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坎地沙坦酯对高血压患者靶器官功能的保护作用

Preserving target-organ function with candesartan cilexetil in patients with hypertension.

作者信息

Zannad F

机构信息

Service de Cardiologie, Hôpital Central, Nancy, France.

出版信息

Blood Press Suppl. 2000;1:36-9.

PMID:11059635
Abstract

Epidemiological evidence suggests that reducing blood pressure alone in hypertensive patients delays the onset of cardiovascular events without necessarily preventing the progression of chronic target-organ disease, such as end-stage renal failure and heart failure. Successful clinical management of hypertensive patients will therefore not be possible unless therapies are aimed both at the effective control of blood pressure and at the preservation of target-organ function. The new angiotensin II type I (AT1) receptor blocker candesartan cilexetil has been shown to be effective in reducing target-organ damage in animal models of hypertension, even at doses that do not produce significant reductions in blood pressure. Protective effects of candesartan cilexetil towards the heart and kidney have also been demonstrated in the clinical studies that have been conducted to date. Thus, candesartan cilexetil has been shown to induce regression of left ventricular hypertrophy within 8-12 weeks of treatment and to improve renal haemodynamics, both acutely and after 6 weeks of treatment in hypertensive patients. Furthermore, in hypertensive patients with co-existent non-insulin-dependent diabetes mellitus and microalbuminuria, 12 weeks of treatment with candesartan cilexetil, 8-16 mg, significantly reduced urinary albumin excretion. Clinical evidence is therefore accumulating that the antihypertensive efficacy and tolerability profile already established for candesartan cilexetil is combined with the renal and cardioprotective effects necessary for optimal management of hypertension.

摘要

流行病学证据表明,仅降低高血压患者的血压虽可延缓心血管事件的发生,但不一定能阻止慢性靶器官疾病(如终末期肾衰竭和心力衰竭)的进展。因此,除非治疗既针对有效控制血压又针对保护靶器官功能,否则高血压患者的成功临床管理将无法实现。新型血管紧张素II 1型(AT1)受体阻滞剂坎地沙坦酯已被证明在高血压动物模型中可有效减少靶器官损伤,即使在未显著降低血压的剂量下也是如此。坎地沙坦酯对心脏和肾脏的保护作用在迄今为止开展的临床研究中也得到了证实。因此,已证明坎地沙坦酯在治疗8 - 12周内可使左心室肥厚消退,并在高血压患者治疗6周后及急性治疗时改善肾脏血流动力学。此外,在合并非胰岛素依赖型糖尿病和微量白蛋白尿的高血压患者中,使用8 - 16 mg坎地沙坦酯治疗12周可显著降低尿白蛋白排泄量。因此,越来越多的临床证据表明,坎地沙坦酯已确立的降压疗效和耐受性与高血压最佳管理所需的肾脏和心脏保护作用相结合。

相似文献

1
Preserving target-organ function with candesartan cilexetil in patients with hypertension.坎地沙坦酯对高血压患者靶器官功能的保护作用
Blood Press Suppl. 2000;1:36-9.
2
Preserving Target-organ Function with Candesartan Cilexetil in Patients with Hypertension.坎地沙坦酯对高血压患者靶器官功能的保护作用
Blood Press. 2000;9(sup1):36-39. doi: 10.1080/080370500439218.
3
Efficacy and tolerability of candesartan cilexetil in special patient groups.坎地沙坦酯在特殊患者群体中的疗效和耐受性。
Blood Press Suppl. 2000;1:27-30.
4
Improving antihypertensive efficacy while maintaining placebo-like tolerability.提高降压疗效,同时维持类似安慰剂的耐受性。
Blood Press Suppl. 2000;1:19-22.
5
Achieving quality 24-h blood pressure control with candesartan cilexetil.使用坎地沙坦酯实现24小时血压的优质控制。
Blood Press Suppl. 2000;1:23-6.
6
Candesartan cilexetil: a new, long-acting, effective angiotensin II type 1 receptor blocker.坎地沙坦酯:一种新型长效、有效的血管紧张素II 1型受体阻滞剂。
J Hum Hypertens. 1997 Sep;11 Suppl 2:S91-5.
7
Improving prognosis in hypertension: exploring the benefits of angiotensin II type 1 receptor blockade.改善高血压预后:探索血管紧张素II 1型受体阻滞剂的益处
Blood Press Suppl. 2000;1:31-5.
8
Candesartan cilexetil: an angiotensin II receptor blocker.坎地沙坦酯:一种血管紧张素II受体阻滞剂。
Ann Pharmacother. 1999 Dec;33(12):1287-98. doi: 10.1345/aph.19005.
9
The efficacy and tolerability of candesartan cilexetil in an elderly hypertensive population.坎地沙坦酯在老年高血压人群中的疗效及耐受性
J Hum Hypertens. 1997 Sep;11 Suppl 2:S75-80.
10
Reducing cardiovascular morbidity and mortality in the elderly.降低老年人的心血管发病率和死亡率。
Blood Press Suppl. 2000;1:40-3.

引用本文的文献

1
Electrocardiographic left ventricular hypertrophy regression induced by an angiotensin receptor blocker-based regimen in hypertensive patients with the metabolic syndrome: data from the SARA Study.基于血管紧张素受体阻滞剂方案诱导高血压合并代谢综合征患者心电图左心室肥厚消退:SARA研究数据
J Clin Hypertens (Greenwich). 2008 Mar;10(3):208-14. doi: 10.1111/j.1751-7176.2008.07596.x.