Wu T J, Kim Y H, Yashima M, Athill C A, Ting C T, Karagueuzian H S, Chen P S
Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital and Institute of Clinical Medicine, Cardiovascular Research Center, National Yang-Ming University School of Medicine, Taipei, Taiwan.
J Am Coll Cardiol. 2001 Nov 15;38(6):1757-65. doi: 10.1016/s0735-1097(01)01606-0.
We sought to evaluate the effects of progressive shortening of the action potential duration (APD) on atrial wave front stability.
The mechanisms of conversion from atrial flutter to atrial fibrillation (AF) are unclear.
Isolated canine right atria were perfused with 1 to 5 micromol/l of acetylcholine (ACh). We mapped the endocardium by using 477 bipolar electrodes and simultaneously recorded transmembrane potentials from the epicardium. The APD(90) was measured during regular pacing (S(1)) with cycle lengths of 300 ms. Atrial arrhythmia was induced by a premature stimulus (S(2)).
At baseline, only short runs of repetitive beats (<10 cycles) were induced. After shortening the APD(90) from 124 +/- 15 ms to 72 +/- 9 ms (p < 0.01) with 1 to 2.5 micromol/l of ACh, S(2) pacing induced single, stable and stationary re-entrant wave fronts (307 +/- 277 cycles). They either anchored to pectinate muscles (5 tissues) or used pectinate muscles as part of the re-entry (4 tissues). When ACh was raised to 2.5 to 5 micromol/l, the APD(90) was further shortened to 40 +/- 12 ms (p < 0.01); S(2) pacing induced in vitro AF by two different mechanisms. In most episodes (n = 13), AF was characterized by rapid, nonstationary re-entry and multiple wave breaks. In three episodes with APD(90) <30 ms, AF was characterized by rapid, multiple, asynchronous, but stationary wave fronts.
Progressive APD shortening modulates atrial wave front stability and converts atrial flutter to AF by two mechanisms: 1) detachment of stationary re-entry from the pectinate muscle and the generation of multiple wave breaks; and 2) formation of multiple, isolated, stationary wave fronts with different activation cycle lengths.
我们试图评估动作电位时程（APD）的逐渐缩短对心房波前稳定性的影响。
心房扑动转变为心房颤动（AF）的机制尚不清楚。
用1至5微摩尔/升的乙酰胆碱（ACh）灌注离体犬右心房。我们使用477个双极电极绘制心内膜图，并同时记录心外膜的跨膜电位。在周长为300毫秒的规则起搏（S1）期间测量APD（90）。通过早搏刺激（S2）诱发房性心律失常。
在基线时，仅诱发了短阵重复搏动（<10个周期）。用1至2.5微摩尔/升的ACh将APD（90）从124±15毫秒缩短至72±9毫秒（p<0.01）后，S2起搏诱发了单个、稳定且固定的折返波前（307±277个周期）。它们要么锚定在梳状肌上（5个组织），要么将梳状肌用作折返的一部分（4个组织）。当ACh浓度升至2.5至5微摩尔/升时，APD（90）进一步缩短至40±12毫秒（p<0.01）；S2起搏通过两种不同机制诱发出体外AF。在大多数发作中（n = 13），AF的特征是快速、非固定的折返和多个波裂。在APD（90）<30毫秒的三个发作中，AF的特征是快速、多个、异步但固定的波前。
APD的逐渐缩短调节心房波前稳定性，并通过两种机制将心房扑动转变为AF：1）固定折返从梳状肌脱离并产生多个波裂；2）形成具有不同激活周期长度的多个孤立固定波前。
