Activation or dysregulation of the immune system plays an important role in the development and progression of many cardiovascular diseases and cardiac arrhythmias. Atrial fibrillation (AF) is the most common… Click to show full abstract
Activation or dysregulation of the immune system plays an important role in the development and progression of many cardiovascular diseases and cardiac arrhythmias. Atrial fibrillation (AF) is the most common cardiac arrhythmia. Inflammation contributes to both electrical and structural atrial remodeling and thrombosis in patients with AF, and therapy targeting specific inflammatory cascades may be a potential strategy to prevent and treat AF (Hu et al., 2015). However, AF has a complex and multifactorial developmental mechanism that involves more than just inflammation. Clinical studies have shown that AF can be triggered by autonomic stimulation, bradycardia, atrial premature beats, tachycardia, accessory pathways, and acute atrial stretch (Weil and Ozcan, 2015). The electrical or focal mechanisms of AF include abnormal automatism, trigger activity and multiple variable reciprocal patterns (Wakili et al., 2011; January et al., 2014). Reduced L-type Ca (ICaL) current, Ca overload, changes in K current (IKACh, IK1), Na current (INa), and transient outward current (Ito) have each been reported in AF (Nattel, 2002). In turn, ionic currents can directly affect the function of cardiomyocyte mitochondria, since it was previously shown that a high content of Ca inhibits mitochondrial respiration, dissipates the membrane potential, and suppresses ATP production (Holmuhamedov et al., 2001; Jahangir et al., 2001). Remodeling of the calcium cycle can contribute to the progression of AF to persistent and activate profibrotic pathways (Denham et al., 2018). In addition to the electrophysiological aspects, the complex anatomical structure of the atria is of great importance (Platonov et al., 2008). It is known that the conduction of an electrical impulse goes through wide muscle bundles with a parallel arrangement of muscle fibers (Anderson et al., 1983). The anatomy of the pulmonary veins promotes reentry due to the combination of abrupt changes in fiber orientation and reduced electrical connectivity between muscle bundles creating areas of heterogeneous conduction velocity and localized block (Hocini et al., 2002; Arora et al., 2003; Hsueh et al., 2013). OPEN ACCESS
               
Click one of the above tabs to view related content.