title: Pioglitazone induces regression of coronary atherosclerotic plaques in patients with type 2 diabetes mellitus or impaired glucose tolerance: a randomized prospective study using intravascular ultrasound.
abstract: BACKGROUND
  A large clinical trial clarified that pioglitazone reduces cardiovascular events in diabetic patients. However, effects of pioglitazone on structure of coronary atherosclerotic plaques have not been demonstrated. We examined whether pioglitazone reduces volumes of coronary atherosclerotic plaques using intravascular ultrasound (IVUS).
  
  
  METHODS
  Twenty-six consecutive patients with type 2 diabetes mellitus (DM) or impaired glucose tolerance (IGT) undergoing percutaneous coronary intervention (PCI) were enrolled. Echolucent plaques without significant stenosis were selected in IVUS video images at non-PCI-influenced coronary segments and volumetric analysis of the targeted plaques was performed. The patients were randomly assigned into 2 groups: pioglitazone group consisted of 13 patients taking pioglitazone 15 mg/day for initial 14 days after PCI and subsequent 30 mg/day during 6-month follow-up, and control group with 13 patients as control. The plaque volumes and some parameters such as plasma lipid profiles and high-sensitive C-reacting protein (hs-CRP) levels were compared between baseline and the follow-up in those groups.
  
  
  RESULTS
  In the pioglitazone group after 6 months, the plaque volume was significantly reduced (101.3+/-32.1 to 94.6+/-33.6 mm(3), -7.2%; p=0.0023), plasma triglyceride was significantly decreased (- 14.9%) and high density lipoprotein cholesterol was substantially increased (+20.0%) without any significant change in low density lipoprotein cholesterol (LDL-C). Also, hs-CRP level tended to be decreased. However, no significant change in plaque volumes and those parameters was observed in the control group.
  
  
  CONCLUSIONS
  Pioglitazone may induce regression of coronary atherosclerotic plaques without LDL-C reduction in patients with DM and IGT.
authors.affiliation: Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Nakayama
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Komiyama
authors.forename: Masaki
authors.initials: M
authors.lastname: Yokoyama
authors.forename: Susumu
authors.initials: S
authors.lastname: Namikawa
authors.forename: Nakabumi
authors.initials: N
authors.lastname: Kuroda
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Issei
authors.initials: I
authors.lastname: Komuro
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy*; D005260:Female; D005500:Follow-Up Studies; D018149:Glucose Intolerance / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D047495:PPAR gamma / Q000037:antagonists & inhibitors; D000077205:Pioglitazone; D011446:Prospective Studies; D045162:Thiazolidinediones / Q000008:administration & dosage*; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D008055:Lipids; D047495:PPAR gamma; D045162:Thiazolidinediones; D000077205:Pioglitazone