REVIEW ARTICLE

Supraventricular Tachycardia
Jack C. Salerno, MD; Stephen P. Seslar, MD, PhD

S
upraventricular tachycardia is the most common rhythm disturbance in children. We
reviewed the spectrum of this common rhythm disorder from symptom recognition and
epidemiology to management, with special attention to advancements in the available
treatment options. Arch Pediatr Adolesc Med. 2009;163(3):268-274

Supraventricular tachycardia (SVT) is the
most common rhythm disturbance in chil-
dren.1 It is estimated to occur in as many
as 1 in 250 otherwise healthy children. Epi-
sodes are often recurrent and, although
rarely life threatening, they may be life al-
tering. Treatment of this disorder has un-
dergone a remarkable transformation in
the past quarter century. Although SVT ac-
counts for a small proportion of children
treated in an outpatient setting, the preva-
lence is high enough that most general pe-
diatric practitioners will, at some point,
care for a patient with this disorder. This
review will cover the spectrum of this
common rhythm disorder, from symp-
tom recognition and epidemiology to man-
agement, with special attention to ad-
vancements in the available treatment
options.
WHAT IS SVT?
Normal Conduction
Before reviewing the mechanism underly-
ing most forms of SVT, a review of how the
electrical signals normally propagate
through the heart is worthwhile. The car-
diac conduction system extends from the
atrium to the ventricular myocardium. In
the normal heart, the atrial and ventricular
myocardium are electrically insulated from
one another except at the atrioventricular
node (AVN) and bundle of His. Impulse
generation typically originates in the sinus
Author Affiliations: Department of Pediatrics, Seattle Children’s Hospital,
University of Washington School of Medicine.
node, and the impulse is conducted through
the atrial myocardium to the AVN. The ma-
jor role of this structure is to allow conduc-
tion of the impulse to the ventricle; how-
ever, equally important is the inherent delay
in the AVN that slows conduction from the
atrium to the ventricle, allowing ventricu-
lar filling. From the AVN, there is rapid con-
duction via the specialized His-Purkinje sys-
tem with associated right and left bundle
branches that intercalate to the ventricular
myocardium.
Supraventricular Tachycardia
Supraventricular tachycardia is broadly de-
fined as a narrow, complex tachycardia that
requires atrial tissue or the AVN as an in-
tegral part of the arrhythmia substrate. The
majority (⬎90%) of the clinically impor-
tant SVT in otherwise healthy children is
caused by the presence of an additional (or
accessory) electrical connection between
the atrium and ventricle (ie, the bundle of
Kent) or within the AVN itself.2 As such,
SVT mediated by these accessory connec-
tions will be the focus of the remainder of
this article. The mechanism underlying
these forms of SVT is known as reentry,
and the fundamental aspects of this ar-
rhythmia mechanism were elucidated dur-
ing the past century.3 Reentry requires the
presence of 2 electrophysiologically dis-
tinct pathways around an insulated core
(eg, the atrioventricular valve annulus)
(Figure 1). In reentrant rhythms, the elec-
trical impulse can cycle and recycle re-
petitively in a manner similar to a dog chas-
ing its tail. Understanding the mechanism

