Advances in Arrhythmia and Electrophysiology
Contemporary Management of
Arrhythmias During Pregnancy
Alan D. Enriquez, MD; Katherine E. Economy, MD; Usha B. Tedrow, MD, MSc
C ardiac arrhythmias are among the most common cardiac
complications encountered during pregnancy.1 In some,
pregnancy may trigger exacerbations of pre-existing arrhyth-
mias, whereas in others arrhythmias may manifest for the first
time.2 Fortunately, severe arrhythmias requiring aggressive or
invasive therapies are rare. There are unfortunately few ran-
domized studies, little data on the efficacy or safety of antiar-
rhythmic drugs (AADs), or even explicit guidelines to support
decision making on pregnant women with arrhythmias. Thus,
much of the clinical care is guided by knowledge of the
physiology of pregnancy and educated risk/benefit decisions
made in collaboration with high-risk obstetric colleagues in
Maternal-Fetal Medicine, as well as with the patient.
Mechanism of Arrhythmia During Pregnancy
The precise mechanism of increased arrhythmia burden dur-
ing pregnancy is unclear, but it is likely because of a combi-
nation of hemodynamic, hormonal, and autonomic changes.
Increases in effective circulating blood volume of 30% to 50%
are seen beginning at 8 weeks of gestation and peaking at ≈34
weeks. Cardiac output is increased as well, with an average
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of 6.7 L/min in the first trimester and ≤8.7 L/min in the third
trimester. This is the result of a 35% increase in stroke volume
and a 15% increase in heart rate. The increase in plasma vol-
ume causes stretching of atrial and ventricular myocytes, and
this may result in early after depolarizations, shortened refrac-
toriness, slowed conduction, and spatial dispersion through
activation of stretch-activated ion channels.3,4 A larger heart
can also potentially sustain re-entry more easily because of
an increase in path length of potential reentrant circuits. The
increase in heart rate during pregnancy, seen predominantly
in the third trimester, may also predispose to arrhythmia, as
a high resting heart rate has been associated with markers of
arrhythmogenesis.5
Hormonal and autonomic changes may also contribute
to arrhythmogenesis. Estradiol and progesterone have been
shown to be proarrhythmic in animal studies and in case
reports of pregnant patients with arrhythmias.6,7 In addition,
estrogen has been shown to increase the number of adrenergic
receptors in the myocardium, and adrenergic responsiveness
seems to be increased in pregnancy.8,9
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
Received March 25, 2014; accepted July 8, 2014.
From the Cardiac Arrhythmia Service, Cardiovascular Division (A.D.E., U.B.T.) and Department of Obstetrics and Gynecology (K.E.E.), Brigham and
Women’s Hospital, Boston, MA.
The Data Supplement is available at http://circep.ahajournals.org/lookup/suppl/doi:10.1161/CIRCEP.114.001517/-/DC1.
Correspondence to Usha B. Tedrow, MD, MSc, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail
utedrow@partners.org
(Circ Arrhythm Electrophysiol. 2014;7:961-967.)
© 2014 American Heart Association, Inc.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org DOI: 10.1161/CIRCEP.114.001517
961
General Management Issues
In general, the therapeutic approach to arrhythmias in preg-
nancy is similar to that in the nonpregnant patient. Hyperthy-
roidism should be excluded, and other systemic disorders that
can result in arrhythmia such as pulmonary embolism should
be considered. Treatment of arrhythmias should be reserved
for significant symptoms or arrhythmias resulting in hemody-
namic compromise and risk to the mother and fetus. Patients
with a known history of uncontrolled arrhythmia should
undergo treatment before becoming pregnant when possible.
Antiarrhythmic Drugs
There are a lack of randomized trials and little or no system-
atic data on the efficacy and safety of AADs in pregnancy. The
majority of AADs are Food and Drug Administration category
C, meaning that risk to the fetus cannot be ruled out (Table 1).
Thus, a primary concern when administering AADs is the
potential risk to the fetus. Organogenesis occurs in the first tri-
mester (gestational weeks, 5–10), and the fetus is most sensi-
tive to the effect of teratogens during this time.10 Medications
of modest risk that have long been effective in controlling
significant arrhythmias should be continued in most clinical
settings during this period as the stability of the patient may
supersede the potential risks of the medication.11 During the
second and third trimesters, effects of AADs on fetal growth
and development, fetal arrhythmias, and uterine contractility
become a concern.12 The lowest effective dose should be used.
