Yang Yanfei, Mangat Iqwal, Glatter Kathryn A, Cheng Jie, Scheinman Melvin M
Cardiovascular Research Institute and Section of Cardiac Electrophysiology, University of California, San Francisco, California 94143-1354, USA.
Am J Cardiol. 2003 Jan 1;91(1):46-52. doi: 10.1016/s0002-9149(02)02996-x.
The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional "breaks" in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 +/- 9 months for the atypical group and 18 +/- 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.
本研究的目的是探讨非典型心房扑动(AFL)转变为心房颤动(AF)的机制,以及这些患者行三尖瓣峡部消融的长期结果。我们回顾性分析了我院221例行典型AFL消融患者的病历。共有25例患者为非典型AFL,其中23例依赖峡部的非典型AFL患者以及180例典型逆时针和/或顺时针AFL患者接受了三尖瓣峡部消融。总共17例患者中有11例记录到13次非典型AFL自发转变为AF。在AF发作前,13例患者中有11例(85%)观察到下环折返模式,3例(1例同时存在两种模式)为上环折返。13例患者中有6例(46%)在AFL期间沿三尖瓣环出现多个早期传导阻滞中断。在13次转变中,5例下环折返患者和1例上环折返患者(46%)在AF发作前出现离散的房性早搏。其余患者中,2例AF发作与肺静脉起源的更快房性心律有关。在某些情况下,AF发作前功能性阻滞线出现额外的“中断”。与典型AFL患者(38%)相比,非典型AFL患者AF发生率显著增加(68%)(p = 0.004)。非典型组平均随访28±9个月,典型组平均随访18±11个月,AF复发率相似(57%对48%,p = 0.4)。离散的房性早搏或房性心动过速可能直接引发AF,或通过在功能性阻滞线上产生进一步中断引发AF。双向三尖瓣峡部阻滞与约50%的AFL患者AF的治愈或控制相关。