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血管紧张素II拮抗作用与心脏:缬沙坦治疗左心室肥厚

Angiotensin II antagonism and the heart: valsartan in left ventricular hypertrophy.

作者信息

Thürmann P A

机构信息

Institute of Clinical Pharmacology, University Witten/Herdecke, Wuppertal, Germany.

出版信息

J Cardiovasc Pharmacol. 1999;33 Suppl 1:S33-6; discussion S41-3.

PMID:10028952
Abstract

Left ventricular hypertrophy (LVH) represents an independent risk factor for cardiovascular morbidity and mortality, and normalization of left ventricular mass has become a desirable goal of antihypertensive treatment. In a randomized, double-blind study, the angiotensin II (AT1-receptor) antagonist valsartan (Diovan ; 80-160 mg q.d.) was compared with the beta-blocker atenolol (50-100 mg q.d.) over 8 months in previously untreated patients with essential hypertension and LVH. Sixty-nine patients were randomized, of whom 58 were evaluated by echocardiography. After 8 months of treatment in the atenolol group [n = 8 with additional hydrochlorothiazide (HCTZ)], initial blood pressure was reduced from 160/103 to 147/92 mm Hg (p < 0.0001). In the valsartan group (n = 9 with HCTZ), blood pressure decreased from 163/101 to 146/90 mm Hg (p < 0.0001). Left ventricular mass index decreased from 127 to 117 g/m2 in the atenolol group and from 127 to 106 g/m2 in the valsartan group. Long-term treatment with valsartan resulted in a significant reduction of LVH in patients with essential hypertension.

摘要

左心室肥厚(LVH)是心血管疾病发病率和死亡率的独立危险因素,使左心室质量恢复正常已成为抗高血压治疗的理想目标。在一项随机、双盲研究中,将血管紧张素II(AT1受体)拮抗剂缬沙坦(代文;80 - 160毫克,每日一次)与β受体阻滞剂阿替洛尔(50 - 100毫克,每日一次)对未经治疗的原发性高血压合并LVH患者进行了8个月的比较。69例患者被随机分组,其中58例接受了超声心动图评估。在阿替洛尔组(n = 8,加用氢氯噻嗪(HCTZ))治疗8个月后,初始血压从160/103降至147/92毫米汞柱(p < 0.0001)。在缬沙坦组(n = 9,加用HCTZ),血压从163/101降至146/90毫米汞柱(p < 0.0001)。阿替洛尔组左心室质量指数从127降至117克/平方米,缬沙坦组从127降至106克/平方米。缬沙坦长期治疗可使原发性高血压患者的LVH显著降低。

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