Download Multifocal Atrial Tachycardia4

Multifocal Atrial
Tachycardia4
James McCord, MD; and Steven Rorzak, MD
is typically seen in elderly patients with severe illnesses, most
tachycardia
ofthe arrhythmia may be delayed afterdepolarizations leading
The
mechanism
COPD.
commonly
Multifocal atrial
but this has not been firmly established. The initial treatment of multifocal
triggered activity,should
include supportive measures and aggressive reversal of precipitating
atrial tachycardia
causes. Since multifocal atrial tachycardia is commonly a secondary phenomenon, the role for
antiarrhythmic therapy is unclear. Metoprolol, magnesium, and verapamil have been evaluated
in a few treatment studies, and may have a role in the treatment of multifocal atrial tachycardia.
to
(CHEST 1998; 113:203-09)
Key words: magnesium; metoprolol; multifocal atrial tachycardia; verapamil
Abbreviations: AV=atrioventricular; CHF=congestive heart failure;
M AT=multifocal atrial
PE=pulmonary embolism
HP he term multifocal atrial tachycardia (MAT) was
¦*¦ first used in 1968
by Shine et al,1 but this rhythm
has been described previously by other names such
as chaotic atrial tachycardia,2 chaotic atrial rhythm,3
chaotic atrial mechanism,4 and repetitive multifocal
atrial tachycardia.56 In addition, in the
paroxysmal
1930s, there were rhythms described as "polymorphe extrasystole"7 and "anarchi auriculaire"8 that
represented MAT.
probably
Shine et al1 defined MAT
(Fig 1) as a rhythm with
atrial rate >100 beats/min, at least three morpho¬
and
irregularP P-P intervals,
logically distinct P waves,between
waves (to further
an isoelectric baseline
differentiate MAT from atrial fibrillation and atrial
flutter). Some authors have suggested that there
should be three distinct P waves different from the
sinus P wave,9 while others have stated that two
distinct P waves in addition to the sinus P wave are
There is no clear consensus
adequate forthisdiagnosis.10
criteria for MAT have
Other
issue.
regarding
been suggested, such as >50% of all atrial beats
an
varying R-R intervals, varying P-R
being ectopic,
and
atrial rate >120 beats/min,12 but
intervals,11
these are less well accepted.
MAT can easily be misinterpreted as atrial fibril¬
lation on an ECG. One retrospective study showed
that in patients hospitalized with MAT, only 22% had
their ECG interpreted correctly on admission.13 The
differentiation of atrial fibrillation from MAT is
Henry Ford Hospital, De¬
accepted June 13.
Manuscript received April 30, 1997; revision
MD,
ReprintFord
requests: James McCord, MD, or Steven Borzak,
Cardiovascular Division, 2799 W Grand
Hospital,
Henry
MI 48202
*From the Cardiovascular Division,
troit.
Blvd, Detroit,
important because their
atrial ECG may
from MAT.23
tachycardia;
differ. Intraatrial fibrillation
treatments
help distinguish
Population
The prevalence of MAT in the hospitalized popu¬
lation has been estimated to be 0.05 to 0.32%o.1'2-414
Review of >300 patients with MAT from nine
studies demonstrated an average age of 72 years, and
an in-hospital mortality rate of 45%o.1-4111316 The
mortality rate is most likely a consequence of
high
the severe underlying illnesses of these patients,
rather than a direct result of the arrhythmia itself.
MAT occurs even less commonly in the pediatric
In 28 patients from six reports, the ages
population.
to 18 years, but these young
from
ranged did newborn
have
serious medical conditions as
as
not
patients
their adult counterparts:1722 54% had no other
condition besides the arrhythmia, 21% had congen¬
ital heart disease, and 25% had a variety of other
conditions. Also, a few young adults have been noted
to have MAT without any underlying illness.23
Clinical Setting
COPD
An exacerbation of COPD is the most common
setting in which MAT arises. COPD was present in
55% of patients with MAT described in various
studies1-41113-16'24"33 (Table 1). Patients with the
and COPD have a high mortality rate:
arrhythmia
80% in one study.1
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203
tions.34 Theophylline may also be arrhythmogenic by
causing increased urinary excretion of potassium and
magnesium,3538 and thereby hypokalemia and hypomagnesemia.
