Download Bradycardia-Tachycardia Syndrome

Bradycardia-Tachycardia Syndrome: Results
In Twenty-elsht PatIentr Treated b y
Combined Pharmacologic Therapy and
Pacemaker Implantation*
Julian M. Aroesty, M.D., Staford I . Cohen, M.D., and
Eugene Morkin, M.D.
The bradycardia-tachycardia syndrome was treated
with pacemaker implantation and drugs in 28 patients.
All patients survived pacemaker implantation and 26
of 28 patients experienced good control of their arrhythmias. Nineteen patients survived for more than one
year (group 1); nine patients survived for less than one
year (group 2), including two patients whose arrhythmias
were not well controlled by pacemaker plus drugs. There
was no significant difference in mean age between the
two groups (75 2 5 years in group 1 and 79 -c 3 years
in group 2). Gout, diabetes, hypertension, angina pectoris, and cardiomegaly were equally common in both
groups. Prior to implantation, 14 of 19 patients in group
1 were in NYHA class 1-2; 8 of 9 patients in group
2 were in NYHA class 3-4. Generally, the clinical classification of cardiac status was not changed by treatment.
Myocardial infarction, ventricular tachycardia, and primary renal disease were distinctly more common in
group 2. Massive myocardial infarctions, both d d and
recent, were found at necropsy. It is concluded that:
(1) permanent pacemaker implantation, when combined
with drug therapy, is effective in the control of the
bradycardia-tachycardia syndmme; (2) the prognosis of
patients successfuUy treated for the bradycardia-tachycardia syndrome is dependent on the extent of the underlying cardiac and renal disease.
lternating episodes of bradycardia and supraventricular tachycardia, the so-called bradycardiatachycardia syndrome, represents a vexing therapeutic problem.' Attempts to control tachyarrhythmias with 8-adrenergic blocking agents and
antiarrhythmic drugs may contribute to the severity
of the bradyarrhythmias, while the treatment of
bradyarrhythmias with ephedrine, belladonna alka-
procainamide or propranolol. The bradyarrhythrnias were
treated with ephedrine, atropine or belladonna. These medications were administered either parenterally or orally, in
progressively increasing dosage, until the occurrence of drug
side effects precluded a further increase.
Frequently, pharmacologic therapy was accompanied by
insertion of a temporary transvenous pacemaker. After the
patient's status stabilized, a fixed rate (Ventricor fixed-rate
pacemaker, Cordis Corp.) or R wave coupled (Ectocor
demand pacemaker, Cordis Corp.) permanent pacemaker
was implanted by the transvenous route.4 In all cases the
pacemaker rate was 70 to 72 stimuli per minute. The patients
were kept at rest for 12 to 24 hours following the operative
procedure, and were discharged from the hospital a t the
discretion of the primary physician caring for each patient.
The patients' electrocardiograms were reviewed using
standard criteria for left ventricular hypertrophy, left atrial
enlargement, bifascicular heart block, and myocardial infarction.5.6 The diagnosis of congestive heart failure and left
atrial enlargement was made using clinical and radiologic
criteria.6 A diagnosis of aortic stenosis was made on the basis
of an ejection systolic murmur at the base, an absent or
diminished aortic second sound, a diminished upstroke of the
carotid pulse and calcification of the aortic valve on fluoroscopy. A diagnosis of mitral regurgitation was made on the
basis of an apical systolic murmur and calcification of the
mitral valve or mitral annulus on fluoroscopy. Valvular or
coronary calcification was specifically sought on image intensified fluoroscopy at the time of temporary and permanent
pacemaker implantation.
The results were analyzed by the chi square method using
correction for small numbers. The age data are presented as
mean f standard error of the mean.7
A
For editorial comment, see page 223
loids, or catecholamines may increase the severity of
the tachyarrhythrnias. Because of these problems,
pacemaker implantation has been combined with
antiarrhythmic the rap^.^ However, patients treated
in this manner have not had a uniformly good res p o n ~ eWe
. ~ have reviewed our own experience in
28 patients with this syndrome to better define factors related to clinical management and prognosis.
Twenty-eight patients with the syndrome of alternating
bradycardia and tachycardia were referred to the cardiac
catheterization laboratory for consideration of permanent
pacemaker implantation. In each case, prior to pacemaker
implantation, an attempt was made to control the arrhythmia
using pharmacologic agents alone. Patients exhibiting the
tachyarrhythmias were usually given digitalis, quinidine,
'From the Cardiac Unit, Department of Medicine, Harvard
Medical School and Beth Israel Hospital Boston.
rted in part by a training grant hom the U.S. Public
Service ( HL-5809). Dr. Morkin is the recipient of
Career Development Award HL-13,639.
