Author + information
- Received July 17, 1990
- Revision received October 24, 1990
- Accepted January 4, 1991
- Published online July 1, 1991.
- Georg Schmidt, MD*,1,
- Kurt Ulm, PhD1,
- Petra Barthel1,
- Andrea Riemenschneider1,
- August Linzmaier1,
- Liselotte Goedel-Meinen, MD1,
- Wolfgang Baedeker, MD1 and
- Hans Blömer, MD1
- ↵*Address for reprints: Georg Schmidt, MD, First Medical Clinic of the Technical University of Munich, Ismaninger Strasse 22, 8000 Munich 80, Germany.
To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom >30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SY) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2+ 0.01/EEday 1+ 0.01) and linked in one, two and three dimensions.
Compared with the consideration of only one type of arrhythmia (one-dimensional model), the simultaneous use of two or three types of arrhythmia (two-or three-dimensional model) resulted in considerably lower reduction and aggravation rates as sufficient proof of drug effects. With control intervals up to 1 week, the one-dimensional model yielded reduction rates for ventricular premature complexes, couplets and salvos of −63%, −90% and −95%, respectively. In contrast, with the three-dimensional model, the rates were −28%, −72% and −88%. The corresponding aggravation values were +370, +1,114% and +2,189% versus +38%, +256% and +747%. With longer control intervals, these values increased progressively (in the interval from 3 months to 1 year, with the three-dimensional model, the rates were −71%, −93% and −96% and +240%, +1,253% and +2,482%).
In conclusion, lower reduction rates are required to distinguish between spontaneous variations and therapy effects when the various forms of arrhythmia are assessed simultaneously than when they are assessed separately. The three-dimensional model not only facilitates future drug trials to determine antiarrhythmic drug efficacy, but also is important for controlling antiarrhythmic therapy in clinical practice.
- Received July 17, 1990.
- Revision received October 24, 1990.
- Accepted January 4, 1991.
- American College of Cardiology Foundation