Similarly, the development of MAT has been
related to P-agonist therapy. Six of 14 patients with
MAT who had aggressive treatment with nebulized
isoproterenol had termination of the arrhythmia
when the drug therapy was discontinued.4
Hypoxemia
Hypoxemia was present in 43% of patients with
MAT in several studies.21126 In one study, 85% of
MAT patients were in acute respiratory distress.15
Hypoxemia may contribute to the arrhythmia in
COPD, but may cause MAT in other settings as well.
In two studies, 17% of MAT cases occurred in the
postoperative setting,13 where hypoxemia associated
with atelectasis or pneumonia might have contrib¬
Figure 1. The rhythm strip demonstrates multiple P-wave
atrial rate >100 beats/min, and varying P-P
configurations,
intervals. Right ventricular hypertrophy is noted in \\.
The
of COPD may promote the ar¬
rhythmia.
study of 16 patients with MAT, all
had cessation of the arrhythmia when theophylline
therapy was discontinued.11 Twelve patients had
theophylline levels >20 ng/mL. Five of these pa¬
tients had theophylline therapy restarted, and MAT
recurred in all. An apparent direct relationship was
shown between the theophylline level and the num¬
ber of atrial ectopic beats.11 A study of 50 patients
with MAT showed that patients treated with theo¬
had significantly faster ventricular rates
phylline
when compared to similar patients not receiving the
drug.33 Ry increasing cyclic adenosine monophos¬
phate in myocardial cells, theophylline may promote
catecholamine-mediated delayed afterdepolariza-
uted.
treatment
In
one
Pulmonary Embolism
A weak relationship between MAT and pulmonary
embolism (PE) may exist. In a study of 50 patients
with MAT, PE was present in 4 of 14 patients who
had autopsies.33 In another study of 31 patients with
MAT, there were eight autopsies and only one of
these had a PE.14 In three other
PE was
studies,
cited in 14%), 10%, and 16% ofthe cases of MAT, but
none of these studies described how PE was diag¬
nosed.3'4-11
An association between PE and MAT was not
found in a subgroup analysis of the Prospective
Table 1.Clinical Characteristics
First Author
Arsura26
Hazard25
Levine27
Iseri30
Kouvaras32
Shine1
Phillips14
Wang15
Lipson2
COPD, No.
CHF, No.
(%)
(%)
6/11 (55)
20/25 (80)
3/6 (50)
5/8 (63)
5/9 (56)
10/32 (31)
26/31 (84)
10/41 (24)
12/31
(39)
Scher13
30/37 (81)
17/56 (30)
Levine11
16/16
Kones4
(100)
LowK+,
No.
(%)
of Patients With MAT
Afib/Aflutter,*
No. (%)
Hypoxemia, No.
PE, No.
(%)
10/11 (91)
5/25 (20)
4/32 (13)
(17)
10/31 (32)
22/37 (59)
6/56(11)
2/16 (13)
18/31 (58)
3/6 (50)
3/8 (38)
2/9 (22)
13/32 (41)
7/41
9/31 (29)
Berlinerblau3
Habibzadeh33
29/50 (58)
McCord51
14/14 (100)
Others16'24-28-29"31
38/55 (69)
Totals
250/453 (55)
74/269 (28)
* Afib/Aflutter=atrial fibrillation/atrial flutter.
5/31 (16)
2/37 (5)
5/25
(25)
(20)
4/14
(29)
4/16
41/178 (23)
12/31
19/41
17/31
(38)
(46)
(55)
1/8
10/31
(12)
(32)
5/37 (14)
5/16 (31)
1/16 (16)
3/31 (10)
4/14 (28)
25/58 (43)
14/106 (13)
5/31 (16)
53/134 (40)
204
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Reviews
atrial flutter.2'31415 The arrhythmia typically lasts 1
days, but a few cases of chronic MAT have
been documented.2-413 Paroxysms of atrial fibrilla¬
tion or atrial flutter have been shown in 16 to 55% of
patients with MAT (Table 2). Intra-atrial masses,
such as tuberculomas or metastatic lesions, have
been associated with the arrhythmia.4 Finally, al¬
MAT with digoxin
though onea author has associated
of
toxicity,10 preponderance studies do not support
an association between MAT and digoxin use or
Investigation of Pulmonary Embolism Diagnosis
trial. Of 117 patients with angiographically con¬
firmed PE, 4% had atrial fibrillation, 1% had atrial
flutter, but none had MAT. However, patients with
preexisting cardiac or pulmonary disease were ex¬
cluded from this analysis.39 Thus, a relationship
between PE and MAT cannot be excluded.
