Andresen D, von Leitner E R, Wegscheider K, Schröder R
Z Kardiol. 1984 Aug;73(8):492-7.
The aim of this study was to develop standards to define both antiarrhythmic drug efficacy and a drug-induced arrhytmogenic effect. In 45 patients with frequent and complex ventricular tachyarrhythmias 3 continuous 24-hour Holter recordings were performed. The spontaneous variability of ventricular premature beats and ventricular pairs was calculated using a new statistical method (transformation model). If two 24-hour Holter monitoring periods, one period before and the other with antiarrhythmic therapy, are compared, at least 75% reduction of ventricular premature beats and 90% reduction of ventricular pairs is necessary to be reasonably certain that one is measuring a drug response rather than spontaneous arrhythmia reduction (p less than or equal to 0.05). On the other hand, drug-induced aggravation can be assumed if ventricular premature beats and ventricular pairs have increased by more than 144% and 227%, respectively (p less than or equal to 0.05).
本研究的目的是制定标准,以界定抗心律失常药物的疗效以及药物诱发的致心律失常作用。对45例频发复杂性室性心律失常患者进行了3次连续24小时的动态心电图记录。使用一种新的统计方法(转换模型)计算室性早搏和室性成对搏动的自发变异性。如果比较两个24小时动态心电图监测期,一个是抗心律失常治疗前的时期,另一个是进行抗心律失常治疗的时期,那么室性早搏至少减少75%且室性成对搏动至少减少90%,才能合理确定所测量的是药物反应而非自发心律失常的减少(p小于或等于0.05)。另一方面,如果室性早搏和室性成对搏动分别增加超过144%和227%(p小于或等于0.05),则可假定为药物诱发的病情加重。