title: LDL-Apheresis Atherosclerosis Regression Study (LAARS). Effect of aggressive versus conventional lipid lowering treatment on coronary atherosclerosis.
abstract: BACKGROUND
  Intensive lipid lowering may retard the progression of coronary atherosclerosis. LDL-apheresis has the potential to decrease LDL cholesterol to very low levels. To assess the effect of more aggressive lipid lowering with LDL-apheresis, we set up a randomized study in men with hypercholesterolemia and severe coronary atherosclerosis.
  
  
  RESULTS
  For 2 years, 42 men were treated with either biweekly LDL-apheresis plus medication or medication alone. In both groups a dose of simvistatin of 40 mg per day was administered. Baseline (mean+/-SD) LDL cholesterol was 7.8+/-1.9 mmol x L(-1) and 7.9+/-2.3 mmol x L(-1) in the apheresis and medication groups, respectively. The mean reduction in LDL cholesterol was 63% (to 3.0 mmol x L(-1)) and 47% (to 4.1 mmol x L(-1)), respectively. Primary quantitative coronary angiographic end points were changes in average mean segment diameter and minimal obstruction diameter. No differences between the apheresis and medication groups were found in mean segment diameter (-0.01+/-0.16 mm versus 0.03+/-0.16 mm, respectively) or in minimal obstruction diameter (0.01+/-0.13 mm versus 0.01+/-0.11 mm, respectively), expressed as means per patient. On the basis of coronary segment, mean percent stenosis of all lesions showed a tendency to decrease; only in the apheresis group more minor lesions disappeared in comparison to the medication group. On bicycle exercise tests, the time to 0.1 mV ST-segment depression increased significantly by 39% and the maximum level of ST depression decreased significantly by 0.07 mV in the apheresis group versus no changes in the medication group.
  
  
  CONCLUSIONS
  Two years of lipid lowering both with medication alone or LDL-apheresis with medication showed angiographic arrest of the progression of coronary artery disease. However, more aggressive treatment induced functional improvement, which may precede anatomic changes.
authors.affiliation: Department of Internal Medicine, University Hospital Nijmegen, Nijmegen, The Netherlands.
authors.forename: A A
authors.initials: AA
authors.lastname: Kroon
authors.forename: W R
authors.initials: WR
authors.lastname: Aengevaeren
authors.forename: T
authors.initials: T
authors.lastname: van der Werf
authors.forename: G J
authors.initials: GJ
authors.lastname: Uijen
authors.forename: J H
authors.initials: JH
authors.lastname: Reiber
authors.forename: A V
authors.initials: AV
authors.lastname: Bruschke
authors.forename: A F
authors.initials: AF
authors.lastname: Stalenhoef
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001781:Blood Component Removal; D008078:Cholesterol, LDL / Q000302:isolation & purification*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000628:therapy*; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005080:Exercise Test; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008148:Lovastatin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D019821:Simvastatin
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D004791:Enzyme Inhibitors; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008148:Lovastatin; D019821:Simvastatin