The Remodeling of Connexins Localized at Pulmonary Vein – Left Atria in Triggering and Maintenance of Atrial Fibrillation

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Atrial fibrillation is the most common sustained arrhythmia and the major cardiac cause of stroke (Sellers & Newby, 2011). Recent studies in patients and animals with paroxysmal atrial fibrillation had shown that the arrhythmia was triggered by focal sources from muscular sleeves originated in the left atria extending into pulmonary veins (Date et al.,2007; Chen et al.,2001; Patterson et al., 2007; Honjo et al., 2003). What is more, the autonomic nervous system has a crucial role in the genesis, maintenance and abruption of atrial fibrillation (Duffy& Wit, 2008; Sandres et al.,2004), and there is a fat pad localized in superior vena cava and the root of aorta as the origin of cardiac nerve, being called SVC-Ao fat pad (Kapa et al.,2010; Volders ,2010; Ji et al.,2010). The mechanism of atrial fibrillation involves multiple effects (Chiou et al.,1997; Tsuboi et al.,2000; Hoffmann et al., 2006; Haissaguerre et al.1998; Wit & Boyden,2007), the expression of connexins is changed and is associated with increased propensity for arrhythmias (Kanagaratnam et al., 2002, Herve et al., 2007, Stergiopoulos et al., 1999, Verheule S et al., 2002, Kanagaratnam et al., 2007; Valiunas et al.,2001; Valiunas et al.,2000; Cottrell et al.,2002; Elenes et al.,1999). Pulmonary veins and left atria are the primary structure of genesis, persistence of atrial fibrillation. Vagus nerve plays a key role in the initiation and maintenance of atrial fibrillation, it can mediate the electrical remodeling of atria and pulmonary vein, enhance the maintenance and stability of atrial fibrillation,. However, these effects can be inhibited by avianizing vagus nerve.