title: Local pulse pressure and regression of arterial wall hypertrophy during long-term antihypertensive treatment.
abstract: BACKGROUND
  Local pulse pressure (PP) is an independent determinant of carotid artery wall thickness, stronger than mean blood pressure (BP). The present study was designed to assess whether a beta-adrenoceptor antagonist-based or an ACE inhibitor-based treatment was able to reduce carotid artery wall hypertrophy through a reduction in carotid PP rather than by lowering mean BP and whether the influence of local PP reduction could also be detected at the site of a muscular artery, the radial artery.
  
  
  RESULTS
  Ninety-eight essential hypertensive patients were randomized to 9 months of double-blind treatment with either celiprolol or enalapril. Arterial parameters were determined with high-resolution echo-tracking systems. PP was measured locally with applanation tonometry and independently of mean BP. After 9 months of treatment, mean BP, carotid PP, and intimal-medial thickness (IMT) decreased significantly, with no difference between the 2 groups. The reduction in carotid PP but not in mean BP was a major independent determinant of the reduction in carotid IMT. Radial artery IMT and PP decreased significantly with both treatments. However, the reduction in radial artery IMT was not related to the changes in radial artery PP.
  
  
  CONCLUSIONS
  The regression of carotid artery wall hypertrophy during long-term antihypertensive treatment was dependent on the reduction in local PP rather than on the lowering of mean BP. The effect of PP lowering on IMT reduction was observed at the site of an elastic artery but not at the site of a muscular artery.
authors.affiliation: Department of Pharmacology, INSERM U 337, Broussais Hospital, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Boutouyrie
authors.forename: C
authors.initials: C
authors.lastname: Bussy
authors.forename: D
authors.initials: D
authors.lastname: Hayoz
authors.forename: J
authors.initials: J
authors.lastname: Hengstler
authors.forename: N
authors.initials: N
authors.lastname: Dartois
authors.forename: B
authors.initials: B
authors.lastname: Laloux
authors.forename: H
authors.initials: H
authors.lastname: Brunner
authors.forename: S
authors.initials: S
authors.lastname: Laurent
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D001794:Blood Pressure; D002339:Carotid Arteries / Q000473:pathology*; D017272:Celiprolol / Q000008:administration & dosage*; D004548:Elasticity; D004656:Enalapril / Q000008:administration & dosage; D005260:Female; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000473:pathology*; D006984:Hypertrophy; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D016037:Single-Blind Method
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D004656:Enalapril; D017272:Celiprolol