Po Sunny S, Li Yuhua, Tang David, Liu Hong, Geng Ning, Jackman Warren M, Scherlag Benjamin, Lazzara Ralph, Patterson Eugene
Cardiac Arrhythmia Research Institute, Department of Medicine, Oklahoma City, Oklahoma, USA.
J Am Coll Cardiol. 2005 Jun 7;45(11):1871-7. doi: 10.1016/j.jacc.2005.02.070.
We investigated the hypothesis that re-entrant pulmonary vein (PV) tachycardias may serve as a mechanism for initiating and sustaining paroxysmal atrial fibrillation (PAF).
The mechanisms of rapid repetitive discharges from the PV initiating PAF remain incompletely understood. Pulmonary vein myocardial sleeves appear to provide a favorable substrate for re-entry formation.
The electrophysiologic properties of canine PV sleeves were investigated using a combination of high-resolution optical mapping (n = 5) and extracellular bipolar and intracellular microelectrode recordings (n = 56) in a superfused PV preparation.
From the left atrium to distal PV, there was progressive shortening of the action potential (AP) duration, reduction in AP and bipolar electrogram amplitude, and depolarization of resting membrane potentials. Sustained PV tachycardias were induced exclusively in the presence of acetylcholine (10(-7) to 10(-6) mol/l, n = 12). Sustained PV tachycardias were rapid (mean cycle length = 93 +/- 15 ms), regular, and capable of induction, termination, and resetting by single extrastimuli. Re-entry as the mechanism underlying PV tachycardias was confirmed by optical mapping (n = 5). Acetylcholine also reduced the slope of the AP restitution curve and suppressed AP alternans (n = 6). Importantly, PV tachycardias exhibited 1:1 conduction into the atrium at short cycle lengths (<100 ms), emphasizing the potential role of re-entrant PV tachycardia in atrial fibrillation.
Pulmonary veins provide a favorable substrate for re-entry formation. Heterogeneity of the electrophysiologic properties and marked abbreviation of action potential duration and refractoriness by acetylcholine combine to produce rapid and stable re-entrant PV tachycardias. Elevated parasympathetic tone and re-entrant PV tachycardia may serve as a mechanism underlying the perpetuation of PAF.
我们研究了折返性肺静脉（PV）心动过速可能是引发和维持阵发性心房颤动（PAF）的一种机制这一假说。
PV引发PAF的快速重复放电机制仍未完全明确。肺静脉心肌袖似乎为折返形成提供了有利基质。
在离体灌注的PV标本中，联合使用高分辨率光学标测（n = 5）以及细胞外双极和细胞内微电极记录（n = 56），研究犬PV袖的电生理特性。
从左心房到PV远端，动作电位（AP）时程逐渐缩短，AP和双极电图幅度降低，静息膜电位去极化。仅在乙酰胆碱（10⁻⁷至10⁻⁶ mol/l，n = 12）存在的情况下可诱发持续性PV心动过速。持续性PV心动过速快速（平均周期长度 = 93 ± 15 ms）、规则，且能被单个期前刺激诱发、终止和重整。光学标测（n = 5）证实折返是PV心动过速的潜在机制。乙酰胆碱还降低了AP恢复曲线的斜率并抑制了AP交替现象（n = 6）。重要的是，PV心动过速在短周期长度（<100 ms）时以1:1传导至心房，强调了折返性PV心动过速在心房颤动中的潜在作用。
肺静脉为折返形成提供了有利基质。电生理特性的异质性以及乙酰胆碱使动作电位时程和不应期显著缩短，共同导致了快速且稳定的折返性PV心动过速。副交感神经张力升高和折返性PV心动过速可能是PAF持续存在的一种机制。
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