In-Hospital Arrhythmia Development and Outcomes in Pediatric

Patients With Acute Myocarditis

Cardiac arrhythmias are a complication of myocarditis. There are no large

studies of inhospital arrhythmia development and outcomes in pediatric
patients with acute myocarditis. This was a retrospective 2-center review of
patients 21 years hospitalized with acute myocarditis from 1996 to 2012.
Fulminant myocarditis was defined as the need for inotropic support within
24 hours of presentation. Acute arrhythmias occurred at presentation and
subacute after admission. Eighty-five patients (59% men) presented at a
median age of 10 years (1 day to 18 years). Arrhythmias occurred in 38
patients (45%): 16 acute, 12 subacute, and 9 acute and subacute (1 onset
unknown).

Arrhythmias

were

associated

with

low

voltages

on

the

electrocardiogram (14 of 34, 41% vs 6 of 47,13%; odds ratio [OR] 4.78, 95%
confidence interval [CI] 1.60 to 14.31) and worse outcome (mechanical
support, orthotopic heart transplant, or death; OR 7.59, 95% CI 2.61 to
22.07) but were not statistically significantly associated with a fulminant
course, ST changes, initial myocardial function, lactate, creatinine level, Creactive protein and/or erythrocyte sedimentation rate, or troponin I level,
after adjusting for multiple comparisons. Subacute arrhythmias were
associated with preceding ST changes (10 of 15, 67% vs 15 of 59, 25%, OR
5.87, 95% CI 1.73 to 19.93). All patients surviving to discharge had
arrhythmia resolution or control before discharge (10 on antiarrhythmic),
with 1 exception (patient with complete heart block requiring a pacemaker).
At 1-year follow-up, there were 3 recurrences of ventricular arrhythmias, but
no arrhythmia-related mortality. In conclusion, arrhythmias are common in
pediatric patients with myocarditis, occurring in nearly 1/2 of all hospitalized
children and are associated with a worse outcome. Early identification of
subacute

arrhythmias

using

electrocardiographic

changes

may

help

management. A majority of patients do not require continued postdischarge

arrhythmia treatment. 2014 Elsevier Inc. All rights reserved. (Am J Cardiol
2014;113:535-540)

Cardiac arrhythmias are a common complication of myocarditis, with an

incidence ranging from 29% to 100%.The most common arrhythmias are
ventricular tachycardia (VT), ventricular fibrillation (VF), and atrioventricular
(AV) block. Published literature on arrhythmia development and outcomes in
pediatric myocarditis has been limited to case reports and small patient
populations studying subsets of cardiac arrhythmias. Friedman et alreviewed
12 pediatric patients with ventricular arrhythmias and occult myocarditis,
and Chien et al and Wang et al 10 both evaluated complete heart block (CHB)
in 9 patients. The most substantial pediatric study to date by Lee et al 3
described clinical outcomes of acute myocarditis in 36 children. The purpose
of this study was to evaluate the incidence and outcomes of in-hospital
arrhythmias in a larger cohort of pediatric patients with acute myocarditis
and determine predictors of in-hospital arrhythmia development.
Methods
This was a 2-center retrospective review of all patients aged <21 years
hospitalized with the diagnosis of myocarditis from 1996 to 2012. Medical
records were reviewed with permission from the Internal Review Board at the
Boston Childrens Hospital and Lucile Packard Childrens Hospital. For the
purposes of this study, all patients had (1) a clinical diagnosis of myocarditis
by a pediatric cardiologist, (2) prodromal viral or infectious symptoms <2
weeks before presentation, and (3) evidence of ventricular dysfunction
(ejection fraction <55% by echocardiography within 24 hours of admission).
A diagnosis of acute myocarditis also required at least 1 of the following: (1)
active or borderline biopsy by Dallas criteria, (2) positive infectious origin of
ventricular dysfunction, or (3) delayed enhancement on cardiac magnetic
resonance imaging consistent with myocarditis. In the absence of one of

these findings, we defined additional patients if (4) left ventricular enddiastolic volume z score was <3 and recovery of systolic function occurred
within 1 year of diagnosis. Exclusion criteria included a history of congenital
heart disease, cardiomyopathy, or arrhythmias.