Manuscript received October 29; revision accepted February
5.
Reprint requests: Dr. Aroesty, 330 Brookline Auenue, Boston
02215
%&
CHEST, 66: 3, SEPTEMBER, 1974
Twenty-eight patients with the bradycardiatachycardia syndrome underwent permanent pacemaker implantation. Their clinical data and duration
BRADYCARDIA-TACHYCARDIA SYNDROME 257
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Table I-Bradycardia-Tachycardia Syndrome
Group 1
( > 1 Yr. Survival)
%
Group 2
( < I Yr. Survival)
Total
O/o
%
Patients, No.
Mean eurvival after pacemaker
implantation (mos.)
ECG Findings
Left anterior hemiblock
LBBB
RBBB and left anterior
hemiblock
LVH
S P P ~ ~ ~
syncope
Angina during tachycardia
Medical History
Gout
Diabetes mellitw
Hypertension
Angins pectoris
Mycardial infarction
Effect of Pharmscologic Therapy
No benefit in arrhythmia control
Some benefit in arrhythmia control
Valvular Hesrt Disease
Mitral valvular dieesse
Aortic valvular disease
*P value <.lo
**P value < .05
t P value <.01
LBBB - left bundle branch block
LVH - left ventricular hypertrophy
RBBB - right bundle branch block
of follow-up are summarized in Table 1. Of this
group, 24 (86 percent) had no further episodes of
paroxysmal tachycardia after pacemaker implantation. Two patients ( 7 percent) each had a single
episode of tachycardia requiring adjustment of their
medication, after which there were no further arrhythmias. Thus, 26 of the 28 patients (93 percent of
the total group) had excellent control of their arrhythmias over a mean period of 25 months following pacemaker implantation. Two patients ( 7 percent) failed to achieve a r r h y t h a control following
pacemaker implantation as manifested by eight episodes of tachycardia over a mean follow-up period
of two months.
Despite excellent arrhythmia control, only 19 of
the 28 patients were still alive at the end of a mean
follow-up period of U) months (32 percent mortality). Nine patients died less than one year following
pacemaker implantation (mean survival three
months). This latter group includes two patients
who failed to respond to combined pacemaker and
drug treatment.
To ascertain clinical features of prognostic sign&cance, the 19 patients surviving longer than one year
(group 1) were compared with the nine patients
who survived less than one year ( group 2 ) .
CLINICAL
DATA
History and Major Complaint
The clinical and electrocardiographic features of patients
in both groups are summarized in Table 1. Group 1 arm-
prised 5 men and 14 women ranging in age from 52 to 88
years, with a mean age of 75 k 5 years. Group 2 comprised
five men and four women ranging in age from 72 to 91 years,
with a mean age of 79 2 3 years. The incidence of gout,
diabetes mellitus, hypertension, and angina pectoris was
approximately equal in both groups. Although the occurrence
of syncope and angina pectoris during tachyarrhythrnias was
equally common in both groups, a history of a prior myocardial infarction was distinctly more common in group 2 ( 8
of 9 ) than in group 1 ( 5 of 19) (p<.01).
The major complaints at the time of pacemaker implantation also are shown in Table 1. Palpitations and dizziness
were present in almost all patients. Approximately two-thirds
of the patients had episodes of syncope. In general, this was
the most distressing symptom to the patient and was the most
frequent symptom bringing the patient to the physician's
attention. Angina also was a significant problem in these
patients, occurring in 21 percent of the total group, often in
association with the tachyarrhythmias. This symptom was
more common in group 2 than group 1; however the difference was not statistically significant (P>.10).
V d w l a r Heart Disease
A high incidence of valvular heart disease has been reported in patients with this syndrome.' Review of our cases
confirmed this impression and suggested that the presence of
aortic stenosis may be an unfavorable prognostic factor.
Seven patients had mitral valvular disease and five patients
with mitral valvular disease had mitral regurgitation alone.
One patient had combined mitral stenosis and regurgitation.
Mitral regurgitation was about equally common in both
groups, and its presence carried no prognostic significance.
The incidence of aortic stenosis was higher in the poor
prognosis group. A single patient in group 1 had aortic
stenosis, while this lesion was present in four of nine patients
in group 2. None of the patients had evidence of aortic
regurgitation.
