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Cardiac arrhythmias in pregnancy Robert J. Knotts, MD, and Hasan Garan, MDn Department of Medicine, Columbia University Medical Center, 161 Fort Washington Ave, Suite 648, New York, NY 10032

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Keywords:

As more women with repaired congenital heart disease survive to their reproductive years

cardiac arrhythmia

and many other women are delaying pregnancy until later in life, a rising concern is the

pregnancy

risk of cardiac arrhythmias during pregnancy. Naturally occurring cardiovascular changes

fetal arrhythmia

during pregnancy increase the likelihood that a recurrence of a previously experienced

antiarrhythmic drugs

cardiac arrhythmia or a de novo arrhythmia will occur. Arrhythmias should be thoroughly investigated to determine if there is a reversible etiology, and risks/benefits of treatment options should be fully explored. We discuss the approach to working up and treating various arrhythmias during pregnancy with attention to fetal and maternal risks as well as treatment of fetal arrhythmias. Acute management in stable patients includes close monitoring and intravenous pharmacologic therapy, while DC cardioversion should be used to terminate arrhythmias in hemodynamically unstable patients. Long-term management may require continued oral antiarrhythmic therapy, with particular attention to fetal safety, to prevent complications associated with arrhythmias. & 2014 Elsevier Inc. All rights reserved.

Maternal arrhythmias Introduction As more women with repaired congenital heart disease survive to their reproductive years, a rising concern is the risk of pregnancy and the associated incidence of cardiac arrhythmias. At the same time, a growing number of women are delaying pregnancy until later in life, increasing their risk of developing arrhythmias as the incidence of heart disease increases with age.1,2 During pregnancy, as the cardiac output increases and the plasma volume expands, increased heart size causes a rise in wall tension, thereby stimulating the stretch-activated ion channels.3 These changes may predispose the mother to new-onset arrhythmias but more likely raise the likelihood of recurrence in women with previously documented ones during pregnancy. The increase in heart rate may lead to a shortening of the PR, QRS, and QT intervals. n

Corresponding author. E-mail address: [email protected] (H. Garan).

http://dx.doi.org/10.1053/j.semperi.2014.04.017 0146-0005/& 2014 Elsevier Inc. All rights reserved.

The rotation of the heart on its long axis in a left-upward direction, due to an enlarging uterus and elevation of the diaphragm, can shift the electrical axis to the left. A small Q wave and/or an inverted T wave may be seen in lead III.4,5 Any other change from baseline should be considered abnormal and further evaluated. Ectopic beats during pregnancy are common, usually benign, and require no specific treatment.6 Sustained arrhythmias in patients without any underlying structural heart disease are likely to be pathway-related supraventricular tachycardia (SVT), such as atrioventricular (AV) nodal reentry1,2 or idiopathic ventricular tachycardia (VT). By contrast, in patients who have cardiomyopathy, rheumatic, or other valve disease, or who have undergone corrective cardiac surgery for congenital heart disease, the mechanism is likely to be atrial or ventricular tachyarrhythmia related to the pathological substrate.7 A prior history of arrhythmias or structural heart disease or a family history of sudden death increases the risk of tachyarrhythmias during pregnancy.3

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Epidemiology Cardiac arrhythmias constituted an event rate of 166/100,000 in unselected pregnancy-related admissions in a large series.8 SVTs had an event rate of 24/100,000, atrial fibrillation/flutter (AF/AFL) an event rate of 2/100,000, VT an event rate of 2/100,000, and high-grade AV block an event rate of 1.5/100,000. The 8 cases of cardiac arrest (6/100,000) included 5 patients with asystole and 3 with ventricular fibrillation (VF).8 The incidence of cardiac arrhythmias during pregnancy is much higher in women with previously known cardiac arrhythmia. In a retrospective study conducted during 87 pregnancies in a selected group of 73 patients who had a history of SVT, paroxysmal AF/AFL, persistent AF/AFL, or VT, 44% of the patients with normal sinus rhythm at the beginning of their pregnancy developed a recurrence of their known tachyarrhythmia during or within 1 month after their pregnancy.9 The recurrence rate of SVT, paroxysmal AF/AFL, and VT in women with a history of these arrhythmias was 50%, 52%, and 27%, respectively.

