Hellestrand K J, Burnett P J, Milne J R, Bexton R S, Nathan A W, Camm A J
Pacing Clin Electrophysiol. 1983 Sep;6(5 Pt 1):892-9. doi: 10.1111/j.1540-8159.1983.tb04410.x.
To determine the effect of flecainide acetate, a Class IC antiarrhythmic drug, The medication was given to 28 patients with ventricular pacing electrodes. Eleven patients with temporary pacing electrodes (Group I) received intravenous flecainide (2 mg/kg over 10 minutes). Ten patients with chronic permanent electrodes (Group II) were given the same dose at the time of elective pulse generator change. Seven, with implanted multiprogrammable pacemakers capable of threshold analysis (Group III), were given intravenous flecainide and 5 of these were then given the drug orally for up to 3 weeks (100 mg/day increasing to 400 mg/day). In Group I the threshold measured at a pulse width of 0.5 ms rose from a control value of 0.66 to 1.44 volts after 10 minutes (p less than 0.01). In Group II the threshold rose from 1.73 to 2.13 volts (p less than 0.01) and 2 patients had total suppression of their ventricular escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise escape rhythm for approximately one hour. In Group III patients, intravenous flecainide resulted in a rise of the pulse width threshold measured at 2.7 volts from 0.14 to 0.22 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.11 ms (p less than 0.05) after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen to 0.11 ms /ms (p less than 0.05 after 10 minutes. After 3 weeks of oral therapy the threshold at 2.7 volts had risen from 0.09 to 0.28 ms (p less than 0.02) and at 4.9 volts from 0.06 to 0.16 ms (p less than 0.05) Flecainide significantly increased both acute and chronic thresholds and the most marked rise (greater than 200%) occurred during chronic oral therapy. Both intravenous and oral flecainide should be used with care in patients with either temporary or permanent pacing systems.
为确定ⅠC类抗心律失常药物醋酸氟卡尼的作用,对28例带有心室起搏电极的患者给予了该药物。11例带有临时起搏电极的患者(Ⅰ组)接受了静脉注射氟卡尼(10分钟内注射2mg/kg)。10例带有慢性永久电极的患者(Ⅱ组)在择期更换脉冲发生器时给予相同剂量。7例植入了能够进行阈值分析的多程控起搏器的患者(Ⅲ组)接受了静脉注射氟卡尼,其中5例随后口服该药长达3周(100mg/天,增至400mg/天)。在Ⅰ组中,脉宽为0.5ms时测得的阈值在10分钟后从对照值0.66伏升至1.44伏(p<0.01)。在Ⅱ组中,阈值从1.73伏升至2.13伏(p<0.01),2例患者的心室逸搏节律完全抑制约1小时。在Ⅲ组患者中,静脉注射氟卡尼导致脉冲宽度阈值升高。在Ⅲ组患者中,静脉注射氟卡尼10分钟后,在2.7伏测得的脉冲宽度阈值从0.14ms升至0.22ms(p<0.02),在4.9伏时从0.06ms升至0.11ms(p<0.05)。口服治疗3周后,2.7伏时的阈值从0.09ms升至0.28ms(p<0.02),在4.9伏时从0.06ms升至0.16ms(p<0.05)。氟卡尼显著增加急性和慢性阈值,最显著的升高(超过200%)发生在慢性口服治疗期间。对于有临时或永久起搏系统的患者,静脉和口服氟卡尼均应谨慎使用。