Yamamoto T, Yeh S J, Lin F C, Wu D L
Department of Medicine, Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan, Republic of China.
Am J Cardiol. 1990 Jun 15;65(22):1438-42. doi: 10.1016/0002-9149(90)91351-6.
The effects of isoproterenol on accessory pathway conduction were evaluated in 24 patients with intermittent and 60 patients with concealed pre-excitation, using atrial and ventricular incremental and extrastimulus testing techniques. The atrial paced cycle length that induced block in the accessory pathway could be compared in 11 of the 24 patients with intermittent preexcitation before and after isoproterenol; it decreased from 622 +/- 212 ms to 408 +/- 128 ms (mean +/- standard deviation) after isoproterenol (p less than 0.01). The anterograde effective refractory period of the accessory pathway could be compared in 5 patients before and after isoproterenol; it decreased from 460 +/- 131 to 310 +/- 48 ms after isoproterenol (p less than 0.01). None of the 60 patients with concealed preexcitation showed ventricular preexcitation with isoproterenol infusion. Eighty-one of the 84 patients had clinically documented supraventricular tachycardia, suggesting the accessory pathway was capable of retrograde conduction. Retrograde study was performed in all 84 patients; 83 had retrograde conduction and the other had no retrograde conduction before and after isoproterenol. The ventricular paced cycle length that induced block in the accessory pathway could be compared in 38 patients before and after isoproterenol; it decreased from 342 +/- 71 to 296 +/- 39 ms after isoproterenol (p less than 0.001). The retrograde effective refractory period of the accessory pathway could be compared in 56 patients; it decreased from 293 +/- 76 to 238 +/- 36 ms after isoproterenol (p less than 0.001). In conclusion, isoproterenol facilitates anterograde and retrograde accessory pathway conduction, but the facilitation of anterograde conduction occurs only in those capable of spontaneous conduction.
采用心房和心室递增刺激及期外刺激测试技术，对24例间歇性预激患者和60例隐匿性预激患者评估了异丙肾上腺素对旁路传导的影响。在24例间歇性预激患者中，11例可比较异丙肾上腺素使用前后诱发旁路阻滞的心房起搏周期长度；异丙肾上腺素使用后，该长度从622±212毫秒降至408±128毫秒（平均值±标准差）（p<0.01）。5例患者可比较异丙肾上腺素使用前后旁路的前向有效不应期；异丙肾上腺素使用后，该不应期从460±131毫秒降至310±48毫秒（p<0.01）。60例隐匿性预激患者中，无一例在输注异丙肾上腺素时出现心室预激。84例患者中有81例有临床记录的室上性心动过速，提示旁路能够进行逆向传导。对所有84例患者进行了逆向研究；83例在异丙肾上腺素使用前后均有逆向传导，另一例无逆向传导。38例患者可比较异丙肾上腺素使用前后诱发旁路阻滞的心室起搏周期长度；异丙肾上腺素使用后，该长度从342±71毫秒降至296±39毫秒（p<0.001）。56例患者可比较异丙肾上腺素使用前后旁路的逆向有效不应期；异丙肾上腺素使用后，该不应期从293±76毫秒降至238±36毫秒（p<0.001）。总之，异丙肾上腺素促进旁路的前向和逆向传导，但前向传导的促进仅发生在那些能够自发传导的患者中。