Fulminant myocarditis was defined as the need for intravenous inotropic

support to maintain cardiac output within 24 hours of presentation.
Arrhythmias were classified as acute or subacute, depending on the timing of
arrhythmia development. Acute arrhythmias were defined as those present
before or during initial evaluation by the medical team at the admitting
hospital (e.g., primary care physician, emergency room physician, or
admitting intensive care physician). Subacute arrhythmias occurred after a
patient had completed the initial evaluation. Emphasis was placed on rhythm
disorders that were judged a priori to be clinically significant and included (1)
sustained supraventricular tachycardia (SVT), (2) high-grade ventricular
ectopy (frequent isolated monomorphic or polymorphic ventricular beats or
couplets deemed high grade by a pediatric electrophysiologist), (3) sustained
or nonsustained VT or VF, and (4) high-grade (Mobitz type II) or CHB.
Reported low-grade arrhythmias (e.g., frequent atrial or infrequent single
ventricular ectopic beats) were recorded, although these arrhythmias were
not considered significant for the purpose of this study.
Left ventricular ejection fraction was defined as: normal >55%, mild
dysfunction >45% and <55%, moderate dysfunction >30% and <45%, and
severe dysfunction <30%. The Dallas criteria were used for endomyocardial
biopsy determination of myocarditis. A clinical worse outcome was defined as

the need for any of the following: mechanical support, orthotopic heart
transplant (OHT), or death.
All electrocardiograms (ECGs) obtained during the hospital course were
evaluated by 2 pediatric electrophysiologists. Timing of development and
resolution

of

electrocardiographic

changes

including

ST

elevation

or

depression, low voltages, and left bundle branch block (LBBB) was recorded
and compared with arrhythmia onset. Low voltage was defined as <0.5 mV
in all limb leads or <1.0 mV in all precordial leads. Abnormal ST segments
were defined as >0.2 mV ST elevation or depression in at least 2 leads. ST
segments were not evaluated if the patient had CHB or an intraventricular
conduction delay.
Statistical analysis was performed using SAS, version 9.3 (SAS Institute
Inc., Cary, North Carolina). Continuous variables are presented as medians
with ranges. Categorical variables are presented as counts with percentages.
Univariate binary logistic regression models were built to predict associations
between arrhythmias, worse outcomes, and subacute arrhythmias. Variables
for the primary analysis were chosen before data collection. Because of the
small numbers of patients and to account for multiple comparisons in the
planned primary analysis of arrhythmia predictors, the Bonferroni correction
was applied and statistically significant data were defined as a p value of
<0.0056. Subsequent to the primary analysis, a secondary analysis of
electrocardiographic findings and associations with worse outcomes and
subacute arrhythmias was performed. Because these variables were not
chosen a priori, this analysis was termed exploratory, and a standard p value
of <0.05 was used.
Results
A total of 85 patients (59% men) presented at a median age of10 years
(range, 1 day to 18 years). Demographic data and presenting symptoms are
listed in Table 1. Arrhythmias occurred in 38 (45%) of 85 patients, acutely in

16, subacutely in 12, and both acute and subacute in 9. In 1 patient, the
timing of arrhythmia onset was unknown. Among the 85 patients, a
fulminant course was seen in 41 (50%). A majority (80%) received
intravenous immunoglobulin, and 21% received steroids in addition to
intravenous

immunoglobulin.

Sixteen patients

did

not receive either

intravenous immunoglobulin or steroids.

Median length of hospital stay for all patients surviving to discharge was 11
days (1 to 244 days). Patients with clinically significant arrhythmias had
longer hospital stays than those without arrhythmias (Table 1). Mechanical
support was required in 23 patients (27%), 17 of whom had clinically
significant arrhythmias. OHT was performed in 5 patients (6%) at a median
time of 4 months (1 to 7 months). Death occurred in 8 patients (9%) at a
median time of 1 month (5 hours to 9 months), 7 during initial
hospitalization. There was no arrhythmia-related mortality.

Figure 1. Arrhythmias and outcomes. Data represents number of patients

with specific arrhythmia substrates and their outcome. AF = atrial flutter; D
= death; EAT = ectopic atrial tachycardia; HGVE = high-grade ventricular
ectopy; Mobitz II = Mobitz type II AV block; NSVT = nonsustained VT.

