Guiraudon Gerard M, Jones Douglas L
Canadian Surgical Technologies and Advance Robotics, Lawson Health Research Institute, London Health Science Center, London, Ontario, Canada,
J Interv Card Electrophysiol. 2014 Jun;40(1):9-15. doi: 10.1007/s10840-014-9884-0. Epub 2014 Mar 27.
This discussion paper re-examines the conduction-activation of the atria, based on observations, with respect to the complexity of the heart as an organ with a brain, and its evolution from a peristaltic tube. The atria do not require a specialized conduction system because they use the subendocardial layer to produce centripetal transmural activation fronts, regardless of the anatomical and histological organization of the transmural atrial wall. This has been described as "two-layer" physiology which provides robust transmission of activation from the sinus to the AV node via a centripetal transmural activation front. New productive insights can come from re-examining the physiology, not only during sinus rhythm but also during atrial tachycardias, in particular atrial flutter and atrial fibrillation (AF). During common flutter, the areas of slow conduction, in the isthmus and following trabeculations, particularly the subendocardial layer confines conduction through the trabeculations which supports re-entry. During experimental or postoperative flutter, the circular 2D activation around the obstacle follows the physiological transmural activation. Understanding this physiology offers insights into AF. During acute or protracted AF, the presence of stationary or drifting rotors is characteristic and consistent with normal physiological 2D atrial activation, suggesting that suppressing physiological transmural activation of AF will permanently restore normal sinus node atrial activation. In contrast, during permanent AF, normal 2D activation is abolished; the presence of transmural, serpentine, and chaotic atrial activation suggests that the normal physiological activation pattern has been replaced by a new, irreversible variety of atrial conduction that is a new physiology, which is consistent with evolution of complex systems.
本讨论文件基于观察结果,重新审视心房的传导激活,鉴于心脏作为一个具有“大脑”的器官的复杂性,以及它从蠕动管进化而来的过程。心房不需要专门的传导系统,因为它们利用心内膜下层产生向心的透壁激活前沿,而不管透壁心房壁的解剖和组织学结构如何。这被描述为“两层”生理学,它通过向心的透壁激活前沿,实现从窦房结到房室结的可靠激活传递。新的有价值的见解可以来自重新审视生理学,不仅是在窦性心律期间,也包括房性心动过速期间,特别是心房扑动和心房颤动(房颤)期间。在常见的心房扑动中,峡部及小梁后的缓慢传导区域,尤其是心内膜下层限制了通过小梁的传导,这支持了折返。在实验性或术后心房扑动期间,围绕障碍物的二维环形激活遵循生理性透壁激活。理解这种生理学有助于深入了解房颤。在急性或持续性房颤期间,静止或漂移的转子的存在是其特征,并且与正常生理性二维心房激活一致,这表明抑制房颤的生理性透壁激活将永久恢复正常的窦房结-心房激活。相比之下,在永久性房颤期间,正常的二维激活被消除;透壁、蜿蜒和混乱的心房激活的存在表明,正常的生理激活模式已被一种新的、不可逆转的心房传导形式所取代,这是一种新的生理学,与复杂系统的进化相一致。