Harada Masahide, Van Wagoner David R, Nattel Stanley
Department of Cardiology, Fujita Health University School of Medicine.
Circ J. 2015;79(3):495-502. doi: 10.1253/circj.CJ-15-0138. Epub 2015 Feb 16.
Atrial fibrillation (AF) is the most common clinically relevant arrhythmia, but the methods available for treating AF and its complications (of which the most important is thrombogenesis), as well as for assessing AF risk and underlying pathophysiology, are largely limited. Emerging evidence suggests a significant role of inflammation in the pathogenesis of AF. That evidence includes elevated serum levels of inflammatory biomarkers in AF subjects, the expression of inflammatory markers in cardiac tissues of AF patients and animal models of AF, and beneficial effects of anti-inflammatory drugs in experimental AF paradigms. Inflammation is suggested to be linked to various pathological processes, such as oxidative stress, apoptosis, and fibrosis, that promote AF substrate formation. Inflammation has also been associated with endothelial dysfunction, platelet activation, and coagulation cascade activation, leading to thrombogenesis. Thus, inflammation may contribute to both the occurrence/maintenance of AF and its thromboembolic complications. Here, we review the evidence for a role of inflammation and inflammatory biomarkers in the risk management and treatment of AF. We also summarize the current knowledge of inflammation-dependent cellular and molecular mechanisms in AF pathophysiology and their potential as therapeutic targets.
心房颤动（AF）是临床上最常见的相关心律失常，但目前用于治疗AF及其并发症（其中最重要的是血栓形成）以及评估AF风险和潜在病理生理学的方法在很大程度上受到限制。新出现的证据表明炎症在AF的发病机制中起重要作用。该证据包括AF患者血清炎症生物标志物水平升高、AF患者及AF动物模型心脏组织中炎症标志物的表达，以及抗炎药物在实验性AF模型中的有益作用。炎症被认为与各种病理过程相关，如氧化应激、细胞凋亡和纤维化，这些过程促进了AF基质的形成。炎症还与内皮功能障碍、血小板活化和凝血级联激活有关，从而导致血栓形成。因此，炎症可能促成AF的发生/维持及其血栓栓塞并发症。在此，我们综述炎症和炎症生物标志物在AF风险管理和治疗中作用的证据。我们还总结了目前关于AF病理生理学中炎症依赖性细胞和分子机制的知识及其作为治疗靶点的潜力。
