High-density mapping of pulmonary veins and left atrium during ibutilide administration in a canine model of sustained atrial fibrillation
High-density mapping of pulmonary veins and left atrium during ibutilide administration in a canine model of sustained atrial fibrillation
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DOI：
10.1152/ajpheart.00537.2005
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发表时间：
2005-12-01
影响因子：
4.8
通讯作者：
Chen, PS
中科院分区：
文献类型：
--
作者：
Chou, CC;Zhou, SM;Chen, PS
犬持续性房颤模型中伊布利特给药期间肺静脉和左心房的高密度标测。美国生理学杂志心脏循环生理学289：H2704-H2713，2005年。首次发表于2005年7月29日; doi：10.1152/ajpheart. 00537.2005. - 伊布利特可延长不应期，终止折返。伊布利特是否对肺静脉局灶性放电（FD）具有相同的作用尚不清楚。我们通过快速左心房（LA）起搏74 +/- 46天，在7只犬中诱导了持续性房颤（AF）。重复输注伊布利特，直至终止AF（0.02 +/- 0.01 mg/kg）或达到累积剂量（0.04 mg/kg）。进行高分辨率计算机心外膜标测。我们发现AF期间肺静脉间歇性FD和肺静脉-左心房交界处折返。伊布利特将连续折返的周期长度从97 +/- 13增加到112 +/- 18 ms，并将FD从96 +/- 7增加到113 +/- 9 ms。在4只肺静脉FD和折返的狗中，折返的发生率从基线时的3.5 ± 1.9/s降低到给药伊布利特后的2.2 ± 1.8/s。然而，FD的发生率保持不变。伊布利特显著降低了PV和LA之间的传导波前（10.4 +/- 2.0/s vs. 8.0 +/- 1.6/s）。终止AF所需的伊布利特剂量与PV和LA的基线有效不应期呈负相关。我们的结论是，伊布利特减少折返波前，但不PV FD在犬模型起搏诱导的持续性AF。这些研究结果表明，PV FD在AF是由于nonreentrant机制。大剂量伊布利特可完全终止所有折返活动，在窦性心律恢复前将AF转为PV心动过速。
High-density mapping of pulmonary veins and left atrium during ibutilide administration in a canine model of sustained atrial fibrillation. Am J Physiol Heart Circ Physiol 289: H2704-H2713, 2005. First published July 29, 2005; doi:10.1152/ajpheart. 00537.2005. -Ibutilide can prolong refractory period and terminate reentry. Whether ibutilide has the same effects on pulmonary vein (PV) focal discharge (FD) is unclear. We induced sustained atrial fibrillation (AF) in seven dogs by rapid left atrial (LA) pacing for 74 +/- 46 days. Ibutilide was repeatedly infused until it terminated AF (0.02 +/- 0.01 mg/kg) or when a cumulative dose was reached (0.04 mg/kg). High-resolution computerized epicardial mapping was performed. We found intermittent FD at the PVs and reentry at the PV-LA junction during AF. Ibutilide increased the cycle length of consecutive reentry from 97 +/- 13 to 112 +/- 18 ms and increased FD from 96 +/- 7 to 113 +/- 9 ms. In four dogs with both FD and reentry at the PVs, the incidence of reentry decreased from 3.5 +/- 1.9/s at baseline to 2.2 +/- 1.8/s after ibutilide administration. However, the incidence of FD remained unchanged. The conducted wave fronts between PV and LA were significantly reduced by ibutilide (10.4 +/- 2.0/s vs. 8.0 +/- 1.6/s). The ibutilide dose needed to terminate AF correlated negatively with the baseline effective refractory period of PV and LA. We conclude that ibutilide reduces reentrant wave fronts but not PV FD in a canine model of pacing-induced sustained AF. These findings suggest that the PV FD during AF is due to nonreentrant mechanisms. High doses of ibutilide may completely terminate all reentrant activity, converting AF to PV tachycardia before the resumption of sinus rhythm.