On initial echocardiogram, left ventricular function was mildly depressed in

27 (32%), moderately depressed in 23 (27%), and severely depressed in 35
(41%). A pericardial effusion was seen in 25 patients (29%).
An endomyocardial biopsy was performed in 44 patients (52%), and of
these, 30 (68%) had active lymphocytic myocarditis, 6 (14%) had borderline
myocarditis, and 8 (18%) had no evidence of myocarditis. A cardiac magnetic
resonance imaging was performed in 23 patients (27%), 15 (65%) of whom
demonstrated delayed enhancement consistent with myocarditis. Infectious
disease workup was completed in 64 patients (75%), with a pathogen
identified in 30 (47%).
Initial laboratory values at presentation are listed in Table 1. Of 81 patients
with ECGs available for review, 20 (25%) had low voltages, 26 (33%) had ST
changes (excluding 2 patients with unresolved CHB), and 7 (9%) had an
LBBB pattern. A total of 38 patients (45%) had 54 clinically significant
arrhythmias

occur

either

at

presentation

(acute)

or

during

their

hospitalization (subacute). Sixteen patients had acute arrhythmias only, 12

subacute only, 9 acute and subacute, and 1 had unknown onset (Figure 1).
Clinically significant arrhythmias included 9 SVT (2 atrial flutter, 2 ectopic
atrial tachycardia, and 5 not specified), 2 high-grade ventricular ectopy, 6
nonsustained VT, 21 sustained VT, 3 VF, 1 Mobitz type II AV block, and 12
CHB.
Compared with those patients without arrhythmias, patients with clinically
significant arrhythmias were statistically significantly more likely to have low
voltages on ECG (14 of 34, 41% vs 6 of 47, 13%; odds ratio [OR] 4.8, 95%
confidence interval [CI] 1.6 to 14.3) and have a worse outcome (20 of 38,
53% vs 6 of 47, 13%; OR 7.6, 95% CI 2.6 to 22.1). After adjusting for multiple
comparisons, clinically significant arrhythmias were not associated with a
fulminant course, initial myocardial function, initial troponin I level, elevated
initial C-reactive protein and/or erythrocyte sedimentation rate, elevated

initial creatinine level, elevated initial lactate level, or ST changes on ECG

(see Table 2). Nevertheless, we did observe greatly increased odds (OR >2.9)
of arrhythmias associated with a fulminant course, ST changes, and elevated
initial lactate and creatinine levels.
Ventricular arrhythmias were the most common rhythm disturbance,
occurring in 30 (79%) of 38 patients with arrhythmias and 35% of the entire
patient cohort. Acute ventricular arrhythmias included high-grade ventricular
ectopy (1) and sustained VT (15). Subacute ventricular arrhythmias included
high-grade ventricular ectopy (1), nonsustained VT (6), sustained VT (6), and
VF (3). Subacute ventricular arrhythmias developed at a median time of
2 days (range, 1 to 19 days) after admission. Median time to complete
resolution

of

all

ventricular

arrhythmias,

including

those

for

which

antiarrhythmic therapy was used, was 6 days (1 to 27). No patient received

an implantable cardioverter-defibrillator.
CHB was seen at presentation in 11 patients and developed during
hospitalization in 1 patient on hospital day 6. Among the 11 patients who
presented with CHB, 9 resolved at a median time of 5 days (range, 0 to 23)
and 2 died without resolution of CHB. The 1 patient who developed subacute
CHB never resolved and was discharged home with a pacemaker. Temporary
transvenous pacing wires were placed in 9 patients for a median time of 6
days (range, to 19). Permanent pacemakers were placed in 2 patients during
hospitalization. One patient presented in CHB and a pacemaker was placed
after 17 days. Normal conduction returned 6 days later, and the patient was
discharged in sinus rhythm and then lost to follow-up. The second patient
developed CHB on hospital day 4. A pacemaker was placed 31 days later and
the patient remains in heart block after 11 months of follow-up.
Electrocardiographic

