Circulation, Vol 82, 830-840, Copyright © 1990 by American Heart Association
JL Anderson, MI Anastasiou-Nana, RL Menlove, FL Moreno, JN Nanas and AH Barker
Previous determinations of variability in frequency of ventricular
arrhythmias have been based on repeated recordings obtained in the absence
of therapy. We evaluate variability during "effective" treatment with
antiarrhythmic drugs. Variability in the percent suppression of premature
ventricular complexes (PVCs) was determined in 55 patients with chronic
arrhythmias who underwent multiple ambulatory electrocardiographic
recordings during evaluation of chronic therapy with antiarrhythmic drugs
initially determined to be effective, which was defined as 70% or more
reduction in total PVC frequency or 90% or more reduction in repetitive
forms. During chronic therapy, total PVCs were suppressed by 92%, averaged
after a logarithmic transformation step, and repetitive beats were
suppressed by 88%. Variability in suppression was substantial. The
one-sided 95% confidence intervals required a fall in suppression of total
PVCs to 40% or less to exceed limits of spontaneous variability and of
repetitive PVCs to 66% or less. Suppression declined at least once during
therapy to less than 60% for total PVCs in 24 of 55 patients (44%) and to
less than 80% for repetitive PVCs in 13 of 33 patients (39%); nine patients
(16%) showed increases in PVC frequency at least once to levels above
pretreatment baseline. Seven subgroups were analyzed for their effects on
variability and loss of suppression: age, gender, disease etiology, cardiac
function, baseline PVC frequency, use of beta-blockers, and class of
antiarrhythmic drug. Differences in confidence bounds and loss of
suppression were found to be determined in a complex way by subgroup
differences in variability and in initial levels of PVC suppression.
Variability was greater for patient subgroups with greater PVC frequency,
beta-blocker therapy, and non-coronary artery disease. However, clinical
loss of suppression was more common only in more elderly patients and those
with worse cardiac function. In summary, substantial variability in
arrhythmia frequency occurs during effective antiarrhythmic therapy, and
the 95% confidence limits of spontaneous variability are broad and
determined in a complex way. Careful consideration should be given before
concluding on the basis of a single Holter test that changes (increases) in
arrhythmia frequency, especially in certain subgroups, are caused by
treatment failure.
ARTICLES
Spontaneous variability in ventricular ectopic activity during chronic antiarrhythmic therapy
Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City.
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