Specific arrhythmias in pregnant women with no organic heart disease Pregnant women who develop palpitations, near syncope, or syncope should be evaluated to determine the etiology. Serum electrolyte abnormalities and hyperthyroidism should be ruled out. A resting ECG, ambulatory ECG recording, and echocardiography should be performed. New-onset SVT is rare but the recurrence rate of previously documented SVT reaches 50% during pregnancy. Atrioventricular nodal reentrant tachycardia is the most common form unless the patient has Wolff–Parkinson–White (WPW) syndrome, where the type of SVT would be AV reentrant tachycardia (AVRT), whereas focal ectopic atrial tachycardia (EAT) is generally rare and is usually associated with structural heart disease.4,7 AF and AFL during pregnancy are also rare in patients who do not have structural heart disease or hyperthyroidism1and, if observed, should raise the suspicion of previously undiagnosed cardiomyopathy or valve disease and further investigated with an echocardiogram. Wide-complex tachycardias may be SVT with aberration, or pre-excitation, or VT. Without structural heart disease VT is idiopathic, usually originating from the right ventricular (RV) outflow tract with its typical ECG configuration of an inferior frontal axis and left bundle branch block QRS mimicry10 and less commonly idiopathic left VT, which has a superiorly directed frontal axis and a right bundle branch QRS morphology. A recent study found 73% of the complex ventricular ectopy originating in the RV outflow tract during pregnancy.11 A specific type of polymorphic VT, torsade de pointes, occurs in patients with long QT syndrome. A retrospective study of women affected with congenital long QT syndrome, who had one or more pregnancies, showed no increase in cardiac events during pregnancy but a definite rise in the ventricular arrhythmias during the postpartum period, especially in LQT2 genotype.12

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Specific arrhythmias in pregnant women with organic heart disease Focal EAT, intra-atrial reentry, atrial flutter, atrial fibrillation, and ventricular tachycardia in young and middle-age women are generally associated with structural heart disease, including surgically corrected congenital heart disease, cardiomyopathy, and valve disease. Focal EAT tends to be persistent and has a propensity to be drug-resistant.4,7 Clinically significant arrhythmias occur in 4.6% of the women with an unrepaired atrial septal defect (ASD) and in 3.6% in those with repaired ASD.13 Right atrial EAT and typical AFL are also common in patients with repaired tetralogy of Fallot (TOF) and pulmonic stenosis. In patients with an atrial switch operation for d-transposition of the great arteries (d-TGA) and in patients after a Fontan procedure, the atrial tachycardias and flutters are usually scar related and complex, and may have dire hemodynamic consequences. In women with atrial switch operation, maternal complications include 12.5% incidence of tachyarrhythmias in mid to late pregnancy.14 In a recent report, 33 of the 71 pregnancies in 45 women with Fontan operation were complicated by an adverse maternal cardiac event, primarily atrial arrhythmias, resulting in heart failure.15 Atrial fibrillation may occur in valve disease, and if associated with rheumatic mitral stenosis, pulmonary edema may develop rapidly, especially in late pregnancy, necessitating emergent ventricular rate control and even prompt DC cardioversion.5 Ventricular tachycardia may cause hypotension and even collapse if the rates are high enough, severely compromising both maternal and fetal circulation. A retrospective review of 40 pregnancies in 25 women with repaired TOF reported 17% cardiac events, but only a couple of these were VT related.16 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare genetic disease that causes RV dysfunction and VT. During the third trimester and after delivery there is an increased incidence of arrhythmias in women with ARVC.17 Symptomatic bradycardia due to sinoatrial disease may result from an atrial switch operation, a Fontan operation, or repair of partial anomalous venous return. The incidence of second- and third-degree heart block during pregnancy is rare unless there is congenital heart disease that has been repaired, such as TOF, ventricular septal defect, or endocardial cushion defect.18

Treatment Acute management Without organic heart disease, narrow-complex tachycardias are usually well tolerated, but if there is hemodynamic instability, DC cardioversion should be used to terminate the tachycardia. DC cardioversion is safe in all stages of pregnancy.5 Although the DC current exposure to the fetus is minimum, fetal monitoring during the procedure is recommended. Rare instances of DCCV precipitating prolonged uterine contractions have been reported.19 In hemodynamically stable patients, the preferred method of termination is IV adenosine, which is extremely effective for AV node dependent SVT. Adenosine has a half-life shorter than 10 s and is not placenta permeable; no fetal adverse effects have

