Yoshiga Yasuhiro, Shimizu Akihiko, Yamagata Toshihiko, Esato Masahiro, Ueyama Takeshi, Ohmura Masato, Itagaki Kazuo, Kimura Masayasu, Kakugawa Hiroyuki, Doi Masahiro, Matsuzaki Masunori
The Department of Medical Bioregulation, Faculty of Science, Yamaguchi University School of Medicine, Ube, Japan.
Circ J. 2003 May;67(5):437-42. doi: 10.1253/circj.67.437.
The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.
本研究的目的是评估服用氟卡尼后右心房电生理特性的变化，并阐明氟卡尼是否对人体心房组织有选择性作用。对38例患者在静脉注射氟卡尼（每10分钟2mg/kg）前后进行电生理测量。根据基线研究中是否诱发反复性房性激动（RAF），将患者分为2组，研究右心房的有效不应期（ERP-A）、最大传导延迟（Max.CD）、反复性房性激动区（RAFZ）、碎裂心房活动区（FAAZ）和传导延迟区（CDZ）。在基线研究中有RAF的患者中，氟卡尼显著延长了ERP-A（从202±22ms延长至238±33ms，p<0.001）并缩短了Max.CD（从77±17ms缩短至63±32ms，p<0.05），但在基线研究中无RAF的患者中则没有这种情况。服用氟卡尼后，有RAF的患者的RAFZ（从43±22ms降至13±19ms，p<0.0001）、FAAZ（从51±22ms降至28±26ms，p<0.001）和CDZ（从70±21ms降至48±30ms，p<0.01）均有显著降低。然而，在基线研究中无RAF的2例患者在服用氟卡尼后因刺激诱发了心房颤动（AF）。基线研究中的ERP-A与服用氟卡尼后ERP-A的变化之间存在显著负相关（r=0.45，p<0.01）。氟卡尼可能优先激活房颤和RAF的基质，但该作用主要基于基线研究中发现的电生理特性。
