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Uncontrolled clinical observations
Brodsky and co-workers studied the effects of beta-blockers in 32 patients presenting
with either ventricular fibrillation (18) or sustained ventricular tachycardia (14); in
all, ventricular tachyarrhythmias were associated with impaired left ventricular function
(Brodsky et al, 1988). Antiarrhythmic drug therapy including beta-blockers was guided by
programmed stimulation (n = 10), exercise testing (n = 8), ambulatory monitoring (n = 12)
or was given empirically (n = 2). Long-term therapy with beta-blockers was continued in 23
of 32 (72%) patients. Although over a mean follow-up of 668 days patients treated with
beta-blockers had a relatively low incidence of both sudden (3%) and non sudden (9%)
death, the relative merit of beta-blocker therapy remains undetermined in this
retrospective analysis since the vast majority of patients received simultaneous treatment
with other antiarrhythmic drugs, including amiodarone in 47% of patients (Brodsky et al,
1988).
In ten patients with implanted cardioverter-defibrillators because of ventricular
tachycardia or fibrillation due to coronary artery disease or non-ischaemic underlying
heart disease, periods of treatment with and without beta-blocking agents were compared:
while taking beta-blockers, only four patients received shocks, compared to ten (ie all
cases) not administered beta-blockers (Leclercq et al, 1992). While there are important
study limitations (small patient number, only a few spontaneous shocks were documented on
ECG recordings), the moderate efficacy of beta-blockers to prevent the recurrence of
severe ventricular tachyarrhythmias deserves further investigations using implanted
devices with improved memory functions in a larger group of patients.
The largest experience today comes from a retrospective review on the use of
antiarrhythmic drugs and beta-adrenergic blocking agents in a large community-based
population of 941 patients resuscitated from out-of-hospital cardiac arrest (Hallstrom et
al, 1991). Of these, 18.7% were treated for at least a portion of the follow-up period
with quinidine, 17.5% with procainamide, and 39.4% received no antiarrhythmic agents;
beta-blockers were prescribed for 28.3% of the patients by community cardiologists and
other physicians. After adjustment for baseline risk factors, beta-blocker therapy was
associated with improved survival (p < 0.001). While based on a very large and
consecutive series of patients, it must be kept in mind that these data are observational
and uncontrolled (Hallstrom et al, 1991).
Quite opposite to class I and class III antiarrhythmic agents, which are thought to
produce proarrhythmia in a certain percentage of patients, this has not been shown for
beta-blockers (Velebit et al, 1982). In a few patients it could even be shown that
proarrhythmic effects induced by class IC antiarrhythmic agents could be suppressed by
beta-adrenergic blockade (Myerburg et al, 1989).
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