Aizawa Y, Chinushi M, Naitoh N, Shibata A
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Heart. 1996 Feb;75(2):165-70. doi: 10.1136/hrt.75.2.165.
The efficacy of drugs used to treat inducible monomorphic sustained ventricular tachycardia (VT) has been assessed by investigating their ability to suppress inducibility, but the mechanism of the drug action remains to be determined.
To determine electrophysiological variables that predict inducibility, divided doses of class I antiarrhythmic drugs were given and their effects were analysed, particularly the ability of the final dose to suppress inducibility.
The excitable gap was estimated by the zone of entrainment, which was defined as the difference between the cycle length of VT and the longest paced cycle length that interrupted VT during entrainment of VT with rapid pacing at paced cycle lengths in decrements of 10 ms. The cycle length of VT, the block cycle length, and the zone of entrainment were measured in the drug free state and after intermediate and final doses of procainamide, disopyramide, cibenzoline, and mexiletine.
Sustained monomorphic VT with a mean (SD) cycle length of 285 (43) ms was induced in 8 patients. It was entrained and interrupted at the block cycle length of 231 (31) ms. The width of the zone of entrainment was 54 (23) ms. In 8 studies VT was not inducible at final doses of procainamide in 4, cibenzoline in 1, and mexiletine in 3. In another 10 studies (procainamide in 4, disopyramide in 1, cibenzoline in 2, and mexiletine in 3), VT remained inducible at the intermediate dose and at the final dose. The cycle length of VT was prolonged to a similar degree in studies of effective and ineffective drugs, but the cycle length that blocked VT was longer at the intermediate dose of the effective drugs. Consequently, the width of the zone of entrainment was significantly narrowed at the intermediate dose of effective drugs and the width of the zone of entrainment was narrower than when ineffective drugs were given (22 (13) ms v 76 (18) or 75 (37) ms at the intermediate and final doses respectively (P < 0.02).
Drugs that narrowed the zone of entrainment were associated with non-inducibility of VT after the final dose of the drug was given. The baseline variables did not predict the responses to class I antiarrhythmic drugs.
用于治疗可诱导的单形性持续性室性心动过速(VT)的药物疗效已通过研究其抑制可诱导性的能力进行了评估,但药物作用机制仍有待确定。
为了确定预测可诱导性的电生理变量,给予了Ⅰ类抗心律失常药物的分次剂量并分析其效果,特别是最后一剂抑制可诱导性的能力。
通过拖带区估计可兴奋间隙,拖带区定义为VT的周期长度与在以10 ms递减的起搏周期长度快速起搏VT期间中断VT的最长起搏周期长度之间的差异。在无药状态下以及在给予普鲁卡因胺、丙吡胺、西苯唑啉和美西律的中间剂量和最后剂量后,测量VT的周期长度、阻滞周期长度和拖带区。
8例患者诱发了平均(标准差)周期长度为285(43)ms的持续性单形性VT。在231(31)ms的阻滞周期长度时可被拖带并中断。拖带区宽度为54(23)ms。在8项研究中,最后剂量的普鲁卡因胺使4例患者的VT不能被诱发,西苯唑啉使1例患者的VT不能被诱发,美西律使3例患者的VT不能被诱发。在另外10项研究中(4例使用普鲁卡因胺,1例使用丙吡胺,2例使用西苯唑啉,3例使用美西律),VT在中间剂量和最后剂量时仍可被诱发。在有效药物和无效药物的研究中,VT的周期长度延长程度相似,但有效药物中间剂量时阻滞VT的周期长度更长。因此,有效药物中间剂量时拖带区宽度显著变窄,且拖带区宽度比给予无效药物时更窄(中间剂量和最后剂量时分别为22(13)ms对76(18)ms或75(37)ms,P<0.02)。
使拖带区变窄的药物与给予最后一剂药物后VT的不可诱导性相关。基线变量不能预测对Ⅰ类抗心律失常药物的反应。