Jordan J, Yamaguchi I, Mandel W J
Chest. 1978 Feb;73(2):215-8. doi: 10.1378/chest.73.2.215.
A 66-year-old white woman with a greater than 20-year history of electrocardiographic evidence of the Wolff-Parkinson-White syndrome, including documented recurrent supraventricular tachycardias, was studied. Despite the disappearance of the delta wave after initiation of therapy with digoxin and quinidine sulfate, the patient continued to have frequent episodes of supraventricular tachycardia. At a time when the serum levels of digoxin and quinidine were in the therapeutic range, extensive electrophysiologic studies were performed. Supraventricular tachycardia at a rate of 160 beats per minute was initiated by induced atrial premature depolarizations. The circuit of tachycardia involved anterograde conduction through the pathway of the atrioventricular node and His bundle and retrograde conduction through the bypass tract. We concluded that elimination of the delta wave and other electrocardiographic characteristics of the Wolff-Parkinson-White syndrome cannot be relied upon to indicate successful pharmacologic prophylaxis for induction of tachyarrhythmia associated with this syndrome.
一位66岁的白人女性，有超过20年心电图显示预激综合征的病史，包括记录在案的复发性室上性心动过速，接受了研究。尽管在用洋地黄和硫酸奎尼丁治疗后δ波消失，但患者仍频繁发作室上性心动过速。在洋地黄和奎尼丁血清水平处于治疗范围内时，进行了广泛的电生理研究。通过诱发房性早搏去极化引发了每分钟160次的室上性心动过速。心动过速的环路包括通过房室结和希氏束途径的前向传导以及通过旁路通道的逆向传导。我们得出结论，不能依靠消除预激综合征的δ波和其他心电图特征来表明对与该综合征相关的快速心律失常进行药物预防成功。
