Malcolme-Lawes Louisa, Sandler Belinda C, Sikkel Markus B, Lim Phang Boon, Kanagaratnam Prapa
Imperial College, London, UK.
Imperial College, London, UK.
Auton Neurosci. 2016 Aug;199:80-7. doi: 10.1016/j.autneu.2016.08.007. Epub 2016 Aug 11.
The autonomic nervous system is implicated in the multifactorial pathogenesis of atrial fibrillation (AF) but few studies have attempted neural targeting for therapeutic intervention. We have demonstrated that short bursts of stimulation, at specific sites of left atrial ganglionated plexi (GPs), trigger fibrillation-inducing atrial ectopy and importantly continuous stimulation of these sites may not induce AV block, the 'conventional' marker used to locate GPs. We have shown that these ectopy-triggering GP (ET-GP) sites are anatomically stable and can be rendered inactive by either ablation at the site or by ablation between the site and the adjacent pulmonary vein (PV). This may have important implications for planning patient specific strategies for ablation of paroxysmal AF in the future.
自主神经系统与心房颤动（AF）的多因素发病机制有关，但很少有研究尝试针对神经进行治疗干预。我们已经证明，在左心房神经节丛（GPs）的特定部位进行短时间的刺激会引发诱发房颤的房性早搏，重要的是，对这些部位进行持续刺激可能不会诱发房室传导阻滞，而房室传导阻滞是用于定位GPs的“传统”标志物。我们已经表明，这些引发早搏的GP（ET-GP）部位在解剖学上是稳定的，并且通过在该部位进行消融或在该部位与相邻肺静脉（PV）之间进行消融可以使其失活。这可能对未来制定针对阵发性房颤患者的个体化消融策略具有重要意义。
