title: Relation of impaired left ventricular filling to systolic midwall mechanics in hypertensive patients with normal left ventricular systolic chamber function: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study.
abstract: BACKGROUND
  Patients with hypertensive left ventricular (LV) hypertrophy commonly have diastolic dysfunction with preserved LV ejection fraction. LV systolic midwall shortening (MWS) may be impaired in hypertensive patients with normal LV ejection fraction. However, it is unclear whether impaired LV filling is related to depressed systolic midwall mechanics.
  
  
  METHODS
  Echocardiographic measures of LV diastolic filling and systolic performance were compared in 632 unmedicated patients with stage II or III hypertension and LV hypertrophy determined by electrocardiogram, with LV ejection fraction >55% and <2+ mitral regurgitation.
  
  
  RESULTS
  Stress-corrected LV MWS, an index of myocardial contractility, was lower in patients with abnormal as opposed to normal LV filling patterns (98% +/- 12% vs 102% +/- 10%, P <.001) and in patients with prolonged as opposed to normal isovolumic relaxation time (IVRT) (98% +/- 13% vs 101% +/- 12%, P =.014). Stress-corrected MWS was <85% of predicted levels in more patients with abnormal LV filling patterns (11.8% vs 6.3%) or with long IVRT (> or =105 msec) (34% vs 21%, both P <.05). In regression analyses, lower stress-corrected MWS and higher LV mass were independent correlates of longer IVRT, while lower stress-corrected MWS was the only independent correlate of prolonged mitral valve deceleration time (P =.017). Higher LV mass had strong, statistically independent relationships to longer IVRT (by 0.3 g/msec) and decreased stress-corrected MWS (by 0.5 g/%; both P <.0001), independent of body size and age.
  
  
  CONCLUSIONS
  In patients with moderate hypertension and target organ damage who have normal LV ejection fraction, impaired early diastolic LV relaxation (abnormal E/A ratio, prolonged IVRT and deceleration time) is associated with impaired LV systolic midwall mechanics independent of higher LV mass.
authors.affiliation: Department of Medicine, Copenhagen County University Hospital, Glostrup, Denmark. kristian@wachtell.net
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Vasilios
authors.initials: V
authors.lastname: Papademetriou
authors.forename: Gunnar
authors.initials: G
authors.lastname: Smith
authors.forename: Eva
authors.initials: E
authors.lastname: Gerdts
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlöf
authors.forename: Erik
authors.initials: E
authors.lastname: Engblom
authors.forename: Gerard P
authors.initials: GP
authors.lastname: Aurigemma
authors.forename: Jonathan N
authors.initials: JN
authors.lastname: Bella
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
authors.forename: Jens
authors.initials: J
authors.lastname: Rokkedal
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology*; D016277:Ventricular Function, Left