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[心房颤动中肾素 - 血管紧张素系统的病理生理学]

[Pathophysiology of the renin-angiotensin-system in atrial fibrillation].

作者信息

Heusch G, Schulz R

机构信息

Institut für Pathophysiologie, Universitätsklinikum Essen.

出版信息

Dtsch Med Wochenschr. 2006 Apr 13;131(15):817-20. doi: 10.1055/s-2006-939853.

Abstract

Cardiovascular diseases which are associated with an activation of the renin-angiotensin-system -- myocardial infarction, heart failure, hypertension -- often induce atrial fibrillation. The initiation and maintenance of atrial fibrillation is not only initiated by mechanical distension of the atria, but also by increased atrial expression of components of the renin-angiotensin-system, which initiate an inflammatory signal cascade and oxidative stress and in consequence myolysis and interstitial fibrosis. Ultimately, locally decreased conduction velocity and abbreviated refractory period facilitate reentry circuit(s) as an underlying pathomechanism of atrial fibrillation. In a meta-analysis, ACE inhibitors and AT (1) blockers, both reduce the relative risk of atrial fibrillation by about 30 %. Further prospective randomized clinical studies are required to establish final evidence.

摘要

与肾素 - 血管紧张素系统激活相关的心血管疾病——心肌梗死、心力衰竭、高血压——常常诱发心房颤动。心房颤动的起始和维持不仅由心房的机械性扩张引发,还由肾素 - 血管紧张素系统各组分在心房中的表达增加所引发,这会启动炎症信号级联反应和氧化应激,进而导致肌溶解和间质纤维化。最终,局部传导速度降低和不应期缩短促成折返环,成为心房颤动的潜在发病机制。在一项荟萃分析中,血管紧张素转换酶抑制剂和血管紧张素Ⅱ1型受体阻滞剂均使心房颤动的相对风险降低约30%。还需要进一步的前瞻性随机临床研究来确立最终证据。

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