predictors

for

the

development

of

subacute

arrhythmias were explored by evaluating the presence of ST changes and/or

low voltages before new arrhythmia development. Compared with patients

who did not develop new arrhythmias, patients with subacute arrhythmias
were more likely to demonstrate ST elevation or depression before subacute
arrhythmia onset (10 of 15, 67% vs 15 of 59, 25%; OR 5.9, 95% CI 1.7 to
19.9) but not low voltages (Table 3).
During hospitalization, 32 (84%) of 38 patients received antiarrhythmic
medication(s) for a median period of 11 days (range, 1 to 144).
Antiarrhythmic therapy was initiated for SVT in 13%, high-grade ventricular
ectopy in 3%, and VT or VF in 88%. At discharge, 10 patients remained on
antiarrhythmic therapy (1 for SVT, 1 for high-grade ventricular ectopy, and 8
for VT). Median follow-up for patients with clinically significant arrhythmias
was 2 years (range, 11 days to 13 years). During the follow-up period,
antiarrhythmic medication was discontinued in 4 patients; however, in 2
patients discharged home without medications, antiarrhythmic therapy was
restarted because of nonsustained VT noted on outpatient monitoring at 2
and 3 months after discharge. At the last follow-up, 5 of the 10 patients were
still on antiarrhythmic medications for ventricular arrhythmias (4 VT and 1
high-grade ventricular ectopy). Among these 5 patients who remain on
antiarrhythmic therapy, follow-up ranged from 1 to 30 months.
Cardiopulmonary resuscitation (CPR) was required at presentation for 15
patients.

Four

patients

required

CPR

for

arrhythmias

during

their

hospitalizations at a median time of 5 days from admission (0 to 8 days); in 3

patients, CPR was for subacute arrhythmias (1 VF, 1 VT, and 1 VT and VF)
and in 1 patient a recurrence of acute VT.
Direct current cardioversion was required at presentation for 11 patients
(10 VT and 1 SVT). Cardioversion was performed after admission in 10
patients at a median time of 4 days (range 0 to 18). Seven patients required
direct current cardioversion for new subacute arrhythmia development (2
atrial flutter, 3 VT, 1 VT and VF, and 1 VF) and 3 patients for recurrent VT.

Of the 38 patients with clinically significant arrhythmias, 29 survived to

discharge with their native heart (4 OHT and 5 deaths). One patient had
permanent heart block requiring a pacemaker. No patient was discharged
with an implantable cardioverter-defibrillator. Median follow-up for all
patients was 1 year (range, 7 days to 14 years). Complete resolution of
clinically significant arrhythmias was seen in 23 (79%) of 29 patients,
whereas 5 (17%) of 29 remain on antiarrhythmic therapy for ventricular
arrhythmias with complete control at the last follow-up. One patient
underwent an OHT for heart failure. Three patients had arrhythmia
recurrence after hospital discharge: 2 patients with nonsustained VT for
which antiarrhythmic therapy was started as an outpatient and 1 patient with
sustained VT in the setting of known congestive heart failure required
readmission for antiarrhythmic therapy. The VT was controlled with
antiarrhythmic therapy, but this patient eventually required an OHT for heart
failure (as mentioned previously).
Among all 85 patients, there were 8 deaths (6 among patients with
arrhythmias). All 5 patients who underwent OHT had a history of
arrhythmias. None of the deaths or OHTs were directly attributed to
arrhythmias and occurred almost exclusively in the group with a fulminant
course. Among patients with significant arrhythmias and a fulminant course,
there were 5 deaths and 4 OHT during the initial admission, whereas in the
nonfulminant group, there was a single patient who underwent an OHT after
the initial admission and subsequently died. An exploratory analysis
evaluating the association of LBBB pattern and worse outcomes was
performed and found 5 of 23 patients with a worse outcome (need for
mechanical support, OHT, or death) had an LBBB pattern versus 2 of 58 with
more favorable outcomes (OR 7.8, 95% CI 1.4 to 43.6).
Of the 73 (86%) surviving patients who were discharged with native
hearts, 10 patients were lost to follow-up. Among the remaining 63 patients,
median follow-up time was 13 months (1 day to 13.5 years). Full myocardial