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 Premature beat
Pathway A Pathway B
Figure 1. Schematic representation of reentry. In reentry, electrical signals
generated from an appropriately timed premature beat find pathway B
unprepared, resulting in conduction block in this limb of the circuit.
Meanwhile, conduction down pathway A proceeds unimpeded. Subsequent
recovery of pathway B allows electrical signals to be conducted backward (or
retrograde), resulting in reactivation of pathway A and propagation of the
reentry circuit.
of reentry is critical to understanding the targets of short-
and long-term therapeutic strategies for SVT (Figure 2).
Accessory Connections
As discussed in the preceding subsection, accessory con-
nections provide the generic substrate for reentry SVT.
However, a number of different types of accessory con-
nections have been identified and subcategorized accord-
ing to differing electrophysiological properties. These dif-
ferences alter the clinical characteristics of the patient with
SVT and have allowed us to define different subtypes of
SVT as distinct clinical entities.
The Concealed Accessory Connection. In this case, the
accessory connection between the atrium and ventricle
does not disturb electrical signal transmission during nor-
mal sinus rhythm. Thus, on a routine electrocardio-
gram (ECG), this accessory connection is “concealed”
or not visible, as described in the “Diagnostic Tools” sub-
section. This accessory connection provides abnormal
electrical conduction backward or retrograde from the
ventricle to the atrium. Because of this, the concealed ac-
cessory connection is also known as the unidirectional
retrograde accessory pathway.
The Wolff-Parkinson-White Accessory Connection.
Named after the 3 individuals credited with elucidating
its electrical properties,4 the Wolff-Parkinson-White
(WPW) accessory connection allows abnormal propa-
gation of electrical signals forward (or antegrade) from
the atrium to the ventricle and, in most cases, retro-
grade from the ventricle to the atrium. This not only cre-
ates a characteristic appearance on a baseline ECG
(Figure 3), but also provides a substrate for typical re-
entry SVT and, importantly, may allow the rapid trans-
mission of electrical signals generated in the atrium to
the ventricle with potentially life-threatening conse-
quences (described in the “Prognosis” section).
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β-Blockers Atrium
Accessory connection
Adenosine phosphate
Digoxin AVN
Verapamil Catheter
hydrochloride ablation
Vagal maneuvers
Ventricle
Figure 2. Schematic representation of a supraventricular tachycardia circuit
and targets of common therapies. AVN indicates atrioventricular node.
Permanent Junctional Reciprocating Tachycardia. The
accessory connection in the permanent junctional recip-
rocating tachycardia subform of SVT behaves much the
same way as a concealed accessory pathway, except that
the rate of transmission of the electrical impulse through
the accessory connection is slower than usual. This cre-
ates a unique ECG appearance during SVT and heart rates
in SVT that can be remarkably slow (130-150 beats/
min) by typical SVT standards. Patients with this form
of SVT often have medically refractory arrhythmias that
can be quite challenging to manage.
Atrioventricular Nodal Reentry Tachycardia. Patients
with the atrioventricular nodal reentry tachycardia
(AVNRT) form of SVT have the functional equivalent of
an extra connection within the AVN. Unlike an acces-
sory pathway, these extra connections are not visible his-
tologically. Nonetheless, they provide the necessary sub-
strate for reentry arrhythmias in a manner similar to that
seen with accessory connections.
EPIDEMIOLOGY AND GENETICS
Epidemiology
The true incidence of SVT in children is unknown but
has been estimated to be 1 in 250 to 1 in 1000 children.5
Approximately 50% of children with SVT will present with
their first episode in the first year of life.6,7 After infancy,
the incidence peaks in early childhood (ages 6-9 years)
and then again in adolescence.7,8 In infants, spontane-
ous resolution occurs in more than 90% by 1 year of age.