to 10
Congestive Heart Failure and Electrolyte
Abnormalities
There appears to be an association of congestive
heart failure (CHF) with MAT. Heart failure was
present in 28% of patients with MAT in several
studies, but most patients had coexisting lung disease
(Table 1). In nine studies, 23% of patients with MAT
had potassium levels <3.5 mEq/L, perhaps medi¬
ated by diuretic treatment of CHF (Table 1). There
have been reports of potassium and magnesium
associated with conversion of MAT to
replacement
sinus rhythm.40 In a small study of eight patients,
three of whom were hypokalemic and hypomagnesemic, all converted to normal sinus rhythm after
potassium and magnesium administration.30 Magne¬
sium modulates many of the potassium transport
systems, which may explain why treatment of refrac¬
tory hypokalemia is responsive to reversal of hypo-
toxicity.131315
Mechanisms
Delayedhasafterdepolarization
leading to "triggered
been
as
the mechanism for
activity"
proposed
never
but
this
has
been
our
MAT,274144
provedare(tooscil¬
knowledge). Delayed afterdepolarizations
lations in the cardiac myocyte membrane potential
that occur following repolarization of an action po¬
tential. When the delayed afterdepolarization is large
enough to reach threshold potential, the resultant
action potential is termed "triggered." Afterdepolar¬
izations stand in contrast to increased automaticity,
as an afterdepolarization is dependent on the occur¬
rence of a previous action potential, while automatic
occur de novo.
rhythms
Indirect evidence suggests that MAT may be due
to triggered activity. Intracellular calcium overload
promotes triggered activity. Many conditions associ¬
ated with MAT lead to intracellular calcium over¬
load, such as catecholamine excess,45 phosphodies-
magnesemia.35
Other Clinical
MAT is
ously
Settings
frequently transient and may spontane¬
rhythm, atrial fibrillation, or
convert to sinus
Table 2.MAT Studies
Reference No.
Intervention
No. of
Patients
Decrease in
Ventricular Rate,
p Value
Conversion to NSR*
Placebo-controlled studies
24
28
Metoprolol IV 9
Verapamil IV 9
Placebo 12
Verapamil IV 5
24
7
3
<0.01
Magnesium IV 9
24
3
<0.05
NS
Metoprolol IV 15
Metoprolol po 10
Metoprolol po 11
Verapamil IV 6
Verapamil IV 16
Verapamil IV 13
32
40
32
16
22
22
19
<0.001
<0.001
<0.01
<0.0001
<0.0005
<0.001
<0.01
32
<0.001
NS*
NS
Placebo 5
51
Placebo 5
3/9
1/9
2/12
1/5
0/5
4/9
0/5
Uncontrolled observational studies
25
26
27
29
16
30
31
32
53
52
Magnesium IV 8
Magnesium IV or IM
Amiodarone IV or po
Flecainide IV 4
Diltiazem 8
8
9
24
8/15
3/10
11/11
3/6
8/16
3/13
7/8
8/8
9/9
3/4
4/8
*NSR=normal sinus rhythm.
fNS=not significant.
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205
inhibition,11 acidemia,46 and hypoxemia.47
Triggered activity can be further potentiated by
terase
hypokalemia48
or
hypomagnesemia49 Verapamil,
which inhibits in vitro atrial triggered activity,715 has
been used in the treatment of MAT.16-24-27"29 How¬
ever, the efficacy of verapamil for MAT has been
inconsistent (Table 2), and delayed afterdepolariza¬
tion leading to triggered activity has never been
demonstrated in the setting of MAT (to our knowl¬
edge).
agents to treat patients with MAT16-24"32-51"53 (Table
2). However, these studies were limited to small
numbers of patients, and only four were controlled.24-28'51-53 The studies involved metoprolol,
verapamil, magnesium, diltiazem, flecainide, and
amiodarone.
