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Angiotensin II Type 1 Receptor Antagonist, Losartan, Causes Regression of Left Ventricular Hypertrophy in End-Stage Renal Disease

Shibasaki Y. · Masaki H. · Nishiue T. · Nishikawa M. · Matsubara H. · Iwasaka T.
Department of Medicine II, Kansai Medical University, Moriguchi, Osaka, Japan Nephron 2002;90:256–261 (DOI:10.1159/000049060)

Abstract

Left ventricular hypertrophy (LVH) commonly occurs in patients with end-stage renal disease (ESRD) and is an independent risk factor for cardiovascular events. Angiotensin II type 1 receptor (AT1-R) antagonists may be able to reverse LVH independent to the hypotensive effect in the ESRD setting. Thirty chronically hemodialyzed uremic patients with hypertension were randomly assigned to receive the AT1-R antagonist losartan (n = 10), the angiotensin-converting enzyme (ACD) inhibitor enalapril (n = 10), or calcium antagonist amlodipine (n = 10). Left ventricular mass (LVM) index was measured by echocardiography before and 6 months after treatment. The baseline demographic and clinical characteristics did not differ between the three groups. The mean baseline LVM index also did not differ in the three groups. After 6 months of treatment, losartan treatment significantly reduced the LVM index (–24.7 ± 3.2%) than amlodipine (–10.5 ± 5.2%) or enalapril (–11.2 ± 4.1%) therapy. All three groups had a similar decrease in the mean blood pressure with treatment. The plasma angiotensin II concentration increased 5-fold with losartan treatment. In contrast, the plasma angiotension II concentration did not change with enalapril and only increased 2-fold with amlodipine. Thus, the present study indicates that losartan more effectively regresses LVH in patients with ESRD than do enalapril and amlodipine despite a comparable depressor effect between the three drugs.

 

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