258 AROESTY, COHEN, MORKIN
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CHEST, 66: 3, SEPTEMBER, 1974
Table %Incidence
o f Bradyarrhythrnitu and Tachyarrhythrnias Prior to
Permanent Pacemaker Implantation
Group 1
Group 2
Total %
(9 Pts.)
Bradyarrhythmias
Highest degree of A-V block
3" HB
2" HB
l o HB
Junctional bradycardia
Sinus arrest
Sino+atrial block
Sinus bradycardia
Tachyarrthmias
Junctional tachycardia
Atrial fibrillation with rapid ventricular response
Atrial flutter with rapid ventricular response
Paroxysmal atrial tachycardia
Ventricular tachycardia
l o HB - first degree heart block
2" HB - second degree heart block
3" HB - third degree heart block
Drug Therapy
Prior to pacemaker implantation, pharmacologic therapy
was attempted in all cases. In 11 of the 19 patients in group 1
(58 percent) and in eight of the nine patients in group 2 (89
percent) phannacologic treatment alone did not help control
the arrhythmias. In the remaining patients in both groups,
phannacologic therapy was of some benefit but did not
completely control the arrhythmias. Generally, large doses of
medications were required and side effects of the drugs
necessitated discontinuation before the desired p h m a cologic effect d d be achieved. Occasionally, the desired
effect of the drug was achieved, but only at doses which
either exacerbated the bradyarrhythmias
patients being
treated for tachvcardia or exacerbated the tachvarrhvthmias
. in patients being treated for bradycardia.
Arrhythmias and Other ECG Features
The incidence of various brady and tachyarrhythmias is
summarized in Table 2. Some degree of atrioventricular
block occurred in the majority of the patients in both groups.
Frequently, this followed attempts at control of the tachyarrhythmias using quinidine, procainarnide, digitalis or propranolol. The incidence of the various bradyarrhythmias was
not significantly different in the two groups. Atrial fibrillation,
paroxysmal atrial tachycardia or atrial flutter with a rapid
ventricular response, and junctional tachycardia occurred
about equally often in both groups. In contradistinction,
Table &Renal
ventricular tachycardia was much more common in group 2
(P<.05). Ventricular tachycardia occurred most often as an
immediate complication of a rapid supraventricular tachyarrhythmia, although it sometimes occurred independently of
the supraventricular tachycardia. In either circumstance, control of ventricular tachycardia was usually effected by pacemaker implantation and antiarrhythmic drugs.
A review of the electrocardiograms of the patients in both
groups showed no difference in the incidence of bundle
branch block, left anterior hemiblock, or bifascicular block.
However, left ventricular hypertrophy was somewhat more
common in group 2 ( p < -10), and the electrocardiographic
pattern of a healed myocardial infarction was significantly
more common in group 2 ( p < .01) .
Disease
The results suggest that there was little reversible component to the azotemia seen in these patients (Table 3). A
diagnosis of primary renal disease could be established in
almost all patients in group 2 (seven of nine) on the basis of
an abnormal urine sediment, positive urine culture, intravenous pyelography or postmortem examination. Evidence of
primary renal disease was uncommon among patients in
group 1 ( 2 of 19). This difference in the incidence of primary
renal disease was statistically s i d c a n t ( P < .005) and undoubtedly contributed to the poor survival of patients in
group 2.
Function in Patients with Pacemaker
-
One-year Prior to Pacemaker Implantation
Mean value of BUN
No. pts. with BUN above 40 mg%
At Time of Pacemaker Implantation
Mean value of BUN
No. pts. with BUN above 40 mg%
At Time of Discharge from Hospital
Mean value of BUN
No. pts. with BUN above 40 mg%
Patients with Primary Renal Disease
--
Group 1
%
Group 2
%
28 mg%
2/13
15
31 mg%
3 /9
33
30 ~ 3 %
4/19
21
59 mg%
7/9
78.
29 mg%
5/19
2/19
26
11
57 mg%
5/9
7/9
56
78.'
Total %
5/22 23
11/28 39
l0/28 36
9/28 32
P<.05
** P<.005
BUN - blood urea nitrogen
CHEST, 66: 3, SEPTEMBER, 1974
BRADYCARDIA-TACHYCARDIA SYNDROME 259
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Table 4--Pacemaker Implantation Data o f Patients in Group 1 and Group 2
%
Group 1
Demand Units
Fixed pace units
Competition (stimulus on T )
VPC
Retrograde P wave
Days, implantation to discharge, No.