Metoprolol
Arsura et al24 performed
controlled
study
that
a
double-blind, placebo-
compared metoprolol
with
verapamil (Table 2). Metoprolol demonstrated
THERAPEUTIC INTERVENTIONS
Reversal of precipitating causes remains the cor¬
of treatment for MAT, as this may be all
that is required to control the arrhythmia,1'2-4-13 and
harmful effects of antiarrhythmic agents
potentially
avoided.
be
COPD, CHF, electrolyte imbal¬
may
ance, hypoxemia, and PE should be treated with
consideration of the arrhythmia-promoting effects of
some therapies. Theophylline and (3-agonist therapy
should be decreased or discontinued if clinically
feasible. If a patient remains in MAT, antiarrhythmic
therapy can be considered for restoration of sinus
or rate control.
rhythm
Class 1 antiarrhythmic agents have been used
without perceived success in uncontrolled settings.
These include lidocaine, quinidine, procainamide,
and phenytoin.1'2'4'13'1519"21 In addition, electrical
cardioversion is not effective in converting MAT to
nerstone
rhythm.2'415
digoxin has not been evaluated
in a controlled study, but observational reports sug¬
gest that digoxin is not effective in controlling the
rate or restoring sinus rhythm in patients with
MAT.1215 This may be because slowing atrioventricular (AV) conduction does not address the atrial
mechanism of the tachycardia. Digoxin promotes
which may worsen
afterdepolarizations
delayed
when there is CHF or intermittent
MAT.
sinus
To our knowledge,
However,
atrial fibrillation, both of which are common in the
setting of MAT, digoxin may be beneficial. Digoxin
should be used cautiously as these patients may be
to digoxin toxicity.1 Ventricular ar¬
especially prone
death have been reported
rhythmias, AV block, andhas
been administered to
when excessive digoxin
MAT patients who were incorrectly diagnosed as
atrial fibrillation.1-15-18-50 In one study, pa¬
havingwith
MAT who were receiving digoxin had a
tients
mortality rate when compared
higher
significantly
not
This result, how¬
with patients
taking
digoxin.33worse
the
reflect
ever, may
general
prognosis of
with
heart
who
failure
are
more
patients
likely to be
receiving digoxin.
Thirteen studies have used other
antiarrhythmic
a
significant reduction in ventricular rate of 24%,
while verapamil and placebo had no effect on rate.
With metoprolol, more patients converted to sinus
rhythm. The only adverse effect was a transient drop
in RP with metoprolol from 150/70 mm Hg to 80/60
mm Hg in one patient that responded promptly to
fluids.
In two other studies, metoprolol demonstrated
significant decreases in ventricular rate of 35% and
32% 25,26 jn j-ne study of Hazard and Rurnett,25 one
third of discharged patients were maintained on a
regimen of oral metoprolol. There was no worsening
of pulmonary status; in fact, the average Po2 in¬
creased significantly from 77 to 89 mm Hg in
metoprolol-treated patients. However, there was no
control group for comparison. In the study of Arsura
et al,26 all 11 patients converted to normal sinus
rhythm after metoprolol.
Verapamil
Verapamil resulted in a significant
ventricular rate in three
decrease in
studies,162729 but
in two
other studies that were double-blind and placebocontrolled, there was no significant change24-28 (Ta¬
ble 2). Verapamil may worsen hypoxemia by negat¬
ing hypoxic pulmonary vasoconstriction in underventilated alveoli,16 but worsening oxygenation was not a
consistent finding. Hazard and Rurnett25 showed a
decrease in average Po2 of 105 to 78 mm
significant
while
Salerno et al29 showed no significant
Hg,
decrease in oxygenation. Salerno et al gave the
largest dose of IV verapamil (average, 17 mg) and
showed that pretreatment with calcium gluconate
decreased the hypotensive effect of
significantlywithout
blocking the heart rate-lowering
verapamil
effect (RP decreased 11% with calcium as opposed
to 27% without calcium).