A detailed discussion of AADs in pregnancy is beyond the
scope of this review but can be found in the Data Supplement.
The characteristics and safety profile of AADs in pregnancy
and lactation are listed in Table 2.
Electric Cardioversion
Electric cardioversion is a reasonable option at all stages of
pregnancy when arrhythmias are associated with hemody-
namic instability.12 It can be considered electively for drug
refractory arrhythmias, and cardioversion does not compro-
mise blood flow to the fetus.13 In addition, because only a
small amount of energy reaches the fetus, the risk of induc-
ing fetal arrhythmias is small.12,14 In later stages of pregnancy
there is a theoretical risk of initiating preterm labor. There
 962  Circ Arrhythm Electrophysiol  October 2014

Table 1.  US Food and Drug Administration Ratings of Drugs in Pregnancy (www.fda.gov)
Category Definition
A Controlled studies show no risk
 Controlled studies in pregnant women have failed to demonstrate a risk to the fetus in the first trimester without evidence of risk in later
trimesters. The possibility of fetal harm seems remote.
B No evidence of risk in studies
 Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no controlled studies in pregnant women; or animal
studies have shown an adverse effect that was not confirmed in controlled studies in pregnant women. The possibility of harm seems remote but
cannot be ruled out.
C Risk cannot be ruled out
 Animal reproduction studies have been shown to have an adverse effect of the fetus and there are no controlled studies in women or there are no
animal or human studies. Drugs should be used only if the potential benefits justify the potential risks to the fetus.
D Positive evidence of risk
 There is positive evidence of human fetal risk based on investigational or marketing experience or studies in women. The potential benefits of the
drug may outweigh the potential risks, but the patient should be apprised of the potential risk to the fetus.
X Contraindicated in pregnancy
 Studies in animals or humans have demonstrated fetal abnormalities or there is evidence of risk based on investigational or marketing
experience, or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. The drug is contraindicated in
women who are or may become pregnant.

are case reports of emergency cesarean delivery because of
fetal arrhythmias after cardioversion, and fetal monitoring is
advised.15
Catheter Ablation in Pregnancy
There are few studies on catheter ablation in the pregnant
patient. In general, this option should only be undertaken in
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refractory arrhythmias during pregnancy with good mater-
nal and fetal outcome.19–21 With the more widespread use of
electroanatomic mapping and intracardiac echocardiography,
future radiation risks may be reduced even further, or ionizing
radiation will not be required at all.22–24 Abdominal shielding
should be routinely used in pregnancy.

a situation where reasonable medical therapy is ineffective, Management of Specific Arrhythmias

and the potential risks to the mother and fetus are outweighed
by the expected benefit. Potential additional risks of catheter
ablation in a pregnant patient versus a nonpregnant patient
include fetal radiation exposure and fetal compromise in the
event of maternal hemodynamic instability. In addition, the
gravid uterus may play a role in difficult patient positioning,
as well as present challenges performing pericardiocente-
sis and resuscitation in the event of a complication. If pro-
cedures are performed after 20 weeks of gestation, placing a
wedge beneath the patient for left lateral uterine displacement
is recommended. If ablation is performed when the fetus is
viable, emergent availability of surgical delivery options with
Maternal-Fetal Medicine colleagues should be part of the pro-
cedural planning.
Radiation exposure to the fetus should be minimized partic-
ularly in early pregnancy during organogenesis and neuronal
development. From implantation through 8 weeks of gesta-
tion, the threshold dose for fetal abnormalities rises from 100
to 250 mGy. Mental retardation may result with exposures
from 60 to 310 mGy in weeks 8–25.16 A reasonable thresh-
old for concern on fetal exposure is 50 mGy, as exposure to
this dose has not been associated with fetal anomalies or preg-
nancy loss.17 Damilakis et al18 investigated theoretical fetal
radiation exposure during catheter ablation for supraventricu-
lar tachycardia (SVT; 20 female patients, 12 with atrioven-
tricular node re-entry, and 8 with Wolff–Parkinson–White).
