title: Plasma low-density lipoprotein reduction and structural effects on coronary atherosclerotic plaques by atorvastatin as clinically assessed with intravascular ultrasound radio-frequency signal analysis: a randomized prospective study.
abstract: BACKGROUND
  Plaque stabilization by statins is important for reduction of cardiovascular events but has not been demonstrated enough in vivo. We examined whether statins clinically alter the structure of coronary atherosclerotic plaques using intravascular ultrasound (IVUS) radio-frequency (RF) signal analysis.
  
  
  METHODS
  Fifty consecutive patients undergoing percutaneous coronary intervention were enrolled. Intravascular ultrasound radio-frequency signals were acquired from non-percutaneous coronary intervention-targeted echolucent plaques. The patients were randomly assigned into 2 groups: group S (n = 25) taking atorvastatin 10 mg/d and group C (n = 25) as control. After 6-month follow-up, IVUS-RF signals were sampled at the same plaque sites. Several regions of interest were placed on each plaque. Intravascular ultrasound radio-frequency parameters were blindly calculated in all regions of interests (group S, n = 148; group C, n = 191). Targeted plaque volumes were also measured. Those data were compared between baseline and follow-up.
  
  
  RESULTS
  In group S after 6 months, plasma low-density lipoprotein level was significantly decreased (133 +/- 13 to 87 +/- 29 mg/dL, P < .0001), integrated backscatter of IVUS-RF signals was substantially increased (-53.8 +/- 4.5 to -51.2 +/- 4.9 dB, P < .0001), and plaque volume was significantly reduced, whereas no change was demonstrated in group C.
  
  
  CONCLUSIONS
  These results suggest that statins alter properties as well as volumes of coronary plaques within 6 months, which may be related to plasma low-density lipoprotein reduction. Intravascular ultrasound radio-frequency signal analysis may be useful to evaluate the effects of drugs on stabilization of coronary atherosclerotic plaques.
authors.affiliation: Department of Cardiovascular Science and Medicine, Chiba University Graduate School, Japan.
authors.forename: Masaki
authors.initials: M
authors.lastname: Yokoyama
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Komiyama
authors.forename: Brian K
authors.initials: BK
authors.lastname: Courtney
authors.forename: Takashi
authors.initials: T
authors.lastname: Nakayama
authors.forename: Susumu
authors.initials: S
authors.lastname: Namikawa
authors.forename: Nehiro
authors.initials: N
authors.lastname: Kuriyama
authors.forename: Tomomi
authors.initials: T
authors.lastname: Koizumi
authors.forename: Mizuo
authors.initials: M
authors.lastname: Nameki
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.forename: Issei
authors.initials: I
authors.lastname: Komuro
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000209:etiology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000069059:Atorvastatin; D002317:Cardiovascular Agents / Q000627:therapeutic use; D008078:Cholesterol, LDL / Q000097:blood*; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology; D005260:Female; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000178:diet therapy / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D011846:Radio Waves; D016037:Single-Blind Method; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D002317:Cardiovascular Agents; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin