Neuberger Hans-Ruprecht, Schotten Ulrich, Blaauw Yuri, Vollmann Dirk, Eijsbouts Sabine, van Hunnik Arne, Allessie Maurits
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
J Am Coll Cardiol. 2006 Feb 7;47(3):644-53. doi: 10.1016/j.jacc.2005.09.041. Epub 2006 Jan 18.
This study was designed to investigate the mutual effects of chronic atrial dilation and electrical remodeling on the characteristics of atrial fibrillation (AF).
Both electrical remodeling and atrial dilation promote the inducibility and perpetuation of AF.
In seven goats AF was induced during 48 h by burst pacing, both at baseline and after four weeks of slow idioventricular rhythm (total AV block). Atrial size and refractory period (AERP) were monitored together with the duration and cycle length of AF paroxysms (AFCL). After four weeks of total atrioventricular (AV) block, the conduction in both atria was mapped during AF. Six non-instrumented goats served as controls.
At baseline, AF-induced electrical remodeling shortened AERP and AFCL to the same extent (from 185 +/- 9 ms to 149 +/- 14 ms [p < 0.05] and from 154 +/- 11 ms to 121 +/- 5 ms [p < 0.05], respectively). After four weeks of AV block the right atrial diameter had increased by 13.2 +/- 3.0% (p < 0.01). Surprisingly, in dilated atria electrical remodeling still shortened the AERP (from 165 +/- 9 ms to 132 +/- 15 ms [p < 0.05]) but failed to shorten the AFCL (140 +/- 19 ms vs. 139 +/- 11 ms [p = 0.98]). Mapping revealed a higher incidence of intra-atrial conduction delays during AF. Histologic analysis showed no atrial fibrosis but did reveal a positive correlation between the size of atrial myocytes and the incidence of intra-atrial conduction block (r = 0.60, p = 0.03).
In a goat model of chronic atrial dilation, AF-induced electrical remodeling was unchanged. However, AFCL no longer shortened during electrical remodeling. Thus, in dilated atria a wider excitable gap exists during AF, probably caused by intra-atrial conduction defects and a higher contribution of anatomically defined re-entrant circuits.
本研究旨在探讨慢性心房扩张与电重构对心房颤动（AF）特征的相互影响。
电重构和心房扩张均促进AF的诱发和持续。
对7只山羊，在基线状态以及在缓慢心室自主节律（完全性房室传导阻滞）4周后，通过短阵猝发刺激诱发AF持续48小时。监测心房大小和不应期（AERP）以及AF发作的持续时间和周期长度（AFCL）。在完全性房室（AV）传导阻滞4周后，在AF期间对双心房的传导进行标测。6只未植入仪器的山羊作为对照。
在基线时，AF诱发的电重构使AERP和AFCL缩短程度相同（分别从185±9毫秒缩短至149±14毫秒[p<0.05]，从154±11毫秒缩短至121±5毫秒[p<0.05]）。AV传导阻滞4周后，右心房直径增加了13.2±3.0%（p<0.01）。令人惊讶的是，在扩张的心房中，电重构仍使AERP缩短（从165±9毫秒缩短至132±15毫秒[p<0.05]），但未能缩短AFCL（140±19毫秒对139±11毫秒[p=0.98]）。标测显示AF期间心房内传导延迟的发生率更高。组织学分析未显示心房纤维化，但确实揭示了心房肌细胞大小与心房内传导阻滞发生率之间呈正相关（r=0.60，p=0.03）。
在慢性心房扩张的山羊模型中，AF诱发的电重构未改变。然而，在电重构期间AFCL不再缩短。因此，在扩张的心房中，AF期间存在更宽的可兴奋间隙，这可能是由心房内传导缺陷和解剖学定义的折返环的更高贡献率所致。