After a period of quiescence, up to one-third will have
recurrence of SVT at a mean age of 8 years.7 Although
spontaneous resolution is the norm in infants, only a small
minority (15%) of patients who receive the diagnosis af-
ter 1 year of age will have spontaneous resolution.6 Su-
praventricular tachycardia due to concealed or WPW ac-
cessory pathways predominates throughout childhood
and adolescence, whereas the relative proportion of pa-
tients with AVNRT tends to increase with age.2 Most in-
dividuals with SVT have a structurally normal heart.
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 I aVR V1
II aVL V2
Short PR interval
with delta wave
III aVF V3
II
Figure 3. Electrocardiogram with findings for Wolff-Parkinson-White syndrome.
However, the prevalence of structural congenital heart
disease in patients with SVT has been estimated at 9% to
32%, which is substantially higher than in the general
population. The most common association is noted be-
tween WPW syndrome and the Ebstein anomaly of the
tricuspid valve, but a number of defects have been
found, including ventricular or atrial septal defects,
among others.2,7-9
Genetics
Most cases of reentrant SVT are sporadic, with approxi-
mately 7% of patients having documented SVT in a first-
degree relative.10 Most cases of WPW syndrome are also
sporadic, although patients with WPW syndrome have
a 3-fold higher risk than the general population of hav-
ing an affected first-degree relative with WPW.11
EVALUATION
History
The clinical presentation of SVT is age and duration de-
pendent. In infants with paroxysmal SVT, the heart rate is
usually 220 to 320 beats/minute; in older children, it is 160
to 280 beats/minute.6 In infants, symptoms are usually non-
specific and include poor feeding, irritability, vomiting, cya-
nosis, and pallid spells. If the symptoms are unrecognized
for hours to days, the infant can present with significant
hemodynamic compromise or heart failure symptoms.12 It
is rare for infants who have SVT for less than 24 hours to
develop signs of congestive heart failure at the time of pre-
sentation; however, congestive heart failure is present in
19% of infants who have SVT for 24 to 36 hours and in
50% who have SVT for more than 48 hours.6 Approxi-
mately 20% of infants receive a diagnosis during routine
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V4 V3R
V5 V4R
V6 V7
office visits and during asymptomatic episodes.6,8 In ver-
bal children with SVT, palpitations and fluttering in the chest
are the usual presenting symptoms. Because reentrant ar-
rhythmias are a circuit, they tend to be all or nothing, and
the onset is frequently described as being abrupt, similar
to a light switch being turned on. The offset may be less
dramatic because the catecholamine level is typically el-
evated, with resultant sinus tachycardia at the termina-
tion of SVT and subsequent gradual slowing. Frequently,
lightheadedness and dizziness due to transient hypoten-
sion can occur at the onset, but syncope is rare in SVT, and
its presence should raise suspicion of something other than
SVT. The frequency and duration of the episodes vary greatly
from a few minutes to a few hours and occur as often as
daily or as infrequently as once or twice per year. Al-
though they are rare in verbal children, incessant SVT symp-
toms may go unrecognized until cardiac dysfunction
develops.
Physical Examination
Most patients presenting with episodic palpitations have
a structurally normal heart and will have normal find-
ings on the physical examination, particularly older chil-
dren. Infants are more likely to present with signs of heart
failure because the tachycardia may have gone unrecog-
nized for longer periods.
Diagnostic Tools
Recording a heart rhythm strip during symptoms re-
mains the key to correct diagnosis and management. Op-
tions for this include 24-hour ambulatory monitoring,
event recorders, and ECGs. Each of these means of ob-
taining a recording have associated advantages and dis-
advantages. The Holter monitor provides a continuous
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 Table 1. Common First-Line Medications in the Treatment of SVT