Magnesium
study of Iseri et al,30 during "high-dose"
magnesium (Table 3) infusion, there was a significant
decrease in heart rate, and 88% of patients converted
to normal sinus rhythm. Only one patient had a
In the
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Reviews
Table 3.Drug Protocols for MAT
Reference No.
Drug
Dose
24
Metoprolol
Verapamil
10 mg IV over 5 min
10 mg IV over 5 min
2 g IV over 1 min, then 2 g/h over 5 h
300 mg po tid or 450-1,500 mg IV over 2-24 h
2 mg/kg IV bolus over 10 min, then 1.5 mg/kg for 1 h
0.15 mg/kg IV bolus over 5 min, then 0.005 mg/kg/min for 1 h
20-45 mg IV bolus, then 10-25 mg/h
Magnesium
30
32
Amiodarone
Flecainide
53
Verapamil
Diltiazem
52
of MAT and the average serum magne¬
from 1.6 to 3.5 mEq/L. Utilizing the
same protocol, McCord et al51 showed that magne¬
sium caused a significant decrease in heart rate as
compared with placebo, but only four of nine mag¬
nesium-treated patients converted to sinus rhythm.
Cohen et al31 treated MAT patients with either
magnesium sulfate IV or IM. Although no ventricu¬
lar rates were reported, all patients treated IM
converted to sinus rhythm within 1 to 2 h, while all
patients treated IV converted to sinus rhythm within
4 to 8 h. Cohen et al attributed this difference to the
higher sustained magnesium level in the first few
hours for the IM-treated group. No side effects were
reported in the magnesium studies. Of note, in all of
these studies, metoprolol, verapamil, and magne¬
sium decreased ventricular rate by suppressing atrial
ectopic beats, not by blocking AV conduction.
recurrence
sium level
rose
Other Agents
Kouvaras et al32 administered either oral or IV
amiodarone to patients with MAT. The four patients
who received IV dosing converted to sinus rhythm
within 45 min during a 2-h infusion of amiodarone.
One of these patients reverted to MAT and required
additional IV dosing. Of five patients who received
oral amiodarone, two converted to sinus rhythm on
the third day, one on the fourth day, and two on the
fifth day. All nine patients subsequently received oral
maintenance doses. Since MAT is frequently tran¬
sient, it is uncertain if conversion to sinus rhythm
represents an effect of amiodarone.
Adcock et al,52 in a preliminary report, studied
patients with MAT who received IV diltiazem as a
bolus and then maintenance infusion. Over a 4-h
period, four patients converted to sinus rhythm, and
during the infusion, there was a mean decrease in
ventricular rate of 35 beats/min. There was no
control group.
Rarranco et al53 studied six patients with MAT:
four received flecainide and two received verapamil.
After an IV bolus and then maintenance infusion
over 1 h, three of four patients who received flecain¬
ide and zero of two patients who received verapamil
in sinus rhythm. Two of the patients who
received flecainide converted to sinus rhythm during
the 10-min bolus. The effect on ventricular rates was
were
not
reported.
Limitations of these trials include few patients
(between 4 and 25), limited follow-up (<24 h in
most studies), and uncontrolled study design (only 4
studies were controlled).
Discussion
Should MAT be treated with antiarrhythmic
agents? The arrhythmia is typically an epiphenomenon of an underlying disorder, and perhaps should
not be directly treated. MAT is commonly transient
and will often resolve after precipitating causes are
reversed. If the arrhythmia persists, the clinical
significance of the tachycardia must be evaluated
before the use of antiarrhythmics is considered.
MAT would be clinically significant if it were to
cause hypotension, CHF, or myocardial ischemia as
can atrial fibrillation. Although atrial fibrillation causing
can be demonstrated with improvement in
hypotension
RP after electrical cardioversion, this phenomenon has
not been shown in MAT. The arrhythmia is not respon¬
sive to electrical cardioversion, and hypotension in this
setting is most likely secondary to underlying conditions
such as PE or sepsis.
Theoretically, MAT could exacerbate myocardial
ischemia or CHF, but this has not been described
commonly in the literature. In fact, it is surprising
how infrequently unstable angina or myocardial in¬
farction has been described in this elderly popula¬
tion.54 Myocardial ischemia, although uncommon in
MAT patients, may be the only compelling reason to
the
arrhythmia itself.