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been reported. Initial intravenous dose is 6 mg, and may be followed by a dose of 12 mg if needed. If the tachycardia is AT or AFL, e.g., in the setting of adult congenital heart disease, then IV adenosine usually will not terminate the tachycardia but will still be diagnostic by revealing the atrial rhythm during transient AV block. In such cases rate control should be the first step. For this purpose, beta-blockers metoprolol and propranolol are recommended as drugs of first choice, (metoprolol initial dose 5 mg IV over 5 min, repeated if necessary) to decrease the ventricular rate during AT, AFL, and AF. They also decrease the sympathetic tone and thereby help terminate the tachycardia. Digoxin and verapamil have a long history of use as AV nodal agents for acute treatment of SVT in pregnancy whereas diltiazem has less. There are also case reports of safe and effective use of IV ibutilide for the termination of both AF and AFL during pregnancy.20 All of these drugs are category C in pregnancy.4 Wide-complex tachycardias that result in hemodynamic instability also require prompt termination with DC cardioversion. It should be assumed that the wide-complex tachycardia is VT and verapamil should not be given unless the mechanism is known with certainty to be idiopathic left VT, the only type of VT responsive to calcium channel blockers. Lidocaine is a use-dependent antiarrhythmic agent that is category B in pregnancy, and intravenous lidocaine may be used safely to terminate VT but should not be used during delivery.4 If the wide-complex tachycardia is AF or AFL with pre-excitation (WPW), both digoxin and calcium channel blockers are contraindicated, since they may further increase the ventricular rate by favoring conduction via the accessory pathway, but beta-blockers may be used with greater safety.

Prophylactic antiarrhythmic therapy The usual concerns over fetal toxicity pose unique challenges for defining strategies for antiarrhythmic therapy. No drug is entirely safe and especially during the first trimester daily drug therapy should be avoided if possible. If the rate of recurrence is high and the risk of withholding therapy is greater than the potential side effects, the lowest dose of the most effective recommended agent should be chosen, keeping in mind that absorption and metabolism of many drugs may change during pregnancy. Digoxin is category C and is generally safe, although not very effective. Metoprolol and propranolol are placenta permeable and also category C and may be used during pregnancy. Atenolol, a category D drug, has been associated with hypospadias, birth defects, and low birth weights and should be avoided.4 Daily use of diltiazem should also be avoided, and if calcium channel blocker therapy is desired, verapamil may be used, provided that care is taken to avoid hypotension that may result in fetal hypoperfusion. Sotalol is the only oral antiarrhythmic drug classified as category B in pregnancy and may be quite effective for suppressing AFL, AF, and VT, as long as the patient's renal function is not impaired.2 Class IC agents propafenone and flecainide, both category C drugs in pregnancy, should not be used in patients with organic heart disease. Neither drug has been reported to be teratogenic, and they may be used with caution in refractory cases of atrial tachyarrhythmias in patients with no organic heart disease.21 Amiodarone carries significant toxic risk for the

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fetus4; daily amiodarone and dronedarone should not be used during pregnancy. Patients with congenital long QT syndrome should be maintained on beta-blockade throughout the pregnancy and well into postpartum. These patients need to be monitored on telemetry during labor and delivery, and any episode of syncope during pregnancy should be taken seriously as this may be a symptom of torsade de pointes. Catheter ablation therapy is generally contraindicated and should only be considered in cases of drug-refractory and poorly tolerated tachyarrhythmias. Due to the high radiation exposure, this procedure should be postponed to the second trimester if possible and performed at an experienced center. As for bradyarrhythmias, asymptomatic patients with congenital complete heart block who do not have a pacemaker may be observed, unless their heart rate averages less than 50 per min, in which case permanent pacemaker insertion becomes a class IIa indication, especially if there are symptoms attributable to bradycardia.2 Vaginal delivery in patients with asymptomatic congenital complete heart block does not place the mother at increased risk.4

