Kasper W, Treese N, Meinertz T, Jähnchen E, Pop T
Am J Cardiol. 1983 Jun;51(10):1618-22. doi: 10.1016/0002-9149(83)90197-2.
The electrophysiologic effects of lorcainide, a class I antiarrhythmic agent with local anesthetic properties, were studied in 20 patients with the Wolff-Parkinson-White syndrome. After intravenous administration of lorcainide (2 mg/kg), the sinus cycle length decreased in all patients from 705 +/- 117 to 636 +/- 94 ms (p less than 0.001). The atrioventricular conduction time lengthened from 84 +/- 22 to 94 +/- 22 ms (p less than 0.01) and the QRS duration increased from 92 +/- 19 to 120 +/- 29 ms (p less than 0.001). The effective refractory period of the atrium increased from 230 +/- 27 to 243 +/- 35 ms (p less than 0.05), whereas the ventricular refractoriness was unaffected. Retrograde conduction over the accessory pathway was blocked in 5 of 18 patients after lorcainide; in the remaining 13 patients a prolongation from 107 +/- 32 to 162 +/- 57 ms (p less than 0.001) was found. Anterograde conduction over the accessory pathway was blocked in 6 patients, and in all other patients it increased considerably. Circus movement tachycardia could be induced in 14 patients before and in 10 patients after the drug. The shortest R-R interval during tachycardia lengthened from 326 +/- 40 to 364 +/- 67 ms (p less than 0.05). The tachycardia zone was unaffected by lorcainide. In 15 patients atrial fibrillation was induced. After lorcainide anterograde conduction during atrial fibrillation was blocked (n = 5). The shortest R-R interval over the accessory pathway during induced atrial fibrillation increased from 228 +/- 35 to 304 +/- 103 ms (p less than 0.05). Intravenous administration of lorcainide produced a pronounced negative dromotropic effect on the conduction properties of the accessory pathway. Lorcainide appears to be a promising new antiarrhythmic agent in patients with the Wolff-Parkinson-White syndrome.
对20例预激综合征患者研究了具有局部麻醉特性的Ⅰ类抗心律失常药劳卡尼的电生理效应。静脉注射劳卡尼（2mg/kg）后，所有患者的窦性周期长度从705±117ms降至636±94ms（p＜0.001）。房室传导时间从84±22ms延长至94±22ms（p＜0.01），QRS时限从92±19ms增加至120±29ms（p＜0.001）。心房有效不应期从230±27ms增至243±35ms（p＜0.05），而心室不应期未受影响。18例患者中有5例在使用劳卡尼后旁路逆行传导被阻断；其余13例患者的逆行传导时间从107±32ms延长至162±57ms（p＜0.001）。6例患者旁路前向传导被阻断，所有其他患者的前向传导均显著增加。14例患者在用药前可诱发折返性心动过速，10例患者在用药后可诱发。心动过速期间最短的R-R间期从326±40ms延长至364±67ms（p＜0.05）。心动过速区不受劳卡尼影响。15例患者诱发了心房颤动。使用劳卡尼后心房颤动期间的前向传导被阻断（n = 5）。诱发心房颤动期间经旁路的最短R-R间期从228±35ms增加至304±103ms（p＜0.05）。静脉注射劳卡尼对旁路的传导特性产生显著的负性变传导作用。劳卡尼似乎是预激综合征患者一种有前景的新型抗心律失常药。