FDA
Medication Class Dosing Approved a Cautions
Propranolol hydrochloride ␤-Blocker 2-4 mg/kg/d in divided doses every 6-8 h Yes Contraindicated in asthma,
concern in diabetes
Atenolol ␤-Blocker 1-2 mg/kg/d given in divided doses every 12 h No Similar to propranolol but more
cardioselective
Digoxin Cardiac glycoside Full-term infant to child aged 10 y, 8-10 Yes Arrhythmia with toxic effects
µg/kg/d given in divided doses every 12 h;
child ⬎10 y, 125 µg/d
Verapamil hydrochloride Calcium channel blocker 4-8 mg/kg/d in 3 divided doses No Avoid in infants ⬍12 mo old

Abbreviations: FDA, US Food and Drug Administration; SVT, supraventricular tachycardia.

a Indicates approved for use in children at the time of writing.

multichannel recording that usually allows the inter-
preter to see the whole episode, including onset and ter-
mination. Most patients, however, do not have daily symp-
toms, making the Holter monitor typically impractical
in the evaluation of SVT. Event recorders are often the
optimal solution for patients who have symptoms more
than once per month. Patients can wear the monitor (loop
recorder) or carry it with them (event monitor). In both
cases, patients activate the recording device during symp-
toms. The advantage of the loop recorder is that the re-
cording encompasses the time before, during, and after
the monitor activation. Finally, for infrequent episodes
lasting longer than 10 minutes, patients can often be re-
ferred to the local emergency department or fire station
for acute monitoring.
MANAGEMENT
Short-term Management
Excellent reviews focus on the short-term management
of SVT, including the pediatric advanced life support
algorithm.13
Long-term Management
Once the rhythm has been recorded and the diagnosis
has been confirmed, patients are typically referred to a
pediatric cardiologist. The management of SVT has many
variables that need to be considered, including the age
of the patient, the duration and frequency of the epi-
sodes, and the presence of ventricular dysfunction. There
are also important social and geographical factors, in-
cluding access to care, that play a role. For children with
rare and mildly symptomatic episodes in whom SVT is
easily terminated, the SVT may not merit treatment. For
children with episodes that are difficult to terminate, oc-
cur frequently, or occur during athletic participation, it
may be advisable to offer medical therapy or transcath-
eter ablation as therapeutic options.
Infants with SVT deserve special recognition in re-
gard to treatment options. Most infants will undergo spon-
taneous resolution of SVT. When this is combined with
the increased risk of transcatheter ablation in this age
group, most electrophysiologists opt for medical man-
agement during the first year of life.
Medical Therapy. Optimal medical management (in terms
of who to treat, with which medication, and for how long)
of SVT in infants and children has not been well studied,
and most current clinical practices are extrapolated from
small studies of adults14 and noncontrolled pediatric stud-
ies.15 A multicenter prospective randomized controlled
trial comparing digoxin and ␤-blockers for the treatment
of SVT in children is currently in progress (clinicaltrials
.gov Identifier: NCT00390546; Shubhayan Sanatani, MD,
FRCPC, oral communication, May 14, 2008).
The intended effect of antiarrhythmic medications is to
slow conduction, preferentially within 1 limb of the reen-
trant circuit, thereby terminating the tachycardia as the cir-
culating wave front encounters refractory tissue. Nearly all
classes of antiarrhythmic agents have been used to treat SVT
successfully. The approach to antiarrhythmic therapy in-
cludes the daily prophylactic therapy and the single-dose
“pill-in-the-pocket” approach whereby medication is taken
only during an acute episode.16 The pill-in-the-pocket ap-
proach requires an immediate-release medication and is ap-
propriate for patients who have infrequent episodes that
are prolonged but well tolerated.
In most cases, first-line therapy is directed at modi-
fying the conduction properties of the AVN and in-
cludes treatment with digoxin, ␤-blockers, and calcium
channel blockers17 (Table 1 and Figure 2). Except in
WPW syndrome, when use of calcium channel blockers
and digoxin should be avoided, therapy can be initiated
with limited regard to the underlying mechanism. As is
typical with medical therapy, there is a significant re-
duction in the number of episodes, although complete
suppression is rare.14 In general, a steady state is achieved
after the drug has been administered continuously at the
same dose and interval for at least 5 half-lives; there-
fore, caution is advised if considering recurrence of SVT
a medication failure in the first few days of therapy. Su-
praventricular tachycardia refractory to first-line medi-
cations can often be controlled with more potent anti-
arrhythmic agents such as flecainide acetate, amiodarone,
sotalol hydrochloride, or drug combinations. Sodium
channel blockers such as flecainide are particularly ef-
fective in controlling SVT,16 but these agents are gener-
ally avoided in patients with structural or ischemic heart
disease because of the risk of proarrhythmia. Sotalol, an
agent with ␤-receptor and potassium channel blocking
properties, is also quite effective18 but can lead to QT pro-

