Author + information
- Received July 6, 1987
- Revision received March 23, 1988
- Accepted April 8, 1988
- Published online January 1, 1988.
- Ernst A. Raeder, MD, FACCa,
- Stefan H. Hohnloser1,
- Thomas B. Graboys, MD, FACC,
- Philip J. Podrid, MD, FACC,
- Stephen Lampert, MD, FACC and
- Bernard Lown, MD, FACC
- ↵aAddress for reprints:Ernst A. Raeder, MD, Cardiology Division, Health Sciences Center T-17-020, State University of New York, Stony Brook, New York 11794.
Day to day variability of ventricular ectopic activity was analyzed in 45 patients with a history of malignant ventricular tachyarrhythmias who underwent two successive 24 h periods of ambulatory electrocardiographic (ECG) monitoring in the absence of antiarrhythmic drugs; 26 were male and 19 female, with a mean age of 56 years (range 15 to 76). The total number of single ventricular premature beats, couplets and ventricular tachycardia beats and runs on days 1 and 2 demonstrated a consistent overall correlation (r = 0.76 to 0.84). Individual variability was evaluated by regression analysis with determination of 95% confidence limits.
The minimal decrease in arrhythmia density necessary to distinguish true drug effect from spontaneous variability was 64% for single ventricular premature beats, 83% for couplets, 90% for ventricular tachycardia runs and 93% for ventricular tachycardia beats. To meet the criteria for arrhythmia aggravation, the arrhythmia density had to increase by 400, 877, 1,500 and 2,400%, respectively. Multivariate analysis disclosed an inverse relation between day to day arrhythmia variability and baseline arrhythmia density and age. Variability was more pronounced in patients with coronary artery disease but was not influenced by the type of presenting arrhythmia or left ventricular function.
The diurnal distribution of arrhythmias and heart rate followed a distinct circadian pattern. These data indicate that, despite good group reproducibility, spontaneous arrhythmia variability in individuals is substantial, necessitating standards to define both drug effect and arrhythmia aggravation.
↵1 Dr. Hohnloser was a fellow of the Fritz Thyssen Foundation, Cologne, West Germany.
This study was supported in part by the Rappaport International Program of Cardiology, Boston, Massachusetts.
- Received July 6, 1987.
- Revision received March 23, 1988.
- Accepted April 8, 1988.
- American College of Cardiology