Effects of three dimensional electrical properties on the mechanisms of initiation, maintenance, and termination of atrial fibrillation ; clinical and computer simulation study

为了分析纤颤的机制，我们采用Luo-Rudy第一阶段方程，模拟了从心内膜到心外膜的二维和三维壁组织环境，纤维扭转温度为0 ~ 120℃。在扭曲的三维模型中，涡旋波表现为时空上散射的多个子波，通常伴随着由旋转各向异性引起的突破波，我们利用Luo-Rudy II方程观察了二维组织环境中涡旋波的动力学.螺旋波折返时细胞内Ca ~（2+）浓度升高，诱发DAD。旋转螺旋波阵面被DAD干扰并破裂，导致从心动过速转变为纤颤的发生率很高。DAD在纤颤的发生中起重要作用。相比之下，降低钾通道电流倾向于组织SW，当降低标准值的60%时，SW折返终止，因为SW尖端失去了稳定性。SW头端沿着功能阻滞线弯曲或SW头端与组织边界碰撞。1-K进一步降低，由于功能阻滞线延长，SW折返变得困难。在临床研究中，我们有时观察到右心房和/或左心房的瘢痕组织。在这种情况下，发现各向异性传导。疤痕组织周围的折返性心动过速偶尔会产生纤颤。阵发性心房颤动患者还存在心房自发性异位和肺静脉重复活动等机制，需要进一步的临床和实验研究来阐明其发病机制。

In order to analyze the mechanism of fibrillation, we simulated an environment of two and three dimensional wall tissue with fiber twists of 0℃ to 120℃, from the endocardium to the epicardium employing Luo-Rudy Phase I equations. In a twisted three dimensional model, the scroll waves were demonstrated as multiple wavelets scattered spatiotemporally, frequently accompanied by breakthrough waves that were promoted by rotational anisotropy.We observed the dynamics of spiral waves (SW) on the two-dimensional tissue environment employing Luo-Rudy II equations. Intracellular concentration of Ca ion increased during spiral wave reentry, then DADs were induced. Rotating spiral wave front disturbed by DADs and broke up, leading to a high incidence of transition from tachycardia to fibrillation. DADs play an important role in the genesis of fibrillation. In contrast, reducing the potassium channel current tended to organize the SW, and when reduced 60 % of the standard value, SW reentry terminated because the SW tip lost its stability. The SW tip meandered along the functional block line or the SW tip collided with the tissue boundary. Further reduction of 1-K, it became difficult to generate the SW reentry due to prolonged functional block line.In the clinical studies, we sometimes observed the scar tissue in the right and/or left atrium. Anisotropic conduction was found in such cases. Reentrant tachycardia around the scar tissue occasionally generated fibrillation. Other mechanisms, such as automatic atrial ectopies and repetitive activities in the pulmonary veins, were observed in the patients with paroxysmal atrial fibrillation.Further clinical and experimental studies are necessary to understanding the mechanism of atrial fibrillation.