Group 2
16
%
22
6
3*
3
2
5
2
10
12
26
12
Total, %
2
1
2
22
11
22
6
4
6
4
14
21
14
9
*Includes one demand unit that functioned only in the fixed-rate mode because of failure to sense the patient's ventricular depolarization.
PACEMAKER
IMPLANTATION
Factors relating to pacemaker implantation were
reviewed and are summarized in able 4. Twentytwo of the 28 patients had permanent transvenous
demand pacemakers. There were no episodes of
myocardial perforation, endocarditis, or pacemaker
infection. A careful attempt was made to achieve a
low pacing threshold, and in 26 cases the threshold
obtained was less than 1.0 ma. In two cases, a slightly higher threshold (1.3 and 1.5 ma) was obtained,
with no evidence of loss of pacemaker function. In
one patient pacing became ineffective because of an
increase in threshold from 0.8 ma to 8.0 ma. This
required removal of the pacemaker wire and reimplantation in a new site in the right ventricle
where the threshold was 0.5 ma. Fourteen months
later, the demand pacemaker was replaced electively. The threshold at that time was 1.0 ma.
Ventricular premature depolarizations and competition with the stimulus occurring on the T-wave
were occasionally seen in both groups of patients.
However, repetitive ventricular responses were not
noted. Retrograde capture of the atria was seen in
only two patients of each group. In one of these
patients, the retrograde atrial capture occurred only
intermittently.
Despite the critically-iU state of many of the patients, the surgical procedure was well tolerated and
patients were discharged from the hospital on an
average of ten days following pacemaker irnplantation.
Four patients in group 1 required replacement of
their pacemaker units at intervals of 20 to 31 months
(mean 24 months). These four patients had a mean
threshold of 0.6 ma at the time of primary implantation and a mean threshold of 1.7 ma at the time of
pacemaker replacement. One patient had a rise in
Table &Incidence
threshold six months following primary pacemaker
imp1antati0na
Effect of Pacemaker Implantation on Cardiac Status
Permanent pacemaker implantation resulted in no
immediate change in the cardiac status of patients in
either group (Table 5 ) . Prior to pacemaker implantation congestive heart failure was present in
approximately half of the patients in group 1 and all
of the patients in group 2 (Table 3 ) . Pacemaker
implantation resulted in a decrease in the number of
patients in group 1 with congestive heart failure;
however, this difference was not statistically significant (p>.05). Patients in group 2 were unimproved
despite continued treatment with digitalis, bedrest,
and diuretics.
At the time of implantation, the majority of the
patients in group 1were NYSHA class 1or 2 and the
majority of the patients in group 2 were MSHA
class 3 or 4. Limitation of activity of these patients
was caused by angina pectoris as well as congestive
heart failure. Whatever the etiology of their cardiac
limitation, a one- to six-month followup of these
patients after pacemaker implantation revealed little
change in their cardiac status (Table 6 ) .
Complications and Postmortem Examination
Embolization to a systemic artery occurred in 10
percent of patients in group 1 and 45 percent of the
patients in group 2. These episodes of embolization
occurred both prior to, and following pacemaker
implantation. None of these patients was continually treated with anticoagulant drugs.
Five patients were examined postmortem. All five
were in group 2. In each case, death was caused by a
massive acute myocardial infarction. In addition,
there were scars of large old myocardial infarctions
and Complieatbnr o f Congeative Heart Failure
Group 1
%
Group 2
%
Total, %
CHF prior to implantation of pacemaker
CHF a t pacemaker implantation
CHF 3 mo. after pacemaker implantation
Cardiomegaly by chest x-ray 6lm
Left atrial enlargement
Systemic embolization
*P <.05
CHF - congestive heart failure
260 AROESTY, COHEN, MORKlN
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CHEST, 66: 3, SEPTEMBER, 1974
Table M Y H A Ckurijication of Patientr
in Group 1 and 2
Group 1
%
Group 2
At Pacemaker Implantation
119
74
14/19
NYHA class 1 or 2
26
8/9
5/19
NYHA clam 3 or 4
1 6 Month Following Pacemaker Implantation
14/19
74
1/8*
NYHA clam 1 or 2
5/19
26
718
NYHA clam 3 or 4
%
Total, %
11** 15/28 54
89.. 13/23 46
13** 15/27 56
8 7 ' 12/27 44
*Since one of the group 2 patients died of ventricular tachycardia less than
one month following pacer implantation, there are only eight patients in
this follow-up group. Thk patient failed to achieve arrhythmia control,
and died suddenly three days after the pacemaker implantation.
