Sakai T, Ogawa S, Hosokawa M, Miyazaki T, Sakurai K, Nakamura Y
Department of Medicine, School of Medicine, Keio University, Tokyo, Japan.
Cardiovasc Res. 1989 Mar;23(3):177-83. doi: 10.1093/cvr/23.3.177.
Flecainide has been reported to be effective in suppressing chronic ventricular arrhythmias in clinical studies, but the electrophysiological mechanisms of its action are not understood. We therefore studied its effects on re-entrant ventricular arrhythmias in eight dogs with 7 day old infarction. Epicardial mapping and local refractory periods were obtained using 48 channel bipolar electrodes attached to the epicardium. Epicardial conduction velocity was significantly depressed by flecainide (2 mg.kg-1 intravenously), from 49.3 (SD 11.9) cms-1 to 35.3(11.2) cm s-1 (p less than 0.01). Flecainide prolonged effective refractory periods (ERP) in the normal, border and infarct zones: normal (n = 93), from 189.5 (15.9) to 219.3 (17.7) ms, p less than 0.01; border (n = 54) from 187.4(24.0) to 225.2 +/- 32.5 ms, p less than 0.01; and infarct (n = 93), from 197.7 (30.6) to 247.1 (34.2) ms, p less than 0.01. However, the percent change in refractoriness was greater in the infarct zone than in the normal zone, at 25.7(17.1)% v 16.2 (10.3)%, p less than 0.01. Furthermore, an area of functional unidirectional conduction block developed within the infarct zone where the maximal dispersion of ERP was observed. Inducible sustained ventricular tachycardia (SVT) was prevented in one dog and slowed (300 to 150 beats.min-1) in another by flecainide, while ventricular fibrillation remained inducible in one dog. Pro-arrhythmic effects were observed in two of five dogs without inducible SVT. In conclusion, flecainide significantly depressed conduction velocity and prolonged local refractoriness in the epicardial myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
据报道，氟卡尼在临床研究中对抑制慢性室性心律失常有效，但其作用的电生理机制尚不清楚。因此，我们研究了其对8只梗死7天的犬折返性室性心律失常的影响。使用附着于心外膜的48通道双极电极获取心外膜标测和局部不应期。静脉注射氟卡尼（2mg·kg-1）后，心外膜传导速度显著降低，从49.3（标准差11.9）cm·s-1降至35.3（11.2）cm·s-1（p<0.01）。氟卡尼延长了正常区、边缘区和梗死区的有效不应期（ERP）：正常区（n=93），从189.5（15.9）ms延长至219.3（17.7）ms，p<0.01；边缘区（n=54），从187.4（24.0）ms延长至225.2±32.5ms，p<0.01；梗死区（n=93），从197.7（30.6）ms延长至247.1（34.2）ms，p<0.01。然而，梗死区不应期的变化百分比大于正常区，分别为25.7（17.1）%和16.2（10.3）%，p<0.01。此外，在梗死区内观察到ERP最大离散度的区域出现了功能性单向传导阻滞区。氟卡尼在1只犬中预防了可诱导的持续性室性心动过速（SVT），在另1只犬中使其减慢（从300次/分钟降至150次/分钟），而1只犬仍可诱发出心室颤动。在5只无诱导性SVT的犬中，有2只观察到促心律失常作用。总之，氟卡尼显著降低了心外膜心肌的传导速度并延长了局部不应期。（摘要截短至250字）
