Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, National Yang-Ming University, Number 201, Section 2, Shipai Road, Beitou District, Taipei 11217, Taiwan, Republic of China.
Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Number 111, Section 3, Hsing-Long Road, Taipei 11696, Taiwan, Republic of China.
Nat Rev Cardiol. 2015 Apr;12(4):230-43. doi: 10.1038/nrcardio.2015.2. Epub 2015 Jan 27.
Atrial fibrillation (AF) is the most common cardiac arrhythmia. However, the development of preventative therapies for AF has been disappointing. The infiltration of immune cells and proteins that mediate the inflammatory response in cardiac tissue and circulatory processes is associated with AF. Furthermore, the presence of inflammation in the heart or systemic circulation can predict the onset of AF and recurrence in the general population, as well as in patients after cardiac surgery, cardioversion, and catheter ablation. Mediators of the inflammatory response can alter atrial electrophysiology and structural substrates, thereby leading to increased vulnerability to AF. Inflammation also modulates calcium homeostasis and connexins, which are associated with triggers of AF and heterogeneous atrial conduction. Myolysis, cardiomyocyte apoptosis, and the activation of fibrotic pathways via fibroblasts, transforming growth factor-β and matrix metalloproteases are also mediated by inflammatory pathways, which can all contribute to structural remodelling of the atria. The development of thromboembolism, a detrimental complication of AF, is also associated with inflammatory activity. Understanding the complex pathophysiological processes and dynamic changes of AF-associated inflammation might help to identify specific anti-inflammatory strategies for the prevention of AF.
心房颤动（AF）是最常见的心律失常。然而，预防 AF 的治疗方法的发展一直令人失望。免疫细胞和介导心肌组织和循环过程中炎症反应的蛋白质的浸润与 AF 有关。此外，心脏或全身循环中的炎症存在可以预测 AF 的发作和一般人群中的复发，以及心脏手术后、心脏复律和导管消融后的患者。炎症反应的介质可以改变心房的电生理和结构基质，从而导致对 AF 的易感性增加。炎症还调节钙稳态和连接蛋白，这与 AF 的触发因素和异质性心房传导有关。肌溶解、心肌细胞凋亡以及通过成纤维细胞、转化生长因子-β和基质金属蛋白酶激活纤维化途径也受炎症途径介导，所有这些都可能导致心房结构重塑。血栓栓塞的形成，即 AF 的一种有害并发症，也与炎症活动有关。了解与 AF 相关炎症的复杂病理生理过程和动态变化可能有助于确定预防 AF 的特定抗炎策略。
