Fareh S, Villemaire C, Nattel S
Department of Medicine and Research Center, Montreal Heart Institute and University of Montreal, McGill University, Montreal, Quebec, Canada.
Circulation. 1998 Nov 17;98(20):2202-9. doi: 10.1161/01.cir.98.20.2202.
Rapid atrial activation causes electrical remodeling that promotes the occurrence and the maintenance of atrial fibrillation (AF). Although remodeling has been shown to alter electrophysiological variables, the spatial uniformity of these changes is unknown.
Dogs subjected to rapid atrial pacing (400 bpm) for 24 hours (n=12) were compared with sham-operated dogs (instrumented but not paced, n=12). Epicardial mapping (240 bipolar electrodes) and extrastimulation at a large number of sites (mean+/-SEM, 66+/-4 per dog) were used to evaluate atrial activation and the heterogeneity of the effective refractory period (ERP), respectively. Rapid pacing increased both the percentage of sites at which AF could be induced by single premature stimuli (from 2.6+/-0.9% to 11.8+/-2.8%, P=0.007) and AF duration (from 39+/-28 to 146+/-49 seconds, P=0.03). Atrial tachycardia decreased atrial ERP (from 120+/-4 to 103+/-2 ms, P=0.003), increased the coefficient of variation of ERP (from 14.9+/-0.9% to 20.7+/-0.9%, P<0.0001), and accelerated conduction velocity (from 91+/-2 to 108+/-3 cm/s, P=0.0004), with no change in the wavelength. The increase in ERP heterogeneity was due both to interregional differences in the extent of ERP remodeling and to increased intersite variability within regions. Stepwise multilinear regression indicated that ERP heterogeneity was an independent determinant of the inducibility (P<0.0001) and duration (P<0.0001) of AF, whereas ERP per se and wavelength were not significant determinants. Combined mapping of AF induction and atrial ERP showed that premature extrastimuli induced AF at sites with short ERP by causing local conduction slowing and/or block in adjacent zones with longer ERP values.
Atrial tachycardia causes nonuniform remodeling of atrial refractoriness that plays an important role in increasing atrial vulnerability to AF induction and the duration of induced AF.
快速心房激动会引发电重构，促进心房颤动（AF）的发生和维持。尽管已表明重构会改变电生理变量，但这些变化的空间均匀性尚不清楚。
将接受24小时快速心房起搏（400次/分钟）的犬（n = 12）与假手术犬（仅植入仪器但未起搏，n = 12）进行比较。分别采用心外膜标测（240个双极电极）和在大量部位进行额外刺激（每只犬平均±标准误为66±4个部位）来评估心房激动和有效不应期（ERP）的异质性。快速起搏增加了单个早搏刺激可诱发AF的部位百分比（从2.6±0.9%增至11.8±2.8%，P = 0.007）以及AF持续时间（从39±28秒增至146±49秒，P = 0.03）。房性心动过速使心房ERP缩短（从120±4毫秒降至103±2毫秒，P = 0.003），增加了ERP的变异系数（从14.9±0.9%增至20.7±0.9%，P < 0.0001），并加快了传导速度（从91±2厘米/秒增至108±3厘米/秒，P = 0.0004），而波长无变化。ERP异质性的增加既归因于ERP重构程度的区域间差异，也归因于区域内部位间变异性的增加。逐步多元线性回归表明，ERP异质性是AF诱发性（P < 0.0001）和持续时间（P < 0.0001）的独立决定因素，而ERP本身和波长并非显著决定因素。AF诱发和心房ERP的联合标测显示，早搏额外刺激通过使ERP较短部位相邻ERP较长区域出现局部传导减慢和/或阻滞而诱发AF。
房性心动过速导致心房不应期的不均匀重构，这在增加心房对AF诱发的易感性以及诱发AF的持续时间方面起重要作用。
