title: Diabetes mellitus is a major negative determinant of coronary plaque regression during statin therapy in patients with acute coronary syndrome--serial intravascular ultrasound observations from the Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome Trial (the JAPAN-ACS Trial).
abstract: BACKGROUND
  The Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome (JAPAN-ACS) trial has found that early aggressive statin therapy in patients with acute coronary syndrome (ACS) significantly reduces the plaque volume (PV) of non-culprit coronary lesions. The purpose of the present study was to evaluate clinical factors that have an impact on plaque regression using statin therapy.
  
  
  RESULTS
  Serial intravascular ultrasound observations over 8-12 months were performed in 252 ACS patients receiving pitavastatin or atorvastatin. Linear regression analysis identified the presence of diabetes mellitus (DM) and PV at baseline as inhibiting factors, and serum remnant-like particle-cholesterol level at baseline as a significant factor significantly affecting the degree of plaque regression. Significant correlation between % change of PV and low-density lipoprotein cholesterol (LDL-C) level was found in patients with DM (n=73, P<0.05, r=0.4), whereas there was no significant correlation between the 2 parameters in patients without DM (n=178).
  
  
  CONCLUSIONS
  The regression of coronary plaque induced by statin therapy after ACS was weaker in diabetic patients than their counterparts. Moreover, vigorous reduction of the LDL-C levels might induce a greater degree of plaque regression in ACS patients with DM.
authors.affiliation: Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Hiro
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kimura
authors.forename: Takeshi
authors.initials: T
authors.lastname: Morimoto
authors.forename: Katsumi
authors.initials: K
authors.lastname: Miyauchi
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Nakagawa
authors.forename: Masakazu
authors.initials: M
authors.lastname: Yamagishi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Ozaki
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kimura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Saito
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Daida
authors.forename: Masunori
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology; D000368:Aged; D000069059:Atorvastatin; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology*; D003920:Diabetes Mellitus; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*; D011804:Quinolines / Q000627:therapeutic use*; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D011804:Quinolines; D000069059:Atorvastatin; C108475:pitavastatin