title: Marked low-density lipoprotein cholesterol reduction below current national cholesterol education program targets provides the greatest reduction in carotid atherosclerosis.
abstract: BACKGROUND
  Current National Cholesterol Education Program (NCEP) guidelines recognize low-density lipoprotein cholesterol (LDL-C) below 100 mg/dl as an optimal level. Evidence supporting this is scant. Both LDL-C and C reactive protein (CRP) are known correlates of atherosclerosis progression.
  
  
  OBJECTIVE
  We examined the effect of final LDL-C and CRP obtained with statin therapy on carotid intima-media thickness (CIMT), a valid surrogate for clinical benefit of lipid-lowering therapies.
  
  
  METHODS
  In a randomized, single-center trial, 161 patients were assigned to statin therapy of different potencies (pravastatin 40 mg, n = 82; atorvastatin 80 mg, n = 79). The effects on CIMT were assessed in relationship to LDL-C and CRP levels obtained after 12 months of therapy.
  
  
  RESULTS
  Changes in CIMT were directly related to the final LDL-C level obtained on statin therapy after 12 months (R = 0.219, p = 0.015). Carotid intima-media thickness regression was seen in 61% of the subjects in the lowest quartile of final LDL-C (< 70 mg/dl) versus 29% of the subjects with the highest quartile of final LDL-C (> or = 114 mg/dl, p = 0.008). No threshold value was seen, with more favorable effects on absolute change in CIMT with lower values of LDL-C (decrease in CIMT of 0.06 +/- 0.17 mm in the lowest quartile compared with an increase of 0.06 +/- 0.09 in the highest quartile of LDL-C, p = 0.008). On-treatment LDL and CRP concentrations both below the group median values were associated with the greatest likelihood of CIMT regression.
  
  
  CONCLUSIONS
  Regression of carotid atherosclerosis is directly related to the absolute LDL-C level on statin therapy. The greatest regression was obtained with an LDL-C < 70 mg/dl, supporting marked LDL-C reduction to levels below current NCEP guidelines.
authors.affiliation: Cardiology Service, Walter Reed Army Medical Center, Washington, D.C. 20307-5001, USA.
authors.forename: Steven M
authors.initials: SM
authors.lastname: Kent
authors.forename: Louis C
authors.initials: LC
authors.lastname: Coyle
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Flaherty
authors.forename: Thor T
authors.initials: TT
authors.lastname: Markwood
authors.forename: Allen J
authors.initials: AJ
authors.lastname: Taylor
mesh_terms: D001161:Arteriosclerosis / Q000097:blood / Q000000981:diagnostic imaging* / Q000188:drug therapy; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging* / Q000188:drug therapy; D008078:Cholesterol, LDL / Q000097:blood*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D017410:Practice Guidelines as Topic; D017035:Pravastatin / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use; D017539:Tunica Intima / Q000000981:diagnostic imaging; D014463:Ultrasonography
chemical_list: D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin; D017035:Pravastatin