Tai C T, Chen S A, Feng A N, Yu W C, Chen Y J, Chang M S
Department of Medicine, National Yang-Ming University, School of Medicine, Veterans General Hospital-Taipei, Taiwan, ROC.
Circulation. 1998 May 19;97(19):1935-45. doi: 10.1161/01.cir.97.19.1935.
Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear.
The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit.
Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.
I类和III类抗心律失常药物对典型心房扑动折返环的急性作用尚未得到充分研究。此外,抗心律失常药物终止心房扑动的关键电生理决定因素尚不清楚。
研究人群包括36例临床记录有典型心房扑动的患者(平均年龄53±17岁)。将一根20极的“光环”导管置于三尖瓣环周围。进行递增起搏以测量沿峡部和侧壁的传导速度,并进行额外刺激以评估基线状态以及静脉输注伊布利特、普罗帕酮和胺碘酮后的心房不应期。还确定了这些药物在转复典型心房扑动方面的疗效以及终止模式。伊布利特在短起搏周期长度时显著增加心房不应期并降低峡部的传导速度。在12例患者中有8例(67%)在峡部传导时间增加(86±19%)导致心房扑动周期长度延长后,伊布利特终止了心房扑动。普罗帕酮主要通过使用依赖性降低传导速度并显著增加心房不应期,但在12例患者中仅4例(33%)转复了心房扑动。胺碘酮对心房不应期和传导速度的影响比伊布利特和普罗帕酮小,在12例患者中仅4例(33%)终止了心房扑动。典型心房扑动的终止是由于波前通过峡部传播失败,这发生在周期长度振荡时、突然且无周期长度变化时或折返环过早激活后。
伊布利特具有独特的心房不应性增加,在转复心房扑动方面比普罗帕酮和胺碘酮更有效。