Arrhythmias and Pregnancy Management of Preexisting and New-Onset Maternal Arrhythmias

Home , Atrial fibrillation, Atrial flutter, Short QT syndrome, Sinus tachycardia

Dominique S. Williams, MDa,*, Krasimira Mikhova, MDb, Sandeep Sodhi, MDc

KEYWORDS Pregnancy Maternal arrhythmias Arrhythmias Atrial fibrillation Supraventricular tachycardia Ventricular tachycardia Structural heart disease

KEY POINTS Women with preexisting arrhythmias are at high risk for recurrent arrhythmias and/or exacerbation arrhythmias with pregnancy. Arrhythmias may present at any time during pregnancy. Higher risk periods include the latter part of the second trimester, third trimester, and peripartum period. New-onset atrial fibrillation and ventricular arrhythmias should prompt evaluation for structural heart disease.

BACKGROUND minute, and peripheral vascular resistance declines. These changes are amplified in multiple gestation Arrhythmias are the most common cardiovascular pregnancy, with cardiac output increasing by 60% complication of pregnancy. Hospitalizations due to 70%.2,3 Physiologic changes peak in the second to arrhythmias in pregnancy have increased by trimester, and again in labor and delivery where car- 58% from 2000 to 2012, mainly due to a rise in 1 diac output increases due to “auto transfusion” with atrial fibrillation. This rise is likely due to the in- uterine contractions. Sympathomimetic tone is also crease in pregnancy in women with structural increased due multiple factors including neurohor- heart disease. Arrhythmias may present for the monal changes during pregnancy, and pain and first time in pregnancy, and in women with a his- anxiety during labor and delivery.3,4 tory of arrhythmias, pregnancy may lead to an Cardiac myocytes have estrogen and proges- exacerbation of a previously controlled terone receptors. The downstream effects of es- arrhythmia. Identification and appropriate man- trogen and progesterone on cardiac myocytes is agement of arrhythmias are of utmost importance not well understood, but studies have shown these in order to optimize maternal and fetal health. hormones play a role in repolarization.4 Temporary cardiac remodeling during pregnancy may PATHOPHYSIOLOGY contribute to the development of arrhythmias. Cardiac output increases by 30% to 50% in preg- Atrial enlargement and stretch may create a sub- 5,6 nancy, heart rate increases by 10 to 15 beats per strate for atrial arrythmias.

a Cardiovascular Division, John T. Milliken Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, St Louis, MO 63110, USA; b Cardiovascular Division, Electrophysiology, John T. Milliken Department of Internal Medicine, Washington University School of Medi- cine, 660 South Euclid Avenue, Campus Box 8086, St Louis, MO 63110, USA; c Department of Medicine, Cardio- vascular Division, John T. Milliken Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, St Louis, MO 63110, USA * Corresponding author. E-mail address: [email protected]

Cardiol Clin 39 (2021) 67–75 https://doi.org/10.1016/j.ccl.2020.09.013

0733-8651/21/Published by Elsevier Inc. cardiology.theclinics.com Descargado para Irene Ramírez ([email protected]) en National Library of Health and Social Security de ClinicalKey.es por Elsevier en enero 08, 2021. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados. 68 Williams et al

