[Spontaneous variability of ventricular arrhythmias in follow-up of anti-arrhythmia therapy].

The question of the reliability of ambulatory Holter monitoring for assessment of antiarrhythmic treatment has not been adequately resolved. Even though treatment efficacy had been individually assessed with Holter monitoring in the CAST study, during long-term treatment with class IC antiarrhythmic drugs, there were more deaths among patients receiving active drug than in those in the placebo group. Basic biostatistical considerations: Due to the spontaneous variability of frequency and complexity of ventricular arrhythmias, parametric models were developed with the aid of which normal ranges for spontaneous variability of singular ventricular premature complexes (VPC), couplets and salvos can be calculated. We designed a model which enables rapid visual analysis of the results: spontaneous variability = log (EE Day 2 + 0.01/EE Day 1 + 0.01) where EE is the number of ectopic events. For both days, the mean values per hour are applied. The use of parametric models prerequisites normal distribution of the data which can be achieved with logarithmic transformation. A constant is added to all mean values to preclude the mathematically-inadmissible form of log 0. The magnitude of the constant results in some degree of underestimation of the spontaneous variability. We chose the smallest constant, c = 0.01, consistent with a normal distribution of data. Figure 1 shows the normal range of the variability quotients for VPC in patients with cardiac disease and complex ventricular arrhythmias. The contiguous regions above and below the normal range designate active areas indicative of reduction or aggravation. Determinants of spontaneous variability: Frequency of arrhythmias: The number of VPC per unit of time exerts considerable influence on the spontaneous variability. The more infrequent an arrhythmia, the greater is the fluctuation to be anticipated. The differences in the variability of VPC, couplets and salvos are almost exclusively due to their differing frequencies since, in the presence of comparable frequency, they cannot be distinguished statistically from each other (Figure 2). Type and extent of underlying cardiac disease: In our patient population, there were no differences in spontaneous variability of arrhythmias between patients with coronary artery disease and those with dilated cardiomyopathy (Figure 3). Although in patients with coronary artery disease, as compared to those with noncoronary disease, a higher degree of spontaneous variability has been reported for VPC but, due to the inhomogeneity of the latter group, valid comparison is encumbered. The ejection fraction, the left ventricular filling pressure and the end-diastolic volume do not exert meaningful influence on the spontaneous variability (Figures 4 to 6).(ABSTRACT TRUNCATED AT 400 WORDS)