Shiroshita-Takeshita Akiko, Mitamura Hideo, Ogawa Satoshi, Nattel Stanley
Department of Medicine and Research Center, Montreal Heart Institute, Université de Montréal, 5000 Belanger Street, Montreal, Quebec, Canada.
Cardiovasc Res. 2009 Jan 1;81(1):90-7. doi: 10.1093/cvr/cvn249. Epub 2008 Sep 17.
Although atrial-tachycardia remodelling is a significant atrial fibrillation (AF) promoting factor, little information is available about how atrial-tachycardia rate determines remodelling effects. This study assessed the effects of atrial tachypacing (ATP) over a range of clinically relevant rates on atrial electrophysiology and AF.
Chronically instrumented dogs underwent sequential 7 day ATP at 400, 300, 200, and 160 bpm in random order with 2 day recovery intervals between periods of ATP. ATP at 400, 300, and 200 bpm significantly decreased atrial effective refractory period (ERP) by 41 +/- 2, 37 +/- 3, and 7 +/- 1 ms, respectively, with no significant effects at 160 bpm. Mean duration of induced AF was increased by 400 and 300 bpm ATP (404 +/- 284 and 410 +/- 283 s on day 4, respectively, vs. 12 +/- 4 s at baseline, P < 0.01), but not by 200 or 160 bpm ATP. ATP effects developed slowly with 200 bpm pacing, so we studied 5 week ATP at 200 and 160 bpm in additional dogs. ERP shortened gradually over 3 weeks at 200 bpm (131 +/- 5 ms baseline vs. 112 +/- 4 and 105 +/- 4 ms at 2 and 3 weeks, respectively), but no decrease occurred thereafter (5-week value: 104 +/- 3 ms) and AF duration was not significantly affected. No change in ERP or AF duration occurred at 160 bpm. Because of the limited effects of 200 bpm ATP on AF duration despite significant effects on ERP, we tested 200 bpm ATP effects in the presence of AF substrates. When 200 bpm ATP was induced in the presence of a fibrotic AF substrate induced by 2 weeks of ventricular tachypacing followed by 1 week recovery, no change in AF duration or atrial vulnerability occurred. However, when 200 bpm ATP was followed by 400 bpm ATP, the onset of remodelling and AF duration increases was accelerated.
There is a non-linear relationship between atrial rate and the extent of atrial electrical remodelling. Remodelling at rates equivalent to paroxysmal supraventricular tachycardias in man is insufficient to promote AF alone or in the presence of an atrial fibrotic substrate, but can accelerate the remodelling and stabilization of AF when followed by faster atrial tachyarrhythmias.
尽管房性心动过速重塑是心房颤动（AF）的一个重要促发因素，但关于房性心动过速的速率如何决定重塑效应的信息却很少。本研究评估了在一系列临床相关速率下的心房超速起搏（ATP）对心房电生理和房颤的影响。
对长期植入仪器的犬只，以随机顺序在400、300、200和160次/分钟的频率进行连续7天的ATP，每次ATP之间有2天的恢复间隔。400、300和200次/分钟的ATP分别使心房有效不应期（ERP）显著缩短41±2、37±3和7±1毫秒，而160次/分钟的ATP无显著影响。400和300次/分钟的ATP使诱发房颤的平均持续时间增加（第4天分别为404±284和410±283秒，而基线时为12±4秒，P<0.01），但200或160次/分钟的ATP未使其增加。200次/分钟起搏时ATP效应发展缓慢，因此我们对另外的犬只进行了5周的200和160次/分钟的ATP研究。200次/分钟时，ERP在3周内逐渐缩短（基线时为131±5毫秒，2周和3周时分别为112±4和105±4毫秒），但此后不再缩短（5周时的值为104±3毫秒），房颤持续时间也未受到显著影响。160次/分钟时，ERP和房颤持续时间均无变化。由于200次/分钟的ATP尽管对ERP有显著影响，但对房颤持续时间的影响有限，我们在存在房颤基质的情况下测试了200次/分钟ATP的效应。当在由2周心室超速起搏后1周恢复诱导的纤维化房颤基质存在的情况下诱导200次/分钟的ATP时，房颤持续时间或心房易损性没有变化。然而，当200次/分钟的ATP之后紧接着400次/分钟的ATP时，重塑的开始和房颤持续时间的增加加速。
心房率与心房电重塑程度之间存在非线性关系。与人阵发性室上性心动过速相当的速率下的重塑，单独或在存在心房纤维化基质的情况下不足以促发房颤，但在随后出现更快的房性快速心律失常时可加速房颤的重塑和稳定。