PREMATURE BEATS Atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia Premature atrial and ventricular beats are common (AVRT) are the most common subtypes of SVT. in pregnancy, occurring in w59% of pregnancies 7 AVNRT is characterized by dual AV node physi- in one study. Premature beats are often benign ology allowing anterograde and retrograde con- and patient reassurance can be provided. Howev- duction. In AVRT conduction may occur through er, in some patients, premature beats can be asso- the AV node or the accessory pathway. In anti- ciated with structural heart disease and further dromic AVRT, the tachycardia conducts antero- workup and evaluation are prudent. grade down the accessory pathway and Premature ventricular contractions (PVC) may retrograde conduction through the AV node, be an initial presentation of a cardiomyopathy or creating a regular wide complex tachycardia. Anti- lead to the development of a cardiomyopathy. dromic AVRT accounts of 5% to 10% of AVRT.12 PVC burden has been shown to correlate with In patients with SVT, electrocardiograms in si- left ventricular function. Most cases of PVC- nus rhythm are assessed for preexcitation, which induced cardiomyopathy occur in patients with a may be asymptomatic and intermittently present PVC burden of greater than 10% in 24 hours.8 9 on electrocardiogram. Findings of preexcitation Tong and colleagues performed a prospective include a short PR interval less than 120 ms, case control study of 53 pregnancies in 43 women slurred upstroke of the QRS, and QRS prolonga- with a PVC burden of greater than 1%, mean PVC tion greater than 110 ms. Concern arises in pa- burden of 13.9%, and no structural heart disease. tients with preexcited atrial fibrillation that may PVCs presented more commonly in the first degenerate into ventricular fibrillation. Preexcita- trimester. In 25 of 53 pregnancies, beta-blocker tion should be considered in patients with SVT therapy was initiated due to symptoms and/or a who present with syncope or sudden cardiac high burden. Adverse cardiovascular events death. occurred in 11% of pregnancies and included heart failure, and sustained and nonsustained ventricular tachycardia. Pregnancies with adverse ATRIAL FIBRILLATION cardiovascular events all had a PVC burden of Atrial fibrillation (AF) is the most common greater than 5%. Adverse fetal events occurred arrhythmia in pregnancy, accounting for 27 per in 13% of pregnancies and included small for 9 100,000 pregnancy hospitalizations for arryth- gestational age and preterm birth. mias.1,13 In a meta-analysis of 7 studies totaling Patients with significant symptoms and pre- 8 301,638 pregnancies, AF incidence was signifi- served systolic function should be reassured. Med- cantly higher in women with structural heart dis- ical therapy for PVCs is indicated for symptoms or in ease compared with women without structural the setting of a reduced left ventricular ejection frac- heart disease (0.3% vs 2.2%).14 tion. First-line therapy with non-dihydropyridine cal- Risk factors for AF in pregnancy are similar to cium channel blockers or beta-blockers, excluding 8 risk factors in the nonpregnant state. Obesity and atenolol, is recommended. age older than 40 significantly increase risk of Premature atrial contractions (PACs) have primar- AF.15 Additional risk factors for AF identified in ily been studied in the nonpregnant population. the Registry of Pregnancy and Cardiac Disease Frequent PACs (>100 beats in 24 hours) have (ROPAC) include congenital heart disease, preex- been shown to increase the risk of new-onset atrial isting history of AF, beta-blocker use before preg- fibrillation, supraventricular tachycardia, and car- nancy, and valvular heart disease.16 diovascular morbidity and mortality in healthy pa- AF in pregnancy is associated with adverse tients and patients with multiple comorbidities. 10,11 maternal and fetal outcomes. Adverse fetal out- including structural heart disease. comes include intrauterine growth restriction, respiratory distress syndrome, intraventricular SUPRAVENTRICULAR TACHYCARDIA hemorrhage, and higher rates of neonatal intensive care unit admissions. In addition, agents used for Supraventricular tachycardia (SVT) is the second rate control may lead to maternal hypotension most common arrhythmia in pregnancy, occurring and decreased placental perfusion, increasing in 22 per 100,000 pregnancy hospitalizations.1 the risk for preterm labor. Adverse maternal out- SVT may present at any stage of pregnancy, but comes include heart failure and thromboembolic commonly presents in the second trimester. SVT events.15–17 presents with sudden onset of palpitations, which Management of AF is similar to the nonpregnant may be associated with dyspnea, chest discom- state. In the nonpregnant population, trials have fort, or presyncope. not shown a difference in cardiovascular

