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Submitted on June 20, 2003
From Cornell Medical Center, New York, NY (R.B.D., K.W.); Sahlgrenska University Hospital, Östra, and University of Göteborg, Göteborg, Sweden (B.D.); Haukeland University Hospital, Bergen, Norway (F.E.G.); Skellefteå Lasarett and Umeå University, Skellefteå, Sweden (K.B.); Helsinki University Central Hospital, Helsinki, Finland (M.S.N.); Veterans Administration Hospital, Washington, DC (V.P.); Merck and Co, Inc, West Point, Pa (K.E.H., J.M.E.); and Glostrup University Hospital, Glostrup, Denmark (J.R., K.W.). * To whom correspondence should be addressed. E-mail: rbdevere{at}med.cornell.edu.
Background--An echocardiographic substudy of the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial was designed to test the ability of losartan to reduce left ventricular (LV) mass more than atenolol. Methods and Results--A total of 960 patients with essential hypertension and LV hypertrophy (LVH) on screening ECG were enrolled at centers in 7 countries and studied by echocardiography at baseline and after 1, 2, 3, 4, and 5 years randomized therapy. Clinical examination and blinded readings of echocardiograms in 457 losartan-treated and 459 atenolol-treated participants with Conclusions--Antihypertensive treatment with losartan, plus hydrochlorothiazide and other medications when needed for pressure control, resulted in greater LVH regression in patients with ECG LVH than conventional atenolol-based treatment. Thus, angiotensin receptor antagonism by losartan has superior efficacy for reversing LVH, a cardinal manifestation of hypertensive target organ damage.
Revised on May 20, 2004
Accepted on June 10, 2004
Regression of Hypertensive Left Ventricular Hypertrophy by Losartan Compared With Atenolol. The Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) Trial
Richard B. Devereux MD*,
1 follow-up measurement of LV mass index (LVMI) were used in an intention-to-treat analysis. Losartan-based therapy induced greater reduction in LVMI from baseline to the last available study than atenolol with adjustment for baseline LVMI and blood pressure and in-treatment pressure (-21.7±21.8 versus -17.7±19.6 g/m2; P=0.021). Greater LVMI reduction with losartan was observed in women and men, participants >65 or <65 years of age, and with mild or more severe baseline hypertrophy. The difference between treatment arms in LVH regression was due mainly to reduced concentricity of LV geometry in both groups and lesser increase in LV internal diameter in losartan-treated patients.
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