Shibasaki Yasunobu, Nishiue Takashi, Masaki Hiroya, Matsubara Hiroaki, Iwasaka Toshiji
Department of Medicine II, Kansai Medical University.
Nihon Rinsho. 2002 Oct;60(10):1992-8.
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.
左心室纤维化常见于终末期肾病（ESRD）患者，是心血管事件的独立危险因素。1型血管紧张素II受体拮抗剂可能能够逆转ESRD患者的左心室纤维化。心肌壁的超声背向散射积分（IBS）与人体形态学评估的胶原含量直接相关。在本研究中，30例慢性血液透析的高血压患者被随机分配接受1型血管紧张素II受体（AT1-R）拮抗剂氯沙坦（n = 10）、血管紧张素转换酶（ACE）抑制剂依那普利（n = 10）或钙拮抗剂氨氯地平（n = 10）进行抗高血压治疗。在治疗6个月前后，通过IBS测量左心室后壁的IBS。三个亚组的基线人口统计学和临床特征无差异。尽管氯沙坦治疗（从34.2±1.8 dB降至30.2±2.4 dB：p = 0.0094）显示IBS值显著降低，但依那普利治疗（从30.3±1.5 dB升至31.7±1.4 dB：p = 0.3268）和氨氯地平治疗（从31.6±1.6 dB升至33.1±1.9 dB：p = 0.4632）在治疗6个月前后IBS值无显著变化。三组均降低了左心室质量指数（氯沙坦组从154.5±9.9 g/m²降至114.6±5.8 g/m²：p = 0.0002）（依那普利组从155.6±14.3 g/m²降至135.3±10.4 g/m²：p = 0.0275）（氨氯地平组从156.6±7.3 g/m²降至137.2±4.1 g/m²：p = 0.0589）。三组平均血压均有显著下降。氯沙坦治疗组血浆血管紧张素II浓度相对于治疗前对照水平显著升高5.0倍，而依那普利组无变化，氨氯地平治疗组仅升高2.0倍。本研究表明，氯沙坦可减轻左心室纤维化，且这种作用可能是通过抗AT1-R效应实现的。