Descargado para Irene Ramírez ([email protected]) en National Library of Health and Social Security de ClinicalKey.es por Elsevier en enero 08, 2021. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados. Arrhythmias and Pregnancy 69

outcomes and overall mortality between rate and heart rate with pregnancy. During pregnancy, the rhythm control strategies.18,19 There are no data heart rate increases by 10 to 20 beats per minute available comparing maternal and fetal outcomes but the resting heart rate rarely exceeds greater in a rate control versus rhythm control approach. than 95 beats per minute.28 IST is characterized According to the 2018 European Society of Cardi- by an elevated resting heart rate greater than 100 ology Guidelines, a rhythm control strategy is beats per minute or an average heart rate of preferred for management of AF in pregnancy.20 greater than 90 beats per minute over 24 hours Rhythm control allows for lower doses of rate con- in the absence of secondary causes. Symptoms trolling medications, such as beta-blockers, which of IST include palpitations, fatigue, chest discom- can associated with hypotension, intrauterine fort, dizziness, and poor exercise tolerance due to growth restriction, and infant hypoglycemia. exaggerated rise in heart rate. In published case Rhythm control can be accomplished with cardio- reports, IST appears to be well tolerated without version and/or antiarrhythmic therapy. Cardiover- adverse of maternal or fetal outcomes.29,30 sion is safe in pregnancy and should be considered if AF does not terminate within 24 hours VENTRICULAR TACHYCARDIA of onset.21,22 Cardioversion within 48 hours of AF onset does not negate the need for therapeutic Ventricular arrhythmias (VA) pose a significant risk anticoagulation.23 Cardioversion results in atrial to maternal and fetal morbidity and mortality. VAs stunning and activation prothrombotic factors.24 most commonly occur in the setting of structural Thromboembolic events are highest the first heart disease, ischemia, inherited arrhythmia syn- month following cardioversion; thus, anticoagula- dromes, or QT prolongation due to drugs or elec- tion should be continued for a minimum of 4 weeks trolyte abnormalities. In an ROPAC study of 2966 following cardioversion. Extended or long-term pregnancies (56% congenital heart disease, 32% anticoagulation should be based on the patients’ valvular heart disease), VAs occurred in 1.4%. Pre- risk factors for thromboembolic events.23,25,26 If dictors of VAs included New York Heart Associa- the onset of AF cannot be determined with accu- tion Class greater than 1 before pregnancy and racy, transesophageal echocardiogram should moderate/severe left ventricular dysfunction. be performed before cardioversion. There was a trend toward higher mortality in P 5 31 In nonpregnant women, the CHADS2 VASC women with VAs (2.4% vs 0.3%, .15). VAs Score (congestive heart failure, hypertension, age are more likely to occur in women with a prior his- 75 years, diabetes mellitus, stroke or transient tory of VAs. ischemic attack, vascular disease, age 65 to 74 Arrhythmogenic Right Ventricular years, sex category) guides anticoagulation man- Cardiomyopathy agement in AF. Therapeutic anticoagulation in recommended in patients with a nonsex Arrhythmogenic right ventricular cardiomyopathy CHADS2VASC score greater than 1.23 The (ARVC) is characterized by fibrofatty displacement CHADS2VASc score is often used in AF in preg- and thinning of the myocardium leading to ventric- nancy; however, it has not been validated in preg- ular enlargement and dysfunction. ARVC predom- nant women. There are case reports of left atrial inantly affects the right ventricle but left ventricular appendage thrombus in pregnancy with persistent dysfunction may also occur. The degree of ventric- AF and structurally normal hearts.27 Aspirin, thera- ular dysfunction correlates with outcome. ARVC peutic anticoagulation, and prophylactic enoxa- may be symptomatic or present with PVCs, ven- parin have been reported in the literature. tricular tachycardia or sudden cardiac death. VAs Antithrombotic therapy for AF in pregnancies often present before ventricular dysfunction. In pa- varies. Use of aspirin, therapeutic anticoagulation, tients with ARVC, VAs are often triggered by prophylactic enoxaparin and no therapy have all increased adrenergic activity, such as exercise.32 been reported.27 If aspirin is prescribed for AF in Adverse cardiovascular events are not uncommon pregnancy, the dose should not exceed 162 mg. during pregnancy in women with ARVC. Wu and Full-dose aspirin increases the risk of premature colleagues33 reviewed 224 pregnancies in 120 closure of the ductus arteriosus. women with ARVC. Ninety-one (76%) women had pregnancies before the diagnosis of ARVC. INAPPROPRIATE SINUS TACHYCARDIA Adverse events occurred in 12 pregnancies and included VAs and heart failure. Women at highest Inappropriate sinus tachycardia (IST) may present risk of adverse outcomes had earlier onset of during pregnancy and can be difficult to distin- symptoms and left ventricular dysfunction (50% guish from postural orthostatic tachycardia syn- vs 60%, P 5 .004). In the women who became drome as well as the physiologic increase in pregnant after being diagnosed with ARVC, there