**Pvalue C0.01
NYHA - New York State Heart Asaociition
in four of the five patients. An acute pulmonary
embolus was observed in one patient and evidence
of an old pulmonary embolus was found in another
patient. Four of the five patients had primary renal
disease by gross and histologic examination.
In all patients, the pacemaker was properly
wedged at the apex of the right ventricle and was
well covered by endothelium. There were no perforations of the myocardium and no intracardiac
thrombi in the right atrium or right ventricle. In the
two patients with pulmonary emboli at necropsy, the
source of the emboli was thought to be in the peripheral venous system. None of the patients had
evidence of systemic embolization or thrombi within
the left atrium or left ventricle.
The original observation of the relationship between sinoatrial heart block and paroxysmal atrial
fibrillation was made by Levine in 1916.8 Following
this initial observation, there were only sporadic
reportss" until demonstration of improved arrhythmia control by pacemaker implantation2 resulted in renewed interest in the bradycardia-tachycardia syndrome. Subsequently, there have been
many reports of treatment using pharmacologic
agents as well as pacemakers.12"'
The present series represents the largest reported
group of patients with the syndrome of brady- and
tachyarrhythmias treated by permanent pacemaker
implantation. Although the episodes of arrhythmias
were controlled in virtually all cases by a combination of pharmacologic therapy and pacemaker insertion, followup has revealed that one-third of the
total number of patients died within one year. Several factors may have been responsible for this outcome. First, there were more elderly patients in this
series than most other reports. Patients were generally in their seventh or eighth decade and many
had severe coronary artery disease and evidence of
primary renal disease. Secondly, this series includes
only patients with refractory arrhythmias who were
CHEST, 66: 3, SEPTEMBER, 1974
referred for pacemaker implantation. In younger
patients with thyrotoxicosis or valvular heart disease
as the etiology of this syndrome, treatment of the
underlying condition may result in excellent arrhythmia control.' As there is an increasing tendency toward aggressive management of older
patients with cardiac disease, we believe our experience may be useful in defining the results of
combined drug and pacemaker therapy.
At least four factors were identified, which when
present, suggested a poor prognosis: ( 1) severe limitation of physical activity either because of congestive failure or angina pectoris ( NYHA clinical classification 3 or 4 ) ; ( 2 ) valvular heart disease, particularly aortic stenosis, in association with coronary
artery disease; ( 3 ) ECG evidence of left ventricular
hypertrophy, old myocardial infarction or ventricular tachycardia; and (4) evidence of chronic primary renal disease with a blood urea nitrogen
(BUN) level greater than 40 mg percent. Although
the patients in group 1 seemed to achieve better
arrhythmia control by pharmacologic agents prior to
pacemaker implantation than did those in group 2,
this difference was not statistically significant (Table
1). Clinical or x-ray film evidence of cardiomegaly,
angina pectoris, syncopal episodes, diabetes mellitus, and a history of hypertension seemed to be
equally common in patients surviving for more than
one year ( group 1) ,and those surviving for less than
one year (group 2), hence, were of little prognostic
value.
An increased incidence of valvular heart disease
was reported previously in patients with the bradycardia-tachycardia syndrome.1.3.8.20.23,28~27
While
mitral valvular disease was equally common in both
groups of patients, aortic valvular disease was significantly more common in the patients in group 2.
None of these patients was thought to have critically
tight aortic stenosis on clinical grounds. At necropsy
none of the patients had aortic valve areas measuring less than 0.5 ~ m Thus,
. ~ the poor prognosis
observed in patients with aortic stenosis could not be
directly attributed to the hemodynamic consequences of this lesion.
ECG evidence of prior myocardial infarction, left
ventricular hypertrophy or the occurrence of ventricular tachycardia were both poor prognostic signs.
While improving our ability to apply effective antiarrhythmic therapy, pacemaker implantation has
failed to prevent the early death of patients with
prior episodes of ventricular tachycardia. These patients have died of the inexorable progress of their
coronary artery disease. All patients dying within
one year of pacemaker implantation, in whom postmortem data were available, had evidence of adBRADYCARDIA.TACHYCARDIA SYNDROME 261
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vanced coronary artery atherosclerosis, with extensive old and recent myocardial infarctions.
Elevation of blood urea nitrogen levels above 40
mg percent at the time of pacemaker implantation
was a striking sign of poor prognosis. None of the
deaths could be attributed directly to primary renal
disease. Rather, the intrinsic abnormalities in renal
function seemed to be exaggerated by a poorly compensated cardiovascular system.