Unfortunately, since only a small number of pa¬
tients have been studied, and the clinical significance
of the arrhythmia is unclear, the role of antiarrhyth¬
mic therapy remains uncertain. The clinical rele¬
vance of persistent tachycardia must be evaluated on
an individual basis; potential benefits of antiarrhyth¬
mic therapy must be weighed against actual risks.
Since metoprolol is the only agent shown to be
treat
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207
effective for rate control in a double-blind, placebocontrolled trial,24 it should be the first agent consid¬
ered in the treatment of MAT. Metoprolol's mech¬
anism of action may be the blunting of the
stimulus that supports the milieu for
adrenergic
MAT. The use of metoprolol in the setting of MAT
is limited, however, because |3-blockers may worsen
CHF or bronchospasm. In two of the three studies
was an ex¬
involving
metoprolol,24-26 bronchospasm
third
the
while
exclusion
criterion,
study did
plicitmention exclusion
criteria.25 If (3-blockers are
not
esmolol with its short
relatively contraindicated,
adverse effects
be considered as
half-life may
any
may resolve soon after discontinuation.55
If metoprolol is not effective or contraindicated,
Resides
"high-dose" magnesium may be considered.
is
the
only agent
metoprolol, high-dose magnesium
shown to have efficacy in a placebo-controlled trial.51
The use of high-dose magnesium was shown to be
safe in the three MAT trials. The mechanism of
action of magnesium may be the inhibition of afterdepolarizations.49 The use of magnesium may be
limited by renal failure, but side effects such as
headache are minor and transient.
flushing andmeasures
If these
fail, dien verapamil may be con¬
sidered. In the two studies that used a control group,
however, verapamil was no better than placebo. The
use of verapamil is also limited in the presence of CHF
or hypotension. The hypotensive effect may be limited
with calcium.29 Although amiodarone,
by pretreatmentflecainide
and
diltiazem,
may have potential in the
treatment of MAT, they cannot routinely be recom¬
mended because to our knowledge, only one study with
a small number of patients evaluated each of these
three patients with MAT, who were
drugs. Finally,
treated with radioto
medical
therapy, were
refractory
and
ablation
AV
pace¬
frequency junctionAll three permanent
maker placement.56-57
patients had a success¬
ful ablation, and reported improvement in their
symptoms of palpitations and dyspnea. This method
may prove useful in patients with persistent and symp¬
tomatic MAT.
basis for this rhythm is hy¬
electrophysiologic
be
to
afterdepolarizations, which could be
pothesized
further mediated by the high adrenergic state encoun¬
measures and rever¬
tered in these
The
ment
to sinus rhythm and potential side ef¬
spontaneously
fects of antiarrhythmic agents can be avoided. If a
patient remains in MAT and the tachycardia is consid¬
ered clinically significant, a certain priority of antiarcould be considered: (3-blockers
rbythmic agents
or
and then vera¬
esmolol),
(metoprolol these magnesium,
have
been
evaluated in
However,
agents
pamil.
few studies involving small numbers of patients.
References
2
3
4
5
Febiger, 1956; 527
DL, Eaddy JA. Repetitive multifocal paroxysmal
atrial tachycardia with second degree A-V block, type I, and
6 Abrahms
7
8
9
10
MAT is most typically encountered in elderly pa¬
tients with COPD, and although the arrhythmia is
uncommon, its incidence may increase as does the
15
with atrial fibrillation. The distinction
quendy confused
as incorrect diagnosis may lead to ineffectual
and possibly harmful therapy.
is crucial,
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15:871-73
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bundle electrocardiography. Eur J Cardiol 1974; 2:153-59
13 Scher DL, Arsura EL, Oliver L, et al. Clinical profile and
14
aging population. This group commonly has numerous
KI, Kastor JA, Yurchak PM. Multifocal atrial tachycar¬
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1 Shine
Conclusions
concomitant medical problems, and the high mortality
rate is most likely due to the severity of their underlying
illness. MAT can be difficult to diagnose and is fre-
patients. Supportive
causes should be the initial treat¬
as
many patients will convert
strategy
sal of precipitating
prognostic factors in patients with multifocal atrial tachycar¬
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