recovery was achieved in 66 (90%) of the 73 patients at a median time of 9

days from initial presentation (1 to 506 days), although 15 were still on heart
failure medications at the last follow-up.
Discussion
Arrhythmias contribute to significant morbidity and mortality among patients
with myocarditis. To our knowledge, this series of 85 patients is the largest
study to date describing in-hospital arrhythmia development and outcomes
in pediatric patients with acute myocarditis. Clinically significant arrhythmias
occurred in nearly 1/2 of the patients. Overall, the most common arrhythmias
were ventricular in origin, occurring in 35% of all patients (79% of patients
with arrhythmias). The most common acute arrhythmia was VT (15 patients)
and/or CHB (11 patients). Consistent with published literature on adults and
small pediatric populations, this study confirmed the high incidence of
arrhythmias in patients with myocarditis. This study also found that (1)
clinically significant arrhythmias were associated with low voltages on ECG
and worse clinical outcomes, (2) subacute arrhythmias occurred in 25% of
patients, and (3) ST changes on ECG may predict development of subacute
arrhythmias.
Not every child with myocarditis develops an arrhythmia, and it is not clear
why some children develop bradyar- rhythmias, others tachyarrhythmias, or
some a combination of both. Although we have become better adept at
managing acute arrhythmias at presentation, we cannot confidently predict
which children will develop new or subsequent arrhythmias during their
hospital course. Our preliminary analysis evaluated associations between
several initial laboratory and diagnostic (ECG/echocardiogram) values and
the presence of clinically significant arrhythmias that occurred anytime
during the patients hospital course (before or after presentation). Although
not statistically significant, there was a strong trend that the sicker patients
had more clinically significant arrhythmias. A fulminant myocarditis course

places the patient at 3 times the risk for clinically significant arrhythmias, an
elevated lactate level increases the risk eightfold, elevated creatinine level
4.5-fold, and ST changes 2.9-fold. These findings may merit clinical
consideration. Interestingly, the initial degree of myocardial function is not
associated with arrhythmia development. Therefore, mild dysfunction does
not equate to less arrhythmia risk, and clinicians should have a heightened
awareness regardless of the degree of myocardial dysfunction.
Because of multiple comparisons and potentially related predictor values
(i.e., poor myocardial function and elevated lactate or creatinine levels), the
Bonferroni

correction

was

applied

to

prevent

false

positives.

This

conservative approach resulted in several predictors not meeting statistical

significance despite a p value <0.05. Ultimately, the main risk factor for
arrhythmia was low voltages on ECG. Although low voltages are often seen in
myocarditis, the pathophysiology is not known. Morimoto et al looked at low
voltages and myocardial edema in 50 adult patients with biopsy-proven
myocarditis. The investigators unfortunately did not define their criteria for
low voltages. Although the investigators did not find an association between
myocardial edema and low voltages, they did find an association between
myocardial edema and both VT and heart block. Given our findings in this
study, low voltages and myocardial edema may warrant both vigilance and
further investigation to replicate these data, particularly in children.
Myocardial

edema

may

be

an

explanation

for

both

arrhythmia

development and low voltages. The location and degree of myocardial

edema, which may differ based on pathogen and anatomical predilection
(atrium

vs

ventricle

vs

conduction

system

and

subendocardium

vs

epicardium), may explain why some patients have only VT or heart block,
whereas others have both. Progression or extension of myocardial edema
may explain why some patients are susceptible to the development of new
arrhythmias after admission. Such myocardial edema could potentially

contribute to low voltages, similar to those seen in patients with peripheral

edema.
Predicting

which

patients

may

develop

arrhythmias

after

initial

presentation would be advantageous in the management of myocarditis.

Among this cohort of patients, subacute arrhythmias occurred nearly as often
as acute arrhythmias. These subacute arrhythmias required CPR in 4 patients
and direct current cardioversion in 10 patients, demonstrating the associated
morbidity and the importance of being able to predict their occurrence.
Therefore, the development of arrhythmias during the patients hospital
course was of particular interest in this study. We explored potential
electrocardiographic findings that might identify those patients who develop
new arrhythmias not seen at initial presentation. Exploratory analysis
suggests that subacute arrhythmias are associated with preceding ST
changes but not preceding low voltages. ST-segment changes may reflect
ongoing myocardial edema that results in (1) worsening cell membrane leak
leading to changes in membrane potentials and/or (2) accumulation of bioproducts and decreased delivery of myocardial tissue oxygenation or energy
substrates. Progressive myocardial edema and electrophysiological changes
may contribute to arrhythmia development. In this study, preceding ST
changes (requiring changes in 2 leads) would have been noted earlier than
low voltage (requiring changes to occur in all limb/precordial leads) and may
explain why low voltages are associated with arrhythmias but do not predict
their development. The ability to predict potential arrhythmia development
may be beneficial and may warrant managing patients with ST changes more
cautiously (i.e., longer observation period in the intensive care unit and/or a
lower threshold for starting antiarrhythmic medications).
Despite a high rate of arrhythmias in this patient population and the
association with worse outcome, death was not directly attributed to
arrhythmias in any of the patients. Morgera et al 13 found that an LBBB on
ECG in adult patients with myocarditis was associated with a worse outcome.

