title: Different role of wave reflection magnitude and timing on left ventricular mass reduction during antihypertensive treatment.
abstract: OBJECTIVE
  Regression of left ventricular (LV) mass during antihypertensive treatment has been associated with reduction in aortic augmentation index, a composite measure of peripheral wave reflection. The aim of this study was to clarify which of the two reflection factors, that is magnitude or timing, plays the dominant role in this regression.
  
  
  METHODS
  We evaluated the reflection magnitude (RM; the reflected-to-forward pressure wave amplitude ratio), the round-trip travel time of the pressure wave (a parameter for reflection timing), and the aortic pulse wave velocity (PWV) with echocardiographic LV mass in 61 hypertensive patients before and after 1-year standard medical treatment.
  
  
  RESULTS
  Antihypertensive therapy significantly (P < 0.01) decreased brachial and aortic blood pressures and aortic PWV, reduced LV mass, and increased travel time. Neither increase in travel time nor decrease in PWV, however, was related to the reduction in LV mass. By contrast, treatment-induced change in RM was significantly correlated with change in LV mass; the correlation was particularly close in patients with LV hypertrophy (r = 0.61, P < 0.001). Only a marginal correlation was observed between the changes in RM and travel time. The association between RM decrease and LV mass reduction was independent of age, sex, changes in travel time and blood pressure, and use of renin-angiotensin system inhibitors (beta = 0.41, P = 0.001).
  
  
  CONCLUSIONS
  Decreased wave RM contributes to LV mass regression more strongly than, and independently of, delayed reflection timing. Peripheral muscular arteries (from which reflection arises) appear to be more important therapeutic targets in regressing LV mass than central elastic arteries.
authors.affiliation: Department of Planning for Drug Development and Clinical Evaluation, Tohoku University, Japan. jhashimoto@mail.tains.tohoku.ac.jp
authors.forename: Junichiro
authors.initials: J
authors.lastname: Hashimoto
authors.forename: Berend E
authors.initials: BE
authors.lastname: Westerhof
authors.forename: Nico
authors.initials: N
authors.lastname: Westerhof
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Imai
authors.forename: Michael F
authors.initials: MF
authors.lastname: O'Rourke
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects*; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents