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血管紧张素II与糖尿病的心脏并发症

Angiotensin II and the cardiac complications of diabetes mellitus.

作者信息

Connelly K A, Boyle A J, Kelly D J

机构信息

University of Melbourne, Department of Medicine, St Vincent's Hospital, 4th floor Clinical Sciences Building, 29 Regent St Fitzroy 3065, Australia.

出版信息

Curr Pharm Des. 2007;13(26):2721-9. doi: 10.2174/138161207781662984.

DOI:10.2174/138161207781662984
PMID:17897016
Abstract

The prevalence of diabetes has reached epidemic proportions in the developed world and is expect to increase to 5.4% by 2025. This has resulted in an unprecedented number of patients experiencing the macro- and micro-vascular complications of diabetes, such as renal, retinal, neurological and cardiac dysfunction. Premature coronary artery disease and cardiac failure are vastly over-represented in the diabetic population, with significant morbidity and mortality. In fact, the rate of cardiac events in patients with diabetes is equivalent to non-diabetic patients with a previous myocardial infarction. Epidemiological evidence, combined with the results of large scale trials blocking the renin-angiotensin system (RAS) have provided data to support the hypothesis that angiotensin II and its interaction with the metabolic changes associated with diabetes mellitus is responsible for the pathogenesis of many of these complications. This review focuses on the role of the RAS and the development of diabetic cardiac disease.

摘要

糖尿病的患病率在发达国家已达到流行程度,预计到2025年将增至5.4%。这导致出现糖尿病大血管和微血管并发症的患者数量空前增加,如肾脏、视网膜、神经和心脏功能障碍。糖尿病患者中过早发生的冠状动脉疾病和心力衰竭的比例极高,具有显著的发病率和死亡率。事实上,糖尿病患者发生心脏事件的几率等同于曾患心肌梗死的非糖尿病患者。流行病学证据,再加上阻断肾素-血管紧张素系统(RAS)的大规模试验结果,为以下假说提供了数据支持:即血管紧张素II及其与糖尿病相关代谢变化的相互作用是导致许多这些并发症发病机制的原因。本综述重点关注RAS的作用以及糖尿病性心脏病的发展。

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