was no significant change in ventricular remodel- Catecholaminergic Polymorphic Ventricular ing or function 1 year postpartum.33 In a study by Tachycardia Hodes and colleagues34 of 26 women with ARVC CPVT is a rare inherited arrhythmia syndrome that and 39 pregnancies, 5% developed heart failure often presents as syncope, VAs, or sudden death and 13% developed VAs. in the setting of exercise or an emotional stressor in the absence of structural heart disease or pro- Hypertrophic Cardiomyopathy longed QT interval. Polymorphic VT, bidirectional VT and ventricular fibrillation are characteristic of Hypertrophic cardiomyopathy (HCM) is due to mu- CPVT. CPVT mimics LQT1 and is not uncommonly tations in genes encoding sarcomere proteins, misdiagnosed as LQT1 despite a normal QTc in- leading to increased left ventricular wall thickness terval. Medical therapy for CVPT includes nonse- and mass in the absence of secondary causes. It is lective beta-blockers and flecainide. Nadolol is inherited in an autosomal dominant manner and the preferred beta-blocker in CPVT.39 may occur with or without LVOT obstruction. Heart failure, arrhythmias, stroke, and sudden cardiac BRADYARRHYTHMIAS death account for most cardiovascular morbidity and mortality in HCM. In the ROPAC registry, Bradyarrhythmias are uncommon in pregnancy. If VAs occurred in 22% of women with HCM with present, they are often due to chronotropic incom- implantable cardioverter-defibrillators. There was petence or high-degree atrioventricular block, no significant increase in VAs in women with which is often present before pregnancy. Women HCM and no implantable cardioverter defibril- with repaired congenital heart disease or prior car- lator.31 In a pooled cohort of 9 studies with 207 diac surgery are at an increased risk for bradyar- women with HCM and 408 pregnancies, maternal rhythmias. In a study of 25 pregnancies in 18 mortality was less than 1% and 30% of pregnan- women, those with untreated atrioventricular cies were associated with worsening symptoms block were more likely to have progression in con- or arrythmias. Adverse fetal outcomes included duction disease with pregnancy. Women with spontaneous abortion, stillbirth, and premature new-onset atrioventricular block were more likely birth. Maternal deaths were due to sudden cardiac to require intervention compared with women death.35 Validated risk factors of sudden cardiac with stable atrioventricular block before 40 death in HCM should be considered when coun- pregnancy. seling women on adverse cardiovascular outcomes with pregnancy. DIAGNOSIS AND MANAGEMENT Clinical evaluation should be performed in a step- wise approach starting with a detailed clinical his- Inherited Arrhythmia Syndromes tory, obstetric history, family history and physical Inherited arrhythmia syndromes (IAS) include examination. Red flags include exertional syn- congenital long QT syndrome (LQTS), catechol- cope, syncope triggered by emotional stress aminergic polymorphic ventricular tachycardia and/or auditory stimuli, palpitations associated (CPVT), Brugada syndrome, short QT syndrome, with anginal chest pain or syncope, and a family idiopathic ventricular fibrillation, and early repolar- history of sudden cardiac death. ization syndrome. Data on IAS and pregnancy out- An electrocardiogram should be obtained in all comes is limited as few studies specify types of patients with specific attention to signs of preexci- IAS. IAS is not an absolute contraindication to tation, pathologic q waves, ventricular hypertro- pregnancy. LQTS is the most common channelop- phy, and conduction delays and intervals. Mobile athy, occurring in 1 in 2000. QTc greater than cardiac telemetry or Holter monitoring should be 500 ms and severe genotype (LQT2 or LQT3) is considered based on the frequency of symptoms. associated with high risk of torsades de Use of implantable loop recorders in pregnancy pointes.36,37 In a study of 136 pregnancies in 76 have been reported. In a study of 40 pregnant women with LQTS and mean QTc 515 ms, women, implantable loop recorders increased 10.3% of pregnancies were associated with VAs. detection of arrhythmias and led to changes in The increased risk of VAs persisted 9 months post- management.41 Identification of arrhythmias or partum. Beta-blocker therapy was protective of frequent premature ventricular should prompt VAs during pregnancy and postpartum.38 Beta- assessment of structural heart disease. Identifica- blockers are a Class I indication in LQTS and tion of structural heart disease affects risk of car- should be continued in pregnancy and diovascular complications with pregnancy and postpartum.39 medical therapy. Transthoracic echocardiogram

