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心房纤颤(AF)发病机制复杂,血管紧张素转换酶抑制剂(ACEI)和血管紧张素受体阻滞剂(ARB)通过神经-体液、离子通道、信号转导等途径改善心房的结构重构和电重构,从而发挥抗AF作用。大量研究表明,ACEI和ARB在心脏结构异常的AF患者中有抗AF作用,且作用大小与剂量相关,联合其他抗AF治疗能取得良好的疗效。然而,在心脏结构正常的AF患者中抗AF作用尚存争议。ACEI和ARB通过神经-体液、离子通道等途径抗室性心律失常,但其能否降低病死率以及疗效是否与剂量有关尚存争议。
The pathogenesis of atrial fibrillation (AF) is complex. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) improve the structural weight of atria through neuro-humoral, ion channel and signal transduction Structure and electrical remodeling, which play an anti-AF effect. A large number of studies have shown that, ACEI and ARB in AF patients with abnormal cardiac structure have anti-AF effect, and the role of size and dose-related, combined with other anti-AF treatment can achieve good results. However, the anti-AF effect remains controversial in AF patients with normal cardiac structures. ACEI and ARB are anti-ventricular arrhythmias through nerve-body fluid and ion channels, but it is still controversial whether their efficacy can be reduced or not.