title: Change in systolic left ventricular performance after 3 years of antihypertensive treatment: the Losartan Intervention for Endpoint (LIFE) Study.
abstract: BACKGROUND
  We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear.
  
  
  RESULTS
  Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174+/-21 to 147+/-19 over 95+/-11 to 82+/-10 mm Hg and LV mass from 234+/-56 to 194+/-50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4+/-2.0% to 16.8+/-2.1% and stress-corrected midwall FS increased from 97+/-13 to 105+/-12% (all P<0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P<0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (beta=-0.211), RWT (beta=-0.334, all P<0.001), and diastolic BP (beta=-0.088, P<0.05) and directly related to SV (beta=0.192, P<0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (beta=-0.153) and RWT (beta=-0.562) and directly with changes in SV (beta=0.145) and systolic BP (beta=0.s221, all P<0.001) with control for blinded therapy.
  
  
  CONCLUSIONS
  Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.
authors.affiliation: Copenhagen County University Hospital, Glostrup, Denmark. kristian@wachtell.net
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Vittorio
authors.initials: V
authors.lastname: Palmieri
authors.forename: Michael H
authors.initials: MH
authors.lastname: Olsen
authors.forename: Eva
authors.initials: E
authors.lastname: Gerdts
authors.forename: Vasilios
authors.initials: V
authors.lastname: Papademetriou
authors.forename: Markku S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: Gunnar
authors.initials: G
authors.lastname: Smith
authors.forename: Björn
authors.initials: B
authors.lastname: Dahlöf
authors.forename: Gerard P
authors.initials: GP
authors.lastname: Aurigemma
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D004452:Echocardiography; D004562:Electrocardiography; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D019808:Losartan / Q000627:therapeutic use*; D013599:Systole / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D000959:Antihypertensive Agents; D019808:Losartan