is readily available and can be performed with (72%). Beta-blockers significantly reduced birth contrast enhancement in pregnancy. Exercise weight less than 200 g; however, this is unlikely stress testing or advanced imaging should be to be clinically consequential. Metoprolol was considered based on the clinical scenario associated with the smallest reduction in birth (Table 1). weight by 119 g. Atenolol was associated with the largest reduction in birthweight by 466 g and PHARMACOTHERAPY is not recommended for use in pregnancy.44

There are no randomized trials regarding use of Calcium Channel Blockers (Food and Drug cardiovascular disease medication in pregnancy. Administration Class C) Most drugs are Food and Drug Administration (FDA) class C or D. Class C drugs have limited Calcium channel blockers (CCBs) have not been data in human pregnancy but have been studied associated with increased risk of congenital mal- in animal reproduction and shown to have adverse formation. Due to the mechanism of action, fetal effects. Class D drugs have shown adverse CCBs may cause hypotension and tocolysis. Prior fetal effects when given in pregnancy in humans. studies suggested an increased risk of neonatal Given limited data on pharmacotherapy in preg- seizures with CCB use in the third trimester; how- nancy, risk versus benefit must be considered. ever, this was not shown in recent large cohort Triggers to arrhythmias should be considered study with 22,908 pregnancies.45 Diltiazem has before implementation of long-term medical ther- been associated with teratogenicity in animals apy. Triggers include severe electrolytes abnor- but this has not been studied in pregnancy. Verap- malities, illicit drug use, supplements, and certain amil is considered safe in pregnancy and obstetric medications such as terbutaline and breastfeeding.20 magnesium sulfate. Severe hypermagnesemia may lead to cardiac and respiratory arrest. The Digoxin (Food and Drug Administration Class PR interval and QRS duration increase with C) plasma levels of 5 mg/dL to 10 mg/dL. Conduction Digoxin predominantly affects the resting heart defect and cardiac arrest may occur with plasma rate and is often used as an adjunct for rate control levels greater than 10 mg/dL. It is important to in patients treated with beta-blockers or CCBs. remember that to improve fetal and maternal out- Digoxin may also be used in heart failure with comes, maternal health must be prioritized. reduced ejection fraction. Serum levels of digoxin are not reliable in pregnancy due to an increase Beta-Blockers (Food and Drug Administration in unbound digoxin and an increase in renal clear- Class C) ance.46 Clinical signs and symptoms should be Beta-blockers increase the risk of intrauterine used in addition with serum levels to assess for growth restriction (IUGR), preterm birth, and digoxin toxicity. neonatal hypoglycemia, bradycardia and hypotension. In a cohort study of 18,477 women with hy- Adenosine (Food and Drug Administration pertension in pregnancy, beta-blocker use in the Class C) first trimester was not independently associated Adenosine is safe for use in pregnancy and has not with an increased risk of overall malformations or been shown to have adverse fetal effects. Adeno- cardiac malformations.42 Variation in risk of sine has a very short half-life, which prevents deliv- congenital malformation with beta-blocker dose ery to the fetus. It is recommended as first-line in the first trimester has not been studied. therapy for acute termination of supraventricular b1 selective beta-blockers are preferred in preg- tachycardia in pregnancy if vagal maneuvers nancy due to lower rates of IUGR and decreased fail.46 An intravenous line should be placed in the effects on uterine activity and peripheral vasodila- antecubital fossa or more proximal, given the short tion. Nonselective beta-blockers are associated half-life. It is given as a bolus of 6 mg followed by with higher rates of IUGR. Atenolol is the only rapid saline flush. Two subsequent doses of 12 mg beta-blocker listed as FDA Class D due to can be given.12 increased risk of congenital malformations. Use of atenolol is not recommended in pregnancy.43 Flecainide (Food and Drug Administration A recent study by Grewal and colleagues Class C) analyzed the determinants of birth weight to discern the relative impact of beta-blockers.44 Of Flecainide is a sodium channel blocker used in the 1757 pregnancies, 404 women were treated with treatment of supraventricular tachycardia, atrial beta-blockers, most commonly metoprolol arrhythmias and CPVT. Flecainide crosses the