Cardiac device management during pregnancy If a permanent pacemaker implantation becomes necessary during pregnancy, a single-chamber device is preferred and is usually well tolerated after the 8th week of gestation. Echo guidance should be used to avoid fetal radiation exposure during implantation. If the need for fluoroscopy is unavoidable, shielding the mother's abdomen with a lead apron helps minimize any risk to the fetus, which is highest during the first and the third trimesters.2 The presence of implantable cardioverter-defibrillators (ICDs) is not a strict contraindication to future pregnancies, and their placement should be considered prior to pregnancy in patients who have high-risk factors for sudden cardiac death. In women at risk for ventricular tachyarrhythmias, e.g., severe hypertrophic cardiomyopathy, who meet the criteria for primary prevention therapy, ICD implantation should be carried out before pregnancy if possible. In a series reporting on 44 pregnancies in women with previously implanted ICDs, the incidence of device-related complications was 9%. Overall, 11 patients received at least one ICD shock, and 3 received multiple shocks. One woman had a therapeutic abortion and another had a stillborn baby. All other babies survived to term and were delivered safely.22 Recent smaller series seem to confirm these results. ICD shocks are a concern for the safety of the fetus.23 The fetal heart probably has a high fibrillation threshold, but actual available fetal safety data remain very limited. There is no standard recipe for programming ICD parameters during pregnancy. Rather programming and follow-up should be highly individualized and carried out under the supervision of experienced cardiac electrophysiologists.

Fetal arrhythmias Fetal arrhythmias are usually diagnosed echocardiographically by assessment of the chronological relationship between the atrial and ventricular contractions.24 Fetal magnetocardiography may further clarify the mechanism

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underlying the arrhythmia.25 Tachyarrhythmia is diagnosed when the fetal heart rate exceeds 180 per min.26 SVTs include AV nodal reentry, AV reentry (due to an accessory pathway) EAT, or permanent junctional reciprocating tachycardia, and assessment of the RP and PR intervals may give the clue for the diagnosis. Hydrops fetalis is the feared consequence and is present at the presentation or after the detection of the SVT in 40–50% of the cases.24 Treatment becomes necessary for fetuses in heart failure or for those at high risk with incessant SVT, with structural heart disease, or with onset earlier than 32 weeks. Fetal tachycardias may be treated via maternal/ transplacental administration of antiarrhythmic drugs. Digoxin alone has been associated with a relatively high success rate,27 and cases of treatment with verapamil, propranolol, sotalol, flecainide, propafenone, and even amiodarone have been reported.27 Fetal bradycardia, diagnosed when the ventricular rate is less than 110 per min, is usually vagally mediated sinus bradycardia, which is transient and benign. Rarely complete heart block may occur and is associated with maternal autoantibodies half the time28 but may also be the result of structural heart disease. Steroid treatment, maternal and fetal plasmapheresis, and intravenous gamma globulin have been tried.24 If bradycardia is severe and myocardial function is reduced, beta agonist agents may be administered intravenously to the mother.24

Summary Cardiac arrhythmias during pregnancy are being seen with increasing frequency as women with congenital heart disease are surviving into their reproductive years and older women with acquired heart disease are pursuing pregnancy. Prompt evaluation and treatment can make a difference to the wellbeing of both the mother and the fetus.

r e f e r e n c e s

1 Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol. 2003;88:129–133. 2 Burkart TA, Conti JB. Cardiac arrhythmias during pregnancy. Curr Treat Options Cardiovasc Med. 2010;12:457–471. 3 Laksman Z, Harris l, Silversides CK. Cardiac arrhythmias during pregnancy: a clinical approach. Fetal Matern Med Rev. 2011;22:123–143. 4 European Society of Gynecology (ESG); Association for European Paediatric Cardiology (AEPC); German Society for Gender Medicine (DGesGM)Regitz-Zagrosek V, Blomstrom Lundqvist C, et al. ESC guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases During Pregnancy of the European Society of Cardiology (ESC). Eur Heart J. 2011;32: 3147–3197. 5 Adamson DL, Nelson-Piercy C. Managing palpitations and arrhythmias during pregnancy. Heart. 2007;93:1630–1636. 6 Cordina R, McGuire MA. Maternal cardiac arrhythmias during pregnancy and lactation. Obstet Med. 2010;3:8–16.

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7 Lee J, Wetzel G, Shannon K. Maternal arrhythmia management during pregnancy in patients with structural heart disease. Prog Pediatr Cardiol. 2004;19:71–82. 8 Li JM, Nguyen C, Joglar JA, Hamdan MH, