title: Intensive cholesterol reduction lowers blood pressure and large artery stiffness in isolated systolic hypertension.
abstract: OBJECTIVE
  We sought to investigate the effects of intensive cholesterol reduction on large artery stiffness and blood pressure in normolipidemic patients with isolated systolic hypertension (ISH).
  
  
  BACKGROUND
  Isolated systolic hypertension is associated with elevated cardiovascular morbidity and mortality and is primarily due to large artery stiffening, which has been independently related to cardiovascular mortality. Cholesterol-lowering therapy has been efficacious in reducing arterial stiffness in patients with hypercholesterolemia, and thus may be beneficial in ISH.
  
  
  METHODS
  In a randomized, double-blinded, cross-over study design, 22 patients with stage I ISH received three months of atorvastatin therapy (80 mg/day) and three months of placebo treatment. Systemic arterial compliance was measured noninvasively using carotid applanation tonometry and Doppler velocimetry of the ascending aorta.
  
  
  RESULTS
  Atorvastatin treatment reduced total and low-density lipoprotein cholesterol and triglyceride levels by 36 +/- 2% (p < 0.001), 48 +/- 3% (p < 0.001) and 23 +/- 5% (p = 0.003), respectively, and increased high density lipoprotein cholesterol by 7 +/- 3% (p = 0.03). Systemic arterial compliance was higher after treatment (placebo vs. atorvastatin: 0.36 +/- 0.03 vs. 0.43 +/- 0.05 ml/mm Hg, p = 0.03). Brachial systolic blood pressure was lower after atorvastatin treatment (154 +/- 3 vs. 148 +/- 2 mm Hg, p = 0.03), as were mean (111 +/- 2 vs. 107 +/- 2 mm Hg, p = 0.04) and diastolic blood pressures (83 +/- 1 vs. 81 +/- 2 mm Hg, p = 0.04). There was a trend toward a reduction in pulse pressure (71 +/- 3 vs. 67 +/- 2 mm Hg, p = 0.08).
  
  
  CONCLUSIONS
  Intensive cholesterol reduction may be beneficial in the treatment of patients with ISH and normal lipid levels, through a reduction in large artery stiffness.
authors.affiliation: Alfred and Baker Medical Unit, Baker Medical Research Institute, Melbourne, Victoria, Australia.
authors.forename: Kathryn E
authors.initials: KE
authors.lastname: Ferrier
authors.forename: Michael H
authors.initials: MH
authors.lastname: Muhlmann
authors.forename: Jean Philippe
authors.initials: JP
authors.lastname: Baguet
authors.forename: James D
authors.initials: JD
authors.lastname: Cameron
authors.forename: Garry L
authors.initials: GL
authors.lastname: Jennings
authors.forename: Anthony M
authors.initials: AM
authors.lastname: Dart
authors.forename: Bronwyn A
authors.initials: BA
authors.lastname: Kingwell
mesh_terms: D000368:Aged; D000410:Alanine Transaminase / Q000097:blood / Q000187:drug effects; D001158:Arteries / Q000187:drug effects / Q000503:physiopathology*; D001219:Aspartate Aminotransferases / Q000097:blood / Q000187:drug effects; D000069059:Atorvastatin; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010349:Patient Compliance; D011758:Pyrroles / Q000627:therapeutic use; D013599:Systole / Q000187:drug effects / Q000502:physiology; D014280:Triglycerides / Q000097:blood; D014739:Victoria / Q000453:epidemiology
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D014280:Triglycerides; D002784:Cholesterol; D000069059:Atorvastatin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase