title: Intravascular ultrasound evaluation of coronary plaque regression by low density lipoprotein-apheresis in familial hypercholesterolemia: the Low Density Lipoprotein-Apheresis Coronary Morphology and Reserve Trial (LACMART).
abstract: OBJECTIVE
  We sought to assess the effects of low density lipoprotein (LDL)-apheresis (LDL-A) for regression of coronary plaque in familial hypercholesterolemia (FH), we set up a one-year follow-up multicenter trial using coronary angiography and intravascular ultrasound (IVUS).
  
  
  BACKGROUND
  It is still unclear whether aggressive lipid-lowering therapy by LDL-A leads to the regression of coronary plaque in patients with FH.
  
  
  METHODS
  Eighteen patients with FH were assigned to one of two groups: medication + LDL-A (LDL-A group, n = 11) and medication only (medication group, n = 7). Total cholesterol, triglycerides, high density lipoprotein cholesterol and LDL cholesterol were measured in all subjects at the outset of treatment (baseline) and every three months thereafter. Coronary angiography and IVUS were performed at the outset and after the one-year follow-up period to measure minimal lumen diameter (MLD) by coronary angiogram and plaque area (PA) by IVUS.
  
  
  RESULTS
  The LDL-A group showed 28.4% reduction in total cholesterol (from 275 +/- 27 mg/dl to 197 +/- 19 mg/dl) and 34.3% reduction in LDL cholesterol (from 213 +/- 25 mg/dl to 140 +/- 27 mg/dl) after one-year follow-up, while the medication group showed no changes in cholesterol levels. There were significant interactions between both treatments in total cholesterol (p = 0.0001), LDL cholesterol (p = 0.0001), MLD (p = 0.008) and PA (p = 0.017) using two-way repeated-measures analysis of variance by the SAS system (SAS Institute Inc., Cary, North Carolina). Significant differences were seen in net change in MLD (p = 0.004) and PA (p = 0.008) during the one-year follow-up period between both groups.
  
  
  CONCLUSIONS
  These results suggest that aggressive lipid-lowering therapy using the combination of LDL-A and lipid-lowering drugs may induce regression of coronary atherosclerotic plaque in FH patients.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medical Bioregulation, Yamaguchi University School of Medicine, 1-1-1 Minamikogoshi, Ube, Yamaguchi 755-8505, Japan. masunori@po.cc.yamaguchi-u.ac.jp
authors.forename: Masunori
authors.initials: M
authors.lastname: Matsuzaki
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Hiramori
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Akira
authors.initials: A
authors.lastname: Kitabatake
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Hishida
authors.forename: Masanori
authors.initials: M
authors.lastname: Nomura
authors.forename: Takashi
authors.initials: T
authors.lastname: Fujii
authors.forename: Ichiro
authors.initials: I
authors.lastname: Sakuma
authors.forename: Kenichi
authors.initials: K
authors.lastname: Fukami
authors.forename: Takashi
authors.initials: T
authors.lastname: Honda
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogawa
authors.forename: Masakazu
authors.initials: M
authors.lastname: Yamagishi
mesh_terms: D000328:Adult; D000368:Aged; D001781:Blood Component Removal; D008078:Cholesterol, LDL / Q000097:blood*; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000209:etiology / Q000473:pathology*; D005260:Female; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000150:complications / Q000628:therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012107:Research Design; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D008078:Cholesterol, LDL; D008055:Lipids