title: Regression of electrocardiographic left ventricular hypertrophy by losartan versus atenolol: The Losartan Intervention for Endpoint reduction in Hypertension (LIFE) Study.
abstract: BACKGROUND
  Electrocardiographic left ventricular hypertrophy (LVH) predicts cardiovascular morbidity and mortality, and regression of ECG LVH may predict improved prognosis in hypertensive patients. However, uncertainty persists as to how best to regress ECG LVH.
  
  
  RESULTS
  Regression of ECG LVH with losartan versus atenolol therapy was assessed in 9193 hypertensive patients with ECG LVH by Sokolow-Lyon voltage or Cornell voltage-duration product criteria enrolled in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study. Patients had ECGs at study baseline and after 6 months, 1, 2, 3, 4, and 5 years of blinded losartan-based or atenolol-based therapy. After 6 months' follow-up, adjusting for baseline ECG LVH levels, baseline and in-treatment systolic and diastolic pressures, and for diuretic therapy, losartan-based therapy was associated with greater regression of both Cornell product (adjusted means, -200 versus -69 mm. ms, P<0.001) and Sokolow-Lyon voltage (-2.5 versus -0.7 mm, P<0.001) than was atenolol-based therapy. Greater regression of ECG LVH persisted at each subsequent annual evaluation in the losartan-treated group, with between 140 and 164 mm. ms greater mean reductions in Cornell product and from 1.7 to 2.2 mm greater mean reductions in Sokolow-Lyon voltage (all P<0.001). The effect of losartan was consistent across subgroups defined by gender, age, ethnicity, and diabetes.
  
  
  CONCLUSIONS
  After adjusting for baseline and in-treatment blood pressure and baseline severity of ECG LVH, losartan-based antihypertensive therapy resulted in greater regression of ECG LVH by Cornell voltage-duration product and Sokolow-Lyon voltage criteria than did atenolol-based therapy. These findings support the value of angiotensin receptor blockade with losartan for reversing ECG LVH.
authors.affiliation: Department of Medicine, Cornell University Medical Center, 525 East 68th St, New York, NY 10021, USA. pokin@mail.med.cornell.edu
authors.forename: Peter M
authors.initials: PM
authors.lastname: Okin
authors.forename: Richard B
authors.initials: RB
authors.lastname: Devereux
authors.forename: Sverker
authors.initials: S
authors.lastname: Jern
authors.forename: Sverre E
authors.initials: SE
authors.lastname: Kjeldsen
authors.forename: Stevo
authors.initials: S
authors.lastname: Julius
authors.forename: Markku S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: Steven
authors.initials: S
authors.lastname: Snapinn
authors.forename: Katherine E
authors.initials: KE
authors.lastname: Harris
authors.forename: Peter
authors.initials: P
authors.lastname: Aurup
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Edelman
authors.forename: Bjorn
authors.initials: B
authors.lastname: Dahlof
mesh_terms: D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001262:Atenolol / Q000009:adverse effects / Q000627:therapeutic use*; D048909:Diabetes Complications; D004311:Double-Blind Method; D004562:Electrocardiography / Q000187:drug effects*; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D019808:Losartan / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D044469:Racial Groups; D012074:Remission Induction; D012307:Risk Factors; D012737:Sex Factors; D016896:Treatment Outcome
chemical_list: D000889:Anti-Arrhythmia Agents; D000959:Antihypertensive Agents; D001262:Atenolol; D019808:Losartan