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[Angiotensin II type 1 antagonist suppress left ventricular hypertrophy and myocardial fibrosis in patient with end stage renal disease (ESRD)].
Nihon Rinsho. 2002 Oct; 60(10):1992-8.NR

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+Show Affiliations

Department of Medicine II, Kansai Medical University.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Comparative Study
English Abstract
Journal Article
Randomized Controlled Trial

Language

jpn

PubMed ID

12397697

Citation

Shibasaki, Yasunobu, et al. "[Angiotensin II Type 1 Antagonist Suppress Left Ventricular Hypertrophy and Myocardial Fibrosis in Patient With End Stage Renal Disease (ESRD)]." Nihon Rinsho. Japanese Journal of Clinical Medicine, vol. 60, no. 10, 2002, pp. 1992-8.
Shibasaki Y, Nishiue T, Masaki H, et al. [Angiotensin II type 1 antagonist suppress left ventricular hypertrophy and myocardial fibrosis in patient with end stage renal disease (ESRD)]. Nihon Rinsho. 2002;60(10):1992-8.
Shibasaki, Y., Nishiue, T., Masaki, H., Matsubara, H., & Iwasaka, T. (2002). [Angiotensin II type 1 antagonist suppress left ventricular hypertrophy and myocardial fibrosis in patient with end stage renal disease (ESRD)]. Nihon Rinsho. Japanese Journal of Clinical Medicine, 60(10), 1992-8.
Shibasaki Y, et al. [Angiotensin II Type 1 Antagonist Suppress Left Ventricular Hypertrophy and Myocardial Fibrosis in Patient With End Stage Renal Disease (ESRD)]. Nihon Rinsho. 2002;60(10):1992-8. PubMed PMID: 12397697.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Angiotensin II type 1 antagonist suppress left ventricular hypertrophy and myocardial fibrosis in patient with end stage renal disease (ESRD)]. AU - Shibasaki,Yasunobu, AU - Nishiue,Takashi, AU - Masaki,Hiroya, AU - Matsubara,Hiroaki, AU - Iwasaka,Toshiji, PY - 2002/10/26/pubmed PY - 2002/12/19/medline PY - 2002/10/26/entrez SP - 1992 EP - 8 JF - Nihon rinsho. Japanese journal of clinical medicine JO - Nihon Rinsho VL - 60 IS - 10 N2 - 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. SN - 0047-1852 UR - https://www.unboundmedicine.com/medline/citation/12397697/[Angiotensin_II_type_1_antagonist_suppress_left_ventricular_hypertrophy_and_myocardial_fibrosis_in_patient_with_end_stage_renal_disease__ESRD_]_ L2 - https://www.medicalonline.jp/meteo_linkout.php?issn=0047-1852&volume=60&issue=10&spage=1992 DB - PRIME DP - Unbound Medicine ER -