With abdominal shielding, theoretical conceptus exposure
during the ablation procedure was <1 mGy. Subsequent to
this study, others have successfully used catheter ablation for
During Pregnancy
Palpitations and Premature Beats
Palpitations are common during pregnancy and often prompt
cardiovascular evaluation. Many patients are aware of a more
rapid or forceful heart beat with the increases in heart rate,
blood volume, and contractility during pregnancy. In a study
of asymptomatic and symptomatic pregnant women without
structural heart disease, the prevalence of premature atrial
contractions and premature ventricular contractions was high
(57% for premature atrial contractions and >50% for prema-
ture ventricular contractions).25 In patients with intolerable
symptoms, treatment with a cardioselective β-blocker can be
initiated, preferably after the first trimester.
Supraventricular Tachycardia
SVT is the most common sustained arrhythmia encountered
during pregnancy with a prevalence of 24 per 100 000 hospital
admissions, and ≈20% of patients with pre-existing SVT will
experience symptomatic exacerbations during pregnancy.26,27
In women without structural heart disease, paroxysmal SVT
is most commonly because of atrioventricular nodal reentrant
tachycardia (AVNRT) followed by atrioventricular reciprocat-
ing tachycardia.2 It is unclear whether pregnancy increases
the risk of the first onset of SVT.2,28 Patients with pre-existing
SVT may experience exacerbations during pregnancy. SVT
is usually well tolerated but can result in hemodynamic dete-
rioration in patients with structural heart disease and result in
impaired fetal blood flow.29,30
 Enriquez et al   Arrhythmias in Pregnancy   963

Table 2.  Characteristics of Antiarrhythmic Drugs in Pregnancy

Drug Vaughan–Williams Class FDA Risk Category* Potential Adverse Effects Teratogenic Use During Lactation
Quinidine IA C Thrombocytopenia, ototoxicity, No Compatible but caution
torsades de pointes advised
Procainamide IA C Drug-induced lupus, torsades de No Compatible for
pointes short-term use
Disopyramide IA C Uterine contractions No Compatible
Lidocaine IB B Bradycardia, CNS adverse effects No Compatible
Mexiletine IB C Bradycardia, CNS effects, No Compatible
low Apgar score
Flecainide IC C Well tolerated in structurally normal No Compatible
hearts
Propafenone IC C Same as flecainide No Unknown
Propranolol II C Bradycardia, growth retardation, apnea No Compatible
Metoprolol II C Same as propranolol No Compatible
Atenolol II D Low birth weight No No
Pindolol II B ... No Compatible
Sotalol III B β-blocker effects, torsades de pointes No Compatible, but caution
advised
Amiodarone III D Fetal hypothyroidism, growth Yes Avoid
retardation, prematurity
Dofetilide III C Torsades de pointes Unknown Unknown
Dronedarone III X Vascular and limb abnormalities, cleft Yes Contraindicated
palate
Ibutilide III C Torsades de pointes Unknown Unknown
Verapamil IV C Maternal hypotension, fetal No Compatible
bradycardia
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Diltiazem IV C Same as verapamil Unknown Compatible

Adenosine N/A C Dyspnea, bradycardia No Unknown
Digoxin N/A C Low birth weight No Compatible
Adapted from Joglar and Page10,11 with permission of the publisher. Copyright © 1999, Adis International Limited, and Copyright © 2014, Wolters Kluwer Health.
Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or
adaptation. CNS indicates central nervous system; and FDA, Food and Drug Administration.
*See Table 1.

Atrioventricular Nodal Reentrant Tachycardia
AVNRT in pregnant patients should initially be managed with
the avoidance of precipitating factors and the use of vagal
maneuvers to terminate acute episodes of the arrhythmia. In
hemodynamically stable patients who do not respond to vagal
maneuvers, adenosine is the drug of choice as it is safe and
terminates ≈90% of paroxysmal SVT.31 If adenosine is inef-
fective, intravenous metoprolol or propranolol should be used.
