Intrinsic left atrial histoanatomy as the basis for reentrant excitation causing atrial fibrillation/flutter in rats
Intrinsic left atrial histoanatomy as the basis for reentrant excitation causing atrial fibrillation/flutter in rats
复制标题
DOI：
10.1016/j.hrthm.2013.04.021
复制
发表时间：
2013-09-01
期刊：
影响因子：
5.5
通讯作者：
Takamatsu, Tetsuro
中科院分区：
文献类型：
--
作者：
Matsuyama, Taka-aki;Tanaka, Hideo;Takamatsu, Tetsuro
背景 虽然肺静脉被认为是阵发性心房颤动/扑动 (AF/AFL) 的优先触发部位，但持续性 AF/AFL 中折返性兴奋的内在基础尚未确定。 目的 确定大鼠折返性 AF/AFL 的组织解剖学基础。 di-4-ANEPPS 染色的 Langendorff 灌注大鼠心/肺制剂中心房的后表面。结果 19 颗心脏中，15 颗右心房突发（S1-S2）起搏引起 AF/AFL，大多数病例是由通过冠状窦（CS）和左心房（LA）顶部的有组织折返激发引起的，3 例为无组织不规则传播。折返电路沿着 2 条传播路径发展：LA 屋顶的较慢路径（传导速度，42.4 +/- 16.6 cm/s）和沿 CS 的较快路径（传导速度，53.3 +/- 9.2 cm/s）。连续 51 次起搏后的额外刺激 (S2) 下，顶部的脉冲从 CS 逆行传播，导致由房间隔和后 LA 锚定的折返传播。组织学定量显示，左心房后部和隔膜的心肌密度显着低于心房其他部位。此外，LA 顶部的肌细胞比 CS 中的密度更低，在传导方向上排列更随机，并且其特征是连接蛋白 43 在整个细胞膜上的分布更加混乱，这与那里较慢的脉冲传播一致。 结论 LA 中固有的组织解剖异质性将构成一个亲折返基质，负责 永久 AF/AFL。
BACKGROUND Although the pulmonary veins are accepted as preferential trigger sites for paroxysmal atrial fibrillation/flutter (AF/AFL), the intrinsic basis for reentrant excitation is undetermined in persistent AF/AFL.OBJECTIVE To identify histoanatomic substrates for reentrant AF/AFL in rats.METHODS Spatiotemporal patterns of impulse propagation were visualized optically on the posterior surface of the atria in di-4-ANEPPS-stained Langendorff-perfused rat heart/lung preparations. The relevant histology was also analyzed.RESULTS Burst (S1-S2) pacing at the right atrium provoked AF/AFL in 15 of 19 hearts, and most cases developed by organized reentrant excitation through the coronary sinus (CS) and left atrial (LA) roof, with nonorganized irregular propagation in 3 cases. The reentrant circuit developed along 2 pathways of propagation: a slower pathway at the LA roof (conduction velocity, 42.4 +/- 16.6 cm/s) and a faster pathway along the CS (conduction velocity, 53.3 +/- 9.2 cm/s). Upon extra stimulus (S2) after consecutive 51 pacing, the impulse at the roof propagated retrogradely from the CS, resulting in reentrant propagation anchored by the atrial septum and posterior LA. Histologic quantification revealed significantly lower myocardial density in the posterior LA and the septum than elsewhere in the atria. Moreover, myocytes in the LA roof, than in the CS, were of lower density, more randomly arranged in the direction of conduction, and characterized by more disorganized distribution of connexin 43 over the entire cell membrane, which is consistent with the slower impulse propagation there.CONCLUSION The intrinsic histoanatomic heterogeneity in the LA would constitute a pro-reentrant substrate responsible for perpetuating AF/AFL.