Table 1 Diagnosis and management of arrhythmias in pregnancy

Arrhythmia Diagnostic Testing Treatment Clinical Pearls Supraventricular Assess for structural Vagal maneuvers Consider antidromic SVT tachycardia heart disease with b-blockers in differential for a echocardiography Non-dihydropyridine regular wide complex before antiarrhythmic calcium channel tachycardia therapy blockers Flecainide Sotalol Adenosine DCCV Catheter ablation Atrial Assess for structural b-blockers Consider DCCV for fibrillation heart disease with Non-dihydropyridine hemodynamically and flutter echocardiography calcium channel stable AF>24 h and/or advanced blockers Aspirin <162 mg daily cardiac imaging Digoxin Therapeutic Flecainide anticoagulation in Sotalol high risk patients Dofetilide (coumadin, LMWH) Amiodaronea Preexcited AF: DCCV Procainamide, Catheter ablation catheter ablation Sinus Distinguish physiologic Encourage adequate Avoidance of tachycardia tachycardia from hydration precipitating factors inappropriate sinus Compression stockings (eg, alcohol, caffeine) tachycardia and b-blockers postural orthostatic Non-dihydropyridine tachycardia syndrome calcium channel blockers Premature Quantitate PVC burden Correct electrolyte Risk of PVC-induced ventricular with Holter monitor abnormalities cardiomyopathy with contractions Consider assessment for b-blockers higher PVC burden structural heart Non-dihydropyridine disease with calcium channel echocardiography blockers and/or advanced Sotalol cardiac imaging Dofetilide Amiodaronea Catheter ablation Ventricular Assess for structural Cardioversion Avoid QT-prolonging tachycardia heart disease with Correct electrolyte agents echocardiography abnormalities Consider antidromic SVT and/or advanced b-blockers with a regular wide cardiac imaging Non-dihydropyridine complex tachycardia Consider inherited calcium channel Consider preexcited AF channelopathies and blockers with an irregular wide ischemia Sotalol complex tachycardia Dofetilide ICD implantation Amiodaronea (transvenous or Catheter ablation subcutaneous) during pregnancy in qualifying patients

Abbreviations: AF, atrial fibrillation; DCCV, direct current cardioversion; ICD, implantable cardioverter defibrillator; LMWH, low molecular weight heparin; PVC, premature ventricular contractions; SVC, supraventricular tachycardia a Avoid amiodarone use, Food and Drug Administration Class D.

