Department of Cardiac Surgery, The First Affiliated Hospital of China Medical University, Shenyang, P.R. China.
Cardiovasc Pathol. 2013 Sep-Oct;22(5):383-8. doi: 10.1016/j.carpath.2013.02.005. Epub 2013 Mar 23.
Atrial fibrosis causes abnormal conduction through the atria, creating a substrate for atrial fibrillation (AF). In a rabbit model, rapid atrial pacing produces significant atrial fibrosis and the substrate for AF maintenance. This atrial remodeling is a potential therapeutic target.
To evaluate the effects of the losartan on atrial fibrosis.
Thirty rabbit AF models were produced by rapid atrial stimulation. They were randomly divided into three groups: sham group, rapid atrial pacing group, and rapid atrial pacing with losartan group. We performed AF vulnerability studies, atrial histologic, and molecular analyses after 4 weeks.
Only rabbits in the rapid atrial pacing group developed sustained AF (30 min, 4of 10 rabbits). Treatment with losartan resulted in a significant reduction in left atrial fibrosis and AF duration (P<.01). real-time polymerase chain reaction analyses demonstrated the drug's effects on the expression of Collagen I, Collagen III, and TGF-β/Smads signaling pathway.
The treatment of losartan results in significantly reduced atrial fibrosis and AF vulnerability. Pharmacological therapy targeted at the fibrotic substrate itself may play an important role in the management of AF.
心房纤维化导致心房传导异常，为心房颤动（AF）的维持提供了基质。在兔模型中，快速心房起搏会产生显著的心房纤维化和 AF 维持的基质。这种心房重构是一种潜在的治疗靶点。
评估氯沙坦对心房纤维化的影响。
通过快速心房刺激产生 30 只兔 AF 模型。它们被随机分为三组：假手术组、快速心房起搏组和快速心房起搏加氯沙坦组。在 4 周后进行 AF 易损性研究、心房组织学和分子分析。
只有快速心房起搏组的兔子发生了持续的 AF（30 分钟，10 只兔子中有 4 只）。氯沙坦治疗导致左心房纤维化和 AF 持续时间明显减少（P<.01）。实时聚合酶链反应分析表明，该药物对 Collagen I、Collagen III 和 TGF-β/Smads 信号通路的表达有影响。
氯沙坦的治疗可显著减少心房纤维化和 AF 的易损性。针对纤维化基质本身的药物治疗可能在 AF 的治疗中发挥重要作用。