There are a number of electrophysiologic factors
involved in the rapid alteration that occurs between
tachyarrhythmias and bradyarrhythmias. Since the
period of sinus node suppression following ectopic
tachyarrhythrmas is directly proportional to the
~ ~ . to
~ ~sinus
rate of the preceding t a c h y ~ a r d i a and
node function,34it is not surprising that the cessation of paroxysmal atrial tachyarrhythmias may be
accompanied by varying periods of asystole.
Treatment of tachyarrhythmia with quinidine,
procainamide, digitalis or p-blocking agents may
increase the asystolic interval following tachycardia.
Moreover, bradyarrhythmias are known to result not
only in dispersion of the refractory period^,^ but
also in a greater opportunity for an ectopic pacemaker focus to d i s ~ h a r g e Both
. ~ ~ factors are conducive to the development of a reentrant tachyarrhythmia.
In isolated cases, pacemaker implantation with
retrograde capture of the atria has reversed the
propensity toward the development of a supraventricular tachycardia, and it has been suggested that
pacemaker implantation alone may be adequate
therapy in these instance^.^^^^*^^ Although retrograde atrial capture during ventricular pacing is
noted in a high percentage of normal s~bjects,~'
we
have observed ventriculoatrial conduction in only 14
percent of our patients. It should be noted that
retrograde excitation may be confined to A-V junctional tissue without progressing to the atrium. It is
possible that ventricular pacing by this mechanism
may help to abort junctional tachycardias or reentrant tachycardias originating from the A-V junct i ~ nHowever,
.~~
in our experience electrical pacing
as the sole therapy did not control arrhythmias in all
patients with the bradycardia-tachycardia syndrome. Therefore we have treated patients with
drugs as well as pacemaker implantation. The pacemaker acts to prevent serious bradyarrhythmias and
allows treatment with larger doses of antiarrhythmic
agents.
Atrial or A-V sequential pacing may offer s i d cant advantages in controlling the arrhythmias
which may occur in the bradycardia-tachycardia
syndrome. This mode of therapy has not been util-
ized in our patients because of the prevalence of A-V
conduction abnormalities, and the diminished longevity and reliability of the A-V sequential pacemaker. When this problem is solved, demand A-V
sequential pacing may represent an ideal method of
controlling this syndrome while preserving the
hernodynamic advantage of atrial pacing.
Because of the distressing symptomatology of this
syndrome, patients with the bradycardia-tachycardia syndrome require as complete control of their
arrhythmias as possible, potentially reversible etiologic factors such as digitalis toxicity, hyperthyroidism or operable valvular heart disease should be
diligently sought. However, in patients beyond the
seventh decade, the majority of patients have severe
coronary artery disease as the underlying etiology.
Treatment with drugs in these patients is often
ineffective. An occasional patient may be managed
with full doses of digitalk3' While addition of suppressive agents (such as quinidine or procainamide)
may improve control of the tachyarrhythmia, these
agents often exacerbate bradyarrhythmias. Betaadrenergic blocking agents not only tend to exacerbate bradyarrhythmias, but must be used with extreme caution if there is preexisting congestive heart
failure. Because of these disadvantages, it is our
recommendation that permanent pacemaker implantation should be carried out prior to use of
suppressive agents and that p-adrenergic blockers
be used only if other antiarrhythmics fail. Using this
program, almost all patients can be maintained totally free of further episodes of tachycardia or bradycardia. In our experience, discontinuation of antiarrhythmic agents after pacemaker implantation has
resulted in recurrence of the tachyarrhythmia and,
hence, should be avoided.
Systemic embolization occurred in 21 percent of
our patients. The high frequency of this complication which also has been noted recently by others3'
generally has not received sufficient emphasis. Despite the possible increased risk of acute cardiac
tamponade should myocardial perforation by the
pacemaker electrode occur, it is our recommendation at present that continuous therapy with anticoagulants should be considered in the absence of a
strong contraindication. Abnormalities of renal function noted in our patients were not so severe as to
contraindicate continual use of anticoagulant therapy. However, the incidence of bleeding episodes
may be increased. Agents such as salicylates and
dipyridamole, which have been shown to diminish
arterial embolization in patients with prosthetic
valves,39may be useful in this syndrome as well.
ACKNOWLEDGMENTS: We thank Kathleen Kelley, R.N.
and Howard A. Frank, M.D. for their assistance during
pacemaker implantation.
262 AROESTY, COHEN, MORKIN
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CHEST, 66: 3, SEPTEMBER, 1974
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