Department of Pathology and Cell Regulation, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Heart Rhythm. 2013 Sep;10(9):1342-8. doi: 10.1016/j.hrthm.2013.04.021. Epub 2013 May 14.
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.
To identify histoanatomic substrates for reentrant AF/AFL in rats.
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.
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 S1 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.
The intrinsic histoanatomic heterogeneity in the LA would constitute a pro-reentrant substrate responsible for perpetuating AF/AFL.
尽管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 中折返激动的内在基础尚不清楚。
确定大鼠 AF/AFL 折返激动的组织解剖学基质。
在 Di-4-ANEPPS 染色的 Langendorff 灌注大鼠心肺标本的心房后表面上，通过光学方法可视化冲动传播的时空模式。还分析了相关的组织学。
右心房的爆发（S1-S2）起搏在 19 个心脏中的 15 个中引发了 AF/AFL，大多数病例通过冠状窦（CS）和左心房（LA）顶部的有组织折返激动发展，而 3 例则为无组织不规则传播。折返环沿着 2 条传播途径发展：LA 顶部的较慢途径（传导速度为 42.4 ± 16.6 cm/s）和 CS 沿的较快途径（传导速度为 53.3 ± 9.2 cm/s）。在连续 S1 起搏后的额外刺激（S2）后，屋顶上的冲动从 CS 逆行传播，导致以房间隔和后 LA 为锚固的折返传播。组织学定量分析显示，后 LA 和房间隔的心肌密度明显低于心房其他部位。此外，与 CS 相比，LA 屋顶的心肌细胞密度较低，在传导方向上排列更不规则，整个细胞膜上的连接蛋白 43 分布更紊乱，这与那里的冲动传播较慢一致。
LA 中的固有组织解剖异质性将构成维持 AF/AFL 的促折返基质。
