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Title: Losartan Causes Greater Regression of Left Ventricular Hypertrophy Compared to Atenolol

URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
Retrieve&db=PubMed&dopt=Abstract&list_uids=12885747

Circulation 2003 Jul 28;[Epub ahead of print]. "Regression of Electrocardiographic Left Ventricular Hypertrophy by Losartan Versus Atenolol. The Losartan Intervention For Endpoint reduction in hypertension (LIFE) Study"
08/08/2003 02:13:36 PM
By Emma Hitt, PhD

Losartan-based antihypertensive therapy appears to result in greater regression of electrocardiographic left ventricular hypertrophy (ECG LVH) compared to atenolol-based therapy, according to a new analysis of data from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) Study. The LIFE study has previously demonstrated that losartan is more effective than atenolol in preventing cardiovascular morbidity and mortality and was associated with greater reductions in LVH from baseline to the last available ECG. "However, that report did not examine the time course of changes in ECG LVH, the independence of treatment effects from in-treatment blood pressure changes, or the homogeneity of treatment effects on regression of LVH in subgroups of the population defined by gender, age, ethnicity, and diabetes," the authors note. Therefore, Peter M. Okin, MD, with the Department of Medicine at the Cornell University Medical Center, New York, United States, and colleagues compared the effectiveness of losartan compared to atenolol for regression of ECG LVH throughout the LIFE study, adjusting for possible effects of baseline severity of LVH and both baseline and in-treatment blood pressure. They assessed regression of ECG LVH in 9,193 hypertensive patients using Sokolow-Lyon voltage or Cornell voltage-duration product criteria. Patients underwent electrocardiograms at study baseline and after 6 months, 1, 2, 3, 4, and 5 years of treatment. After 6 months of follow up, and after adjusting for baseline ECG LVH levels, baseline and in-treatment systolic and diastolic pressures, and 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," (all p<0.001) they report. According to the researchers, the greater reductions in those receiving losartan in all examined subsets were independent of baseline severity of ECG LVH and of baseline and in-treatment blood pressures and diuretic use in the study groups, "suggesting that the greater treatment effect of losartan on regression of ECG LVH is independent of the blood pressure-lowering effect of the drug." "These findings support the value of angiotensin receptor blockade with losartan for reversing ECG LVH," they conclude.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
Retrieve&db=PubMed&dopt=Abstract&list_uids=12885747

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