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 longation and proarrhythmia. When the potential for pro-
arrhythmia and toxic effects from these agents is con-
sidered, their use should be overseen by an experienced
electrophysiologist and reserved for patients in whom
there is a higher risk of complications from an interven-
tional electrophysiological procedure (eg, in infants and
small children).
Ablation Therapy. The management of SVT has been
revolutionized with the development of catheter-based
ablative techniques that serve to eliminate the abnormal
electrical connections that allow SVT to occur. Al-
though once reserved for the sickest patients, catheter-
based ablative therapy is now considered the standard
of care for older children and adolescents with sympto-
matic SVT owing to its outstanding efficacy and safety
profile.
Overview. Ablation therapy begins with a diagnostic
electrophysiological study. This is performed in a car-
diac catheterization laboratory. For children, the proce-
dure may be performed under general anesthesia to mini-
mize patient movement. Access is obtained to the venous
or the arterial circulation through established tech-
niques,19 and catheters with electrode sensors are ad-
vanced into specific areas of the heart, usually the right
atrium, the crux of the heart near the normal atrioven-
tricular conduction system, in the coronary sinus and the
right ventricle. Using various pacing maneuvers, one can
identify the abnormal electrical connection that serves
as the substrate for SVT by its alteration of the normal
electrical signals. A specialized ablation catheter is then
used to perform millimeter-by-millimeter mapping of the
abnormal electrical signals until the precise location of
the extra electrical connection is identified. The tip of
the mapping catheter is then used to disrupt (or ablate)
the discrete region of tissue beneath the catheter, thus
eliminating the abnormal electrical connection and the
substrate for SVT. Because it is a catheter-based proce-
dure, recovery is minimal. Patients are usually sent home
the same day as the procedure and return to full activity
within a week.
Ablation Energy Source. Some of the greatest ad-
vances in catheter-based ablation therapy since its in-
ception in the early 1980s have been centered on the ab-
lation energy source. Early catheter-based ablation efforts
used energy from a direct current,20 making them rela-
tively crude by today’s standards.21,22
Radiofrequency (RF) ablation followed, with the first
use of RF catheter ablation in children reported in the
early 1990s.23 Radiofrequency energy allows for much
greater control of the energy delivery and therefore greatly
enhanced the safety of catheter-based ablation. Ulti-
mately, RF catheter ablation supplanted ablation that used
direct current. The safety and efficacy of RF ablation in
children was established through the development of an
ablation registry.24 Based on findings in this cohort, the
early results of ablation procedures are quite promising,
with a short-term success rate of 93% and a low inci-
dence of complications (1%).25,26 Follow-up analysis of
the cohort demonstrated that, overall, 90% of patients
who underwent an acutely successful ablation re-
mained free of recurrence at the 1-year follow-up.27
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In the early part of this century, the armamentarium
of the interventional electrophysiologist was expanded
further with the addition of cryoablation technology.
Rather than heat disruption, cryoablation technology causes
tissue disruption by freezing the tissue under the abla-
tion catheter tip. Cryoablation has several advantages com-
pared with RF ablation, particularly for children. Most no-
tably, cryoablation has essentially eliminated the risk of
unintentional heart block during ablation procedures. Un-
fortunately, the enhanced safety afforded by this technol-
ogy may be offset by higher SVT recurrence rates.28 For
this reason, in most centers, cryoablation has not re-
placed RF ablation, but rather serves as an important ad-
junct technology in situations where RF energy would be
deemed higher risk (eg, near the normal conduction sys-
tem, in the coronary sinus). The interested reader is re-
ferred to an outstanding review on this topic.29
PROGNOSIS
In the absence of structural heart disease or cardiomyop-
athy, the prognosis of SVT is believed to be excellent.
Wolff-Parkinson-White syndrome deserves special
consideration with respect to prognosis owing to the small
but real risk of sudden cardiac death associated with this
condition. The principal indicator of risk in adults with
WPW syndrome is the presence of symptoms (eg, pal-
pitations and syncope). Symptomatic patients with WPW
syndrome have an estimated 3% to 4% lifetime risk (0.25%
per year) of sudden cardiac death.30 In children and ado-
lescents, however, asymptomatic may be better termed
presymptomatic. It has been estimated that 55% of asymp-
tomatic children and adolescents will become sympto-
matic by 40 years of age.31 For that reason, all children
or adolescents in whom WPW syndrome is identified on
an ECG, regardless of the presence of symptoms, should
be referred to a pediatric electrophysiologist for evalua-
tion. Patients with WPW accessory pathways who are de-
fined as low risk on the basis of electrophysiological study
findings appear to be at no increased risk of sudden car-
diac death compared with the general population.
ANTICIPATORY GUIDANCE
Patient and Family Education
Empowering families should be one of the priorities of
physicians who treat children with SVT. Physicians should
reiterate that SVT is typically not life threatening but can
be life altering. Education should focus on the diagno-
