Huang Jian, Skinner Jonathan L, Rogers Jack M, Smith William M, Holman William L, Ideker Raymond E
Cardiac Rhythm Management Laboratory, Department of Medicine, University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, AL 35294-0019, USA.
J Am Coll Cardiol. 2002 Jul 17;40(2):375-83. doi: 10.1016/s0735-1097(02)01942-3.
The goal of this study was to evaluate the effects of acute and chronic amiodarone on activation patterns during ventricular fibrillation (VF), ventricular effective refractory period (VERP) and defibrillation threshold (DFT).
Acute and chronic amiodarone may act through different mechanisms.
The VERP, VF activation patterns and DFT were determined in 24 dogs. Twelve dogs received acute intravenous amiodarone (10 mg/kg, n = 6) or saline (n = 6), and 12 dogs received chronic oral amiodarone (20 mg/kg/day, n = 6) or placebo (n = 6). Epicardial VF activation patterns were recorded with 504 electrodes. Quantitative descriptors of VF were calculated.
The DFT was unchanged by acute or chronic amiodarone. Although chronic amiodarone significantly extended the VERP, acute amiodarone did not. In the mapped region, acute and chronic amiodarone decreased the number of VF wavefronts by 42% and 60%. Acute amiodarone decreased conduction block by 22%, while chronic amiodarone increased block by 41% but decreased wave fractionation by 50%. Both chronic and acute amiodarone increased the size of the core of re-entrant circuits and decreased the incidence of re-entry by 44% and 57%; however, chronic amiodarone increased wavelength, while acute amiodarone did not.
Neither acute nor chronic amiodarone change the DFT. While both acute and chronic amiodarone decrease the number of wavefronts, decrease the incidence of re-entry and increase the size of re-entrant cores in the mapped region during VF, they achieve these antiarrhythmic effects through different electrophysiologic mechanisms. Chronic amiodarone prolonged the VF cycle length and slowed conduction velocity, indicating it increased the wavelength and/or the excitable gap.
本研究旨在评估急性和慢性胺碘酮对心室颤动（VF）期间的激活模式、心室有效不应期（VERP）和除颤阈值（DFT）的影响。
急性和慢性胺碘酮可能通过不同机制发挥作用。
对24只犬测定VERP、VF激活模式和DFT。12只犬接受急性静脉注射胺碘酮（10mg/kg，n = 6）或生理盐水（n = 6），12只犬接受慢性口服胺碘酮（20mg/kg/天，n = 6）或安慰剂（n = 6）。用504个电极记录心外膜VF激活模式。计算VF的定量描述指标。
急性或慢性胺碘酮均未改变DFT。虽然慢性胺碘酮显著延长VERP，但急性胺碘酮未出现此情况。在标测区域，急性和慢性胺碘酮使VF波前数量分别减少42%和60%。急性胺碘酮使传导阻滞减少22%，而慢性胺碘酮使传导阻滞增加41%，但使波碎裂减少50%。慢性和急性胺碘酮均增大折返环核心的大小，并使折返发生率分别降低44%和57%；然而，慢性胺碘酮增加波长，急性胺碘酮则未增加。
急性和慢性胺碘酮均未改变DFT。虽然急性和慢性胺碘酮在VF期间均减少波前数量、降低折返发生率并增大标测区域折返核心的大小，但它们通过不同的电生理机制实现这些抗心律失常作用。慢性胺碘酮延长VF周期长度并减慢传导速度，表明其增加了波长和/或可兴奋间隙。