In our exploratory analysis, our data also suggest a similar finding among
pediatric patients, with an LBBB pattern resulting in an eightfold increase in
risk for a clinically worse outcome.
This is a retrospective study limited to available clinical information.
Identifying patients with a definitive diagnosis of myocarditis is a challenge.
Only 1/2 (52%) of all patients received endomyocardial biopsy, and of those,
just >2/3 (68%) had a pathologically confirmed diagnosis. Acute myocarditis
was a clinical diagnosis in most cases. Although we attempted to exclude
patients with primary dilated cardiomyopathy, we cannot eliminate potential
inclusion of this group of patients. By attempting to exclude the patients with
dilated cardiomyopathy, we also likely excluded some patients with chronic
myocarditis. Electrocardiographic interpretation was limited to available
ECGs, and the number of ECGs per patient varied, which may have affected
our data. Potentially, patients who were clinically ill may have undergone
more electrocardiographies. Lastly, follow-up of arrhythmias varied. Some
patients received outpatient Holter or event monitors, whereas others did
not. We therefore cannot exclude the possibility of uncaptured or occult
arrhythmias that occur on an outpatient basis. Although the findings in this
study are very interesting, many predictors were analyzed. Despite the high
ORs suggesting a clinical effect, data that were not statistically significant
should be interpreted with caution because of a greater probability of false
positives. The findings in this study warrant further investigation and
replication.
Table 1. Demographics, clinical presentation, and initial laboratory values
Variable

Arrhythmia

No Arrhythmia

Men

(%)
85 20/38 (53)

Median age

85 8 yrs (1 day17 14 yrs (8 days18

yrs)

Gastrointestinal
Upper

(%)
30/47 (64)
yrs)

85 17/38 (45)
85 12/38 (32)

27/47 (57)
26/47 (55)

85 16/38 (42)

19/47 (40)

respiratory
Dyspnea

Palpitations
85 3/38 (8)
Laboratory values at presentation

Elevated
protein
reactive

C- 46 15/18 (83)

3/47 (6)

23/28 (82)

Elevated

81 9/36 (25)

4/45 (9)

creatinine
Elevated

74 28/34 (82)

26/40 (65)

aspartate
Elevated brain
22 9/12 (75)
natriuretic peptide
ID pathogen found 64 16/32 (50)
Initial echocardiogram

Mechanical

85 17/38 (45)

6/10 (60)
14/32 (44)

6/47 (13)

support
Median length of
85 19 (5 244)
hospital stay (days)

8 (171)

Table 2. Primary analysis comparing patients with (n = 38) and without (n =

47) arrhythmias
Primary Analysis

Arrhythmia (%)

No Arrhythmia (%)

OR

95% CI

79
81

15/32 (47)
14/34 (41)

11/47 (23)
6/47 (13)

0.0319
0.0051*

2.9
4.8

1.1-7.6
1.6-14.3

Elevated creatinine 81
Elevated CRP/ESR
53
Troponin I
49
Myocardial function

9/36 (25)
17/21 (81)
4.4 (0.1-50.0)

4/45 (9)
27/32 (84)
2.0 (0.1-46.4)

0.0102
0.7458
0.7219
0.5783

4.5
0.8
1.0

1.4-14.3
0.2-3.4
0.96-1.1

Mild vs severe
Worse outcome

20/38 (53)

6/47 (13)

1.5
7.6

0.6-4.2
2.6-22.1

Arrhythmia
Any ST change
Any low voltage

85

0.0002*

Worse outcome is defined as the need for mechanical support, orthotopic heart transplant,
or death. CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.
* p <0.0056 considered statistically significant.

Table 3. Exploratory analysis

Exploratory Analysis

Worse Outcome (%)

No Worse Outcome (%)

OR

95% CI

2/58 (3)

0.0197

7.8

1.4-43.6

No Subacute Arrhythmia

OR

95% CI

Worse outcome
LBBB

81

5/23 (22)
n

Subacute arrhythmia

Subacute Arrhythmia

Preceding
voltages
Worse

low

80

3/19 (16)

13/61 (21)

0.6008

0.7

0.2-2.7

outcome is defined as the need for mechanical support, orthotopic heart transplant,

or death.