Verapamil is considered a third line agent.27
For patients with frequent symptomatic episodes, metopro-
lol or verapamil can be used for prevention of SVT. Although
digoxin is safe in pregnancy, it often is ineffective alone but
has been used in combination with a β-blocker for AVNRT.12
For those with significant symptoms who do not respond to
atrioventricular nodal blocking agents, sotalol or flecainide
may be used. In rare cases, drug refractory, hemodynamically
significant AVNRT during pregnancy has been treated with
catheter ablation with low radiation exposure to the fetus.23
Accessory Pathways and Wolff–Parkinson–White
Patients with pre-excitation are more likely to have arrhyth-
mias during pregnancy.32 Most will present with ortho-
dromic atrioventricular reciprocating tachycardia, and the
management of acute episodes is the same as for AVNRT. In
a pregnant patient presenting with atrial fibrillation (AF) and
manifest pre-excitation or with a stable wide complex tachy-
cardia of uncertain pathogenesis, intravenous procainamide is
the drug of choice.
For long-term therapy, β-blockers, calcium channel block-
ers, digoxin, or flecainide may be used in patients with
concealed accessory pathways. For patients with Wolff–
Parkinson–White syndrome, verapamil or digoxin should
not be used because of the risk of rapid accessory pathway
conduction during AF. β-Blockers can be used cautiously in
patients with Wolff–Parkinson–White syndrome, especially if
the accessory pathway is not capable of rapid conduction.27
Otherwise, class I AADs such as flecainide or quinidine
may be used to slow conduction in the accessory pathway.
Although catheter ablation is the treatment of choice for
Wolff–Parkinson–White in the nonpregnant patient, this is
best avoided if possible during pregnancy. However, in select
cases, catheter ablation has been performed safely.19
Atrial Tachycardia
Atrial tachycardia is relatively rare during pregnancy, but
pregnancy may contribute to its initiation and maintenance.33
 964  Circ Arrhythm Electrophysiol  October 2014
Atrial tachycardia is often persistent and refractory to medi-
cal therapy and even cardioversion.34 Tachycardia-induced
cardiomyopathy may be present. For acute treatment, adenos-
ine should be used first as this is diagnostic and occasion-
ally successful in terminating the arrhythmia. Otherwise,
β-blockers, calcium channel blockers, or digoxin can be used
for rate control. If these agents fail to control the arrhythmia,
sotalol or flecainide may be considered. In cases of incessant,
symptomatic atrial tachycardia, catheter ablation has been
performed safely.22
AF and Flutter
AF and flutter are less common during pregnancy than SVT
with a prevalence of 2 in 100 000 hospital admissions.26 AF is
particularly rare in pregnant women without structural heart
disease or a prior personal history of AF. Increasing maternal
age because of increased successful use of infertility treat-
ments may make this a more common pregnancy-associated
arrhythmia in the future. Among women with previously
diagnosed AF, more than half will have symptomatic episodes
during pregnancy.35 Given the increased risk of venous throm-
boembolism during pregnancy, any pregnant woman with
new-onset AF should have pulmonary embolism excluded as
a cause.
Hemodynamically unstable episodes of AF or flutter should
be treated with electric cardioversion. In stable patients, fle-
cainide and ibutilide have been used safely in case reports to
convert AF in pregnancy, but there is not broad experience
with chemical cardioversion in this setting.35–37 For the major-
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ity of patients, rate control with β-blockers, calcium channel
blockers, or digoxin is used in the acute setting as well as for
chronic therapy. In patients where rate control fails or in those
with poorly tolerated episodes of AF (eg, mitral stenosis), a
rhythm control strategy with AADs is reasonable. Sotalol or
flecainide is the preferred AAD in this setting. Dronedarone is
contraindicated, and there is little experience with dofetilide.
Because of the risk of fetal harm, amiodarone should only be
used in the setting of life-threatening arrhythmias. There is no
role at this time for catheter ablation of AF during pregnancy.
Cavotricuspid isthmus ablation for typical atrial flutter can
likely be performed with low radiation exposure to the fetus,
but there are no such case reports available in the literature.
Atypical atrial flutters are more common among patients with
prior surgery for congenital heart disease.
Systemic anticoagulation is recommended for those with
AF and flutter who have risk factors for thromboembolism.
