title: [Angiotensin II type 1 antagonist suppress left ventricular hypertrophy and myocardial fibrosis in patient with end stage renal disease (ESRD)].
abstract: Fibrosis of left ventricle commonly occurs in end stage renal disease(ESRD) patients and is an independent risk factor of cardiovascular events. Angiotensin II type 1 receptor antagonist may be able to reverse fibrosis of left ventricle in ESRD patients. Ultrasonography-integrated backscatter(IBS) of myocardial walls is directly related to the morphometrically evaluated collagen content in humans. In this study, 30 chronically hemodialyzed patients with hypertension were randomly allocated to receive antihypertensive therapy with either angiotensin II type 1 receptor(AT1-R) antagonist losartan(n = 10), angiotensin-converting enzyme(ACE) inhibitor enalapril(n = 10) or calcium antagonist amlodipine(n = 10). IBS of posterior wall of left ventricule were measured by IBS before and after 6 months treatment. Baseline demographic and clinical characteristics did not differ in three subgroups. Although losartan(34.2 +/- 1.8 to 30.2 +/- 2.4 dB: p = 0.0094) treatment demonstrated significant reduce of IBS values, enalapril(30.3 +/- 1.5 to 31.7 +/- 1.4 dB: p = 0.3268) and amlodipine (31.6 +/- 1.6 to 33.1 +/- 1.9 dB: p = 0.4632) did not changed it significantly before and after 6 months treatment. All three groups reduced left ventricular mass index(Losartan 154.5 +/- 9.9 to 114.6 +/- 5.8 g/m2: p = 0.0002) (enalapril 155.6 +/- 14.3 to 135.3 +/- 10.4 g/m2: p = 0.0275) (amlodipine 156.6 +/- 7.3 to 137.2 +/- 4.1 g/m2: p = 0.0589). Three groups manifested a similar significant decrease in the mean blood pressure. Plasma angiotensin II concentration was markedly increased by 5.0-fold relative to the control levels before treatment in Losartan treatment, in contrast unchanged in enalapril and only 2.0-fold increased in amlodipine treatment. This study indicates that losartan reduce of fibrosis of left ventricule and this effect may be via an anti-AT1-R effect.
authors.affiliation: Department of Medicine II, Kansai Medical University.
authors.forename: Yasunobu
authors.initials: Y
authors.lastname: Shibasaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Nishiue
authors.forename: Hiroya
authors.initials: H
authors.lastname: Masaki
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Matsubara
authors.forename: Toshiji
authors.initials: T
authors.lastname: Iwasaka
mesh_terms: D017311:Amlodipine / Q000627:therapeutic use*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D009202:Cardiomyopathies / Q000517:prevention & control*; D004656:Enalapril / Q000627:therapeutic use*; D005260:Female; D005355:Fibrosis; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000517:prevention & control*; D007676:Kidney Failure, Chronic / Q000150:complications*; D019808:Losartan / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D006435:Renal Dialysis
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D017311:Amlodipine; D004656:Enalapril; D019808:Losartan