placenta and is present in breast milk. It is used in ELECTROPHYSIOLOGY PROCEDURES the treatment of both maternal and fetal arrhythmias. Coadministration of atrioventricular (AV) Catheter ablation has been performed safely in nodal blockers are recommended in patients pregnancy. Catheter ablation is considered in pa- with AF and flutter treated with flecainide as there tients with refractory and/or life-threatening arrhythmias that cannot be managed with medical is potential for one-to-one atrioventricular conduc- 20,49 tion. Flecainide should not be used in patients with therapy. If possible, catheter ablations should coronary artery disease or structural heart be performed in the second trimester with use of disease.47 echocardiographic guidance to minimize or elimi- nate radiation exposure. Placement of implantable cardiac-defibrillators (ICD) and pacemakers are Sotalol (Food and Drug Administration Class safe in pregnancy. ICD shocks have not been B) associated with adverse fetal effects.50 Sotalol is a potassium channel blocker with beta- blocker properties. Due to its QT-prolonging effects, there is risk of torsade de pointes. Sotalol SUMMARY exhibits reverse-use dependence on the action Arrhythmias, new-onset or exacerbation of preex- potential. As a result, QT-prolonging effects are isting arrhythmias, are the most common cardio- highest at reduced heart rates. Drug efficacy is vascular complication in pregnancy. A detailed reduced at higher heart rates. evaluation should be performed in patients with arrhythmias and management should be in place Dofetilide (Food and Drug Administration outlining antepartum, intrapartum, and post- Class C) partum care. A multidisciplinary approach with Dofetilide is a potassium channel blocker with cardiology, maternal fetal medicine, pediatrics, reverse-use dependence. The QT prolonging of ef- and anesthesia is of utmost importance to opti- fects are greater when compared with sotalol. mize maternal and fetal outcomes. Dofetilide must be initiated in an inpatient setting with close monitoring of the electrocardiogram.47 CLINICS CARE POINTS Providers should pay close attention to drug inter- actions and avoid coadministration of QT- Arrhythmias are the most common cardiovas- prolonging agents. cular complication of pregnancy, occurring in 68 per 100,000 pregnancies. Amiodarone (Food and Drug Administration Women with a prior history of arrhythmias are Class D) at high risk of recurrence (30%–50%) with pregnancy. Amiodarone is reserved for refractory and/or life- There are no validated risk models to assess threatening arrhythmias due to its adverse fetal ef- risk of thromboembolic events in nonvalvular fects which are independent of dose and duration. AF in pregnancy. The CHA₂DS₂-VASc score Adverse fetal effects include congenital goiter, hy- has not been validated in pregnancy. High- pothyroidism, neurodevelopmental abnormalities, dose aspirin increases the risk of premature and preterm birth. Neonatal hypothyroidism is closure of the ductus arteriosus. often transient and has been reported in 23% of Ventricular tachycardia should prompt evalu- neonates exposed to amiodarone.48 Use of amio- ation for structural heart disease, ischemia darone is not recommended in women (eg, pregnancy associated myocardial infarc- breastfeeding. tion, coronary spasm), use of QT-prolonging agents, and inherited channelopathies. DIRECT CURRENT CARDIOVERSION Amiodarone is associated with adverse fetal effects and should be reserved for refractory Cardioversion is safe and effective in pregnancy and life-threatening arrhythmias. and should be performed immediately in patients Cardioversion, catheter ablation, and implan- with hemodynamic instability.21,22 Continuous tation of cardioverter-defibrillators are safe in fetal monitoring and coordination of care with pregnancy. maternal fetal medicine and pediatric is recommended in viable pregnancies. If anticoagulation is indicated, consideration of gestational age and DISCLOSURE potential need for emergency delivery should play a role in choosing the appropriate agent. The authors have nothing to disclose.

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