Although the benefit of aspirin in lower risk patients with AF
is uncertain, pregnancy is a hypercoagulable state, and we rec-
ommend aspirin in pregnant patients without indications for
anticoagulation.38 Warfarin, particularly early in pregnancy,
has teratogenic potential. Thus, low molecular weight hepa-
rin or unfractionated heparin is preferred, especially in the
first trimester and the last month of pregnancy.35,38 Warfarin
may be used in the second and third trimester. Heparin is also
recommended for patients with persistent episodes in whom
electric cardioversion is planned. There is little data about the
safety or use of newer oral anticoagulants such as dabigatran
or rivaroxaban or intravenous direct thrombin inhibitors in
pregnancy except for case reports of the use of intravenous
agents in patients with heparin-induced thrombocytopenia.39
Therefore, the routine use of these agents is not recommended
in pregnancy.
Ventricular Tachycardia and Sudden Cardiac Death
Ventricular tachycardia (VT) and ventricular fibrillation are
rare during pregnancy with a prevalence of 2 in 100 000 hos-
pital admissions.26 When ventricular arrhythmias do occur, it
is usually in the setting of structural heart disease and a history
of VT, and the risk of recurrent VT in such patients is as high
as 27%.40
VT in Women With Structural Heart Disease
VT has been described during pregnancy in a variety of
cardiomyopathies including hypertrophic cardiomyopathy
and arrhythmogenic right ventricular cardiomyopathy.41,42
Ischemic cardiomyopathy is uncommon in this patient popu-
lation, but myocardial infarction complicated by VT/ventric-
ular fibrillation with or without (coronary dissection, spasm)
coronary artery disease has been observed.43 Patients with
congenital heart disease are at relatively high risk for VT
with a prevalence of 4.5 to 15.9 per 1000 pregnancies.1,44 In
patients without known structural heart disease who develop
symptoms of heart failure in the last month of pregnancy
or in the months after delivery, peripartum cardiomyopathy
should be considered. The prevalence of VT in this patient
population is unknown, but cases of peripartum cardiomy-
opathy presenting with VT during pregnancy have been
reported.45
In pregnant patients with structural heart disease, the treat-
ment of VT should be tailored to the underlying cardiac condi-
tion. For the acute management of VT, electric cardioversion
should be performed in the setting of hemodynamic instabil-
ity. In hemodynamically tolerated VT, pharmacological car-
dioversion with lidocaine should be tried first. Procainamide
or quinidine may then be used if lidocaine is ineffective.
Given the risk of adverse effects to the fetus, amiodarone
should only be used in life-threatening situations when other
therapies have failed. Chronic AAD therapy is often war-
ranted in patients with VT and structural heart disease because
of the risk of hemodynamic compromise and sudden death.
β-Blockade with metoprolol or propranolol is indicated for
most patients. Sotalol may be considered if β-blockers are
ineffective. Mexiletine and quinidine are reasonable alterna-
tive agents, and class IC agents should not be used because
they are associated with increased mortality in nonpregnant
patients with structural heart disease.46 Again, amiodarone
should be reserved for potentially life-threatening arrhythmias
when other AADs have failed.47
As discussed previously, catheter ablation for arrhythmias
has been successfully performed in pregnant patients with low
radiation exposure and good outcomes.21 However, such case
reports are limited to the treatment of SVT. VT ablation cases
are often longer, use more fluoroscopy, and require general
anesthesia. There is only 1 case report of VT ablation in a
pregnant patient, and it was performed safely in a patient with
arrhythmogenic right ventricular cardiomyopathy presenting
with electrical storm at 36 weeks of gestation.48 However,
because of the limited experience and increased risk, VT

ablation in pregnant patients should only be considered as a
last resort in medically refractory patients with life-threaten-
ing arrhythmias.
VT in Pregnant Women Without Structural
Heart Disease
Idiopathic VT
Idiopathic VT is typically hemodynamically stable and asso-
ciated with a good prognosis.49 It may present for the first time
during pregnancy. It is often catecholamine sensitive, and
treatment of outflow tract VT with cardioselective β-blockers
in pregnant patients is usually effective.50,51 Sotalol or fle-
cainide may be considered in patients with significant symp-
toms that fail β-blocker therapy. Fascicular VT is typically
verapamil sensitive, and verapamil can be used for both acute
termination and prevention of recurrences.52 In nonpregnant
patients, catheter ablation is an effective treatment for idio-
pathic VT. However, there are no case reports of idiopathic VT
ablation in pregnant patients.
