Circulation. 2003;108:684-690
Published online before print July 28, 2003, doi: 10.1161/01.CIR.0000083724.28630.C3
Published online before print July 28, 2003, doi: 10.1161/01.CIR.0000083724.28630.C3
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(Circulation. 2003;108:684.)
© 2003 American Heart Association, Inc.
Clinical Investigation and Reports |
Regression of Electrocardiographic Left Ventricular Hypertrophy by Losartan Versus Atenolol
The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study
From the Department of Medicine, Division of Cardiology, Cornell University Medical Center, New York, NY (P.M.O., R.B.D.); Sahlgrenska University Hospital/Östra, Göteborg, Sweden (S.J., B.D.); Ullevål University Hospital, Oslo, Norway (S.E.K.); University of Michigan Medical Center, Ann Arbor (S.J.); the Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland (M.S.N.); Merck Research Laboratories, West Point, Pa (S.S., K.E.H.); and Merck & Co, Inc, Whitehouse Station, NJ (P.A., J.M.E.).
Correspondence to Peter M. Okin, MD, Cornell University Medical Center, 525 East 68th St, New York, NY 10021. E-mail pokin{at}mail.med.cornell.edu
Received October 8, 2002; de novo received March 24, 2003; revision received May 22, 2003; accepted May 22, 2003.
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.
Methods and 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.
Key Words: angiotensin • electrocardiography • hypertension • hypertrophy
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