| Research Abstract |
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.
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