Long QT Syndrome
It is controversial whether women with long QT syndrome
are at increased risk for ventricular arrhythmias during preg-
nancy.53 There is increased risk in the postpartum period that
is potentially related to a decrease in heart rate, stress, and
altered sleep patterns. A retrospective study of 422 women
with long QT syndrome (111 probands) found that probands
were significantly more likely to have syncope, aborted car-
diac arrest, or sudden death in the 40-week postpartum inter-
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val compared with the 40-week prepregnancy period (23.4%
versus 3.8%).53 In addition, β-blocker therapy was associated
with decreased risk of cardiac events before pregnancy, dur-
ing pregnancy, and postpartum. Thus, β-blockers should be
continued throughout pregnancy and postpartum in women
with long QT syndrome and symptoms.47 Propranolol is the
preferred agent, as metoprolol may not be as effective in long
QT syndrome 1 and 2.54
Implantable Cardioverter Defibrillators and Pregnancy
Pregnant patients who present with unstable ventricular
arrhythmias and at high risk for sudden cardiac death during
pregnancy may be candidates for implantable cardioverter
defibrillator (ICD) implantation. Safety considerations on the
placement of ICDs during pregnancy are similar in principle to
those discussed in the section on catheter ablation. One must be
certain of the indication for the device and that all other alterna-
tives have been explored. If indicated, ICDs can be successfully
implanted during pregnancy with little fluoroscopy, and some
have used no fluoroscopy with echocardiographic guidance.55,56
Regarding the presence of an ICD during pregnancy,
little information is available, but the available studies are
reassuring. Natale et al57 assembled a series of 44 pregnant
women with ICDs, 42 of whom had abdominal generators.
Local complications such as implant site pain and generator
migration occurred in 3. Eleven (25%) women received ≥1
shock without direct ill effects on the pregnancy. In addition,
compared with the prepregnancy period, pregnancy was not
associated with an increase in ICD-related complications or
ICD shocks.
Enriquez et al   Arrhythmias in Pregnancy   965
Bradycardia and Conduction Disorders
Sinus node dysfunction and atrioventricular block are rare in
pregnancy, especially in structurally normal hearts.11,26 Con-
genital complete heart block is occasionally diagnosed for the
first time during pregnancy. Asymptomatic patients with com-
plete heart block without other evidence of conduction disease
or structural heart disease often have a good prognosis and can
be managed expectantly.11 In the past, temporary pacing during
labor and delivery was advocated in all patients with complete
heart block because of potential bradycardia and syncope with
Valsalva.58 However, more recent studies suggest that tempo-
rary pacing is unnecessary in stable patients with complete
heart block.59 Pregnant patients with symptomatic or hemody-
namically unstable bradyarrhythmias may require permanent
pacing. As with ICDs, permanent pacemakers can be implanted
successfully during pregnancy using low doses of radiation.60
Fetal Arrhythmias
A complete discussion of fetal arrhythmias is beyond the scope
of this review. SVTs are the most common fetal arrhythmias,
although VT has been reported.61 Fetal SVTs may be paroxys-
mal or sustained and may result in hydrops fetalis, which may
be reversible with treatment. Flecainide, sotalol, and digoxin
are the drugs of choice for the treatment of fetal SVT.62
Conclusions
The incidence of cardiac arrhythmias is higher with preg-
nancy, and all forms of arrhythmia and structural heart disease
may be encountered. The majority of arrhythmias are benign,
but for those patients with severe symptoms or hemodynami-
cally unstable arrhythmias, therapy should be initiated with
the assistance of Maternal-Fetal Medicine colleagues. Mul-
tiple AADs are available for use in pregnancy. However, data
are limited, and there is a need for more prospective and regis-
try studies to evaluate the safety of these agents in pregnancy.
If possible, therapy should be limited during the first trimester,
and drugs with the longest safety record should be used first.
In the case of refractory, life-threatening arrhythmias, higher
risk strategies should be considered. With shielding, modern
electroanatomic mapping systems, and intracardiac echocar-
diography, catheter ablation of many arrhythmias can be per-
formed with minimal radiation exposure.
Disclosures
Dr Tedrow has received consulting fees from St. Jude Medical and
Boston Scientific as well as nonsalary research support from Biosense
Webster and St. Jude Medical. The other authors report no conflicts.
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Key Words: arrhythmias, cardiac ◼ pregnancy