
authors: Matsuzaki
mesh_terms: D000368:Aged; D044466:Asian People; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000208:ethnology / Q000473:pathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000473:pathology; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy* / Q000208:ethnology; D007564:Japan / Q000453:epidemiology; D016014:Linear Models; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D058226:Plaque, Atherosclerotic; D011743:Pyrimidines / Q000627:therapeutic use*; D018570:Risk Assessment; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; D005464:Fluorobenzenes; D006442:Glycated Hemoglobin; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011743:Pyrimidines; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides; C517652:hemoglobin A1c protein, human