title: Association between wasted pressure effort and left ventricular hypertrophy in hypertension: influence of arterial wave reflection.
abstract: BACKGROUND
  Wave reflection during the systole increases left ventricular (LV) pressure, tension-time index (TTI) and myocardial oxygen requirement. The purpose of this study was to extract that component of extra myocardial oxygen requirement that is due to early systolic wave reflection, define it as wasted effort (DeltaE(w)), and examine its relationship to LV hypertrophy (LVH).
  
  
  METHODS
  Radial artery pressure waveforms were recorded using applanation tonometry and central aortic waveforms generated in 98 patients with untreated hypertension. Aortic augmentation index (AI(a)), wave reflection amplitude (i.e., aortic augmented pressure (AG)) and systolic duration (ED-Tr), ejection duration (ED) and round-trip travel time of the pressure wave (Tr) were calculated from the aortic waveform, and DeltaE(w) estimated as 2.09 AG (ED-Tr). Carotid-femoral pulse wave velocity (PWV(e)) was also measured and LV mass index (LVMI) determined by echocardiography.
  
  
  RESULTS
  DeltaE(w) was significantly correlated with age, body height, and LVMI. Women had greater DeltaE(w) than men. The correlation between DeltaE(w) and LVMI was independent of age, gender and body height (P = 0.003). Patients with LVH (LVH (+) group) showed greater DeltaE(w) than patients without LVH (LVH (-) group) (P = 0.003), and this difference remained significant when adjusted for confounding factors. Also, AI(a) and AG were higher in the LVH (+) than in the LVH (-) group (both P < 0.01). In contrast, PWV(e) was not different between the groups, and Tr showed only a marginal difference (P = 0.07).
  
  
  CONCLUSIONS
  DeltaE(w) appears to be directly and positively associated with LVH in untreated hypertensive patients. The amplitude and duration of the reflected wave, rather than its travel time, are probably responsible for this association.
authors.affiliation: Department of Planning for Drug Development and Clinical Evaluation, Tohoku University Graduate School of Pharmaceutical Science and Medicine, Sendai, Japan. jhashimoto@mail.tains.tohoku.ac.jp
authors.forename: Junichiro
authors.initials: J
authors.lastname: Hashimoto
authors.forename: Wilmer W
authors.initials: WW
authors.lastname: Nichols
authors.forename: Michael F
authors.initials: MF
authors.lastname: O'Rourke
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Imai
mesh_terms: D000328:Adult; D000368:Aged; D001011:Aorta / Q000503:physiopathology; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology*; D002339:Carotid Arteries / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D005263:Femoral Artery / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D011673:Pulsatile Flow / Q000502:physiology; D017534:Radial Artery / Q000503:physiopathology
chemical_list: D010100:Oxygen