sis, prognosis, and treatment options. Emphasis should
be placed on decreasing anxiety and alleviating the fear
of the unknown. The family should understand what to
expect, whom to contact when an episode occurs, and
when to contact emergency service personnel. School
emergency plans are also important and should include
similar information (Table 2).
Athletic Participation
Most neighborhood and elementary school activities for
young children involve lesser degrees of physical inten-
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Table 2. Example of Typical School Plan
SVT Diagnosis Typical Events
Expected symptoms Racing heartbeat, palpitations,
mild dizziness
Current medications None
Whom to contact during Parent
an episode
Interventions Age-appropriate vagal maneuvers
(gag reflex, bearing down,
handstand with support)
When to call emergency Prolonged symptoms, inability to
medical services terminate episode with vagal
maneuvers, abnormal mentation,
or syncope
Abbreviation: SVT, supraventricular tachycardia.
sity and should be an allowable component of the school
curriculum for patients with a diagnosis of SVT.32 It is
generally believed that these recreational athletes may be
more likely to report symptoms and willfully stop
participation.
In comparison, competitive athletics require system-
atic training and regular competition against others and
place a high premium on athletic excellence and achieve-
ment.33 There is a strong inclination among competitive
athletes to push beyond their physical limits. Therefore,
the competitive athlete may incorrectly perceive an im-
portant symptom as a normal physiologic response to ex-
treme exertion or may ignore the symptoms entirely to
prevent early extrication from competition. In the case
of high-speed or contact sports, this lack of recognition
may place the athlete at risk of injury, particularly if there
is a transient loss of mental function with a resultant loss
of physical control.34 As an example, a downhill skier or
platform diver with dizziness from episodic SVT may be
at greater risk of injury than a basketball player.
The American Heart Association has published guide-
lines for sports eligibility in patients with SVT.34 In gen-
eral, asymptomatic athletes without structural heart dis-
ease who have reproducible exercise-induced SVT prevented
by medical therapy can participate in all competitive sports.34
Athletes who have undergone successful transcatheter ab-
lation, are asymptomatic, and have no inducible arrhyth-
mia on follow-up testing can return to full competition sev-
eral days after the procedure.34
Because of the small risk of sudden cardiac death,
symptomatic athletes with WPW syndrome should un-
dergo a formal electrophysiological study, risk stratifi-
cation, and possible ablation of their accessory pathway
before participating in competitive sports. In asymptom-
atic athletes, the risks are less clear. Because younger pa-
tients may become symptomatic as they get older, the
Bethesda Guidelines for athletic participation state, “in
younger age groups, a more in-depth evaluation includ-
ing an electrophysiology study may be recommended
before allowing participation in moderate to high-inten-
sity competitive sports.”34(p1359) At a minimum, asymp-
tomatic athletes with a WPW pattern on their ECG should
undergo exercise testing or ambulatory monitoring dur-
ing exercise. Those deemed to be at low risk by demon-
stration of abrupt loss of preexcitation at faster sinus rates
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may not require further testing. Those who remain in a
state of preexcitation at maximal sinus rates should prob-
ably undergo a formal electrophysiological study and risk
stratification.
In conclusion, SVT is a common condition in the pe-
diatric population. In most cases, it represents a benign
heart rhythm disorder, but infants, athletes, and pa-
tients with WPW syndrome deserve special consider-
ation because of greater associated risks in these popu-
lations. Treatment with suppressive medications remains
the first-line therapy for infants and small children. For
symptomatic older children and adolescents, catheter ab-
lation appears to be a safe, effective form of treatment.
Education of patients and caregivers about the implica-
tions of SVT and development of age-appropriate care
plans in conjunction with a pediatric cardiologist is criti-
cal to achieve optimal outcomes.
Accepted for Publication: August 28, 2008.
Correspondence: Jack C. Salerno, MD, Department of
Pediatrics, Seattle Children’s Hospital, 4800 Sand Point
Way NE, Pediatric Cardiology, M/S G-0035, Seattle, WA
98105 (jack.salerno@seattlechildrens.org).
Author Contributions: Study concept and design: Salerno
and Seslar. Acquisition of data: Seslar. Analysis and inter-
pretation of data: Salerno and Seslar. Drafting of the manu-
script: Salerno and Seslar. Critical revision of the manu-
script for important intellectual content: Salerno and Seslar.
Administrative, technical, and material support: Seslar. Study
supervision: Salerno.
Financial Disclosure: None reported.
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Correction

Data Errors in Tables. In the article titled “Pediatri-

cians and the Promotion and Support of Breastfeeding,”
by Feldman-Winter et al, published in the December is-
sue of the Archives (2008;162[12]:1142-1149), a total of
3 errors were introduced in Tables 2 and 4 on pages 1144
and 1146, respectively. On page 1144, in Table 2 the con-
fidence interval in the first line should have been (0.93-
2.01). On page 1146, in Table 4 the confidence interval
in the first line should have been (0.90-1.30), and the
odds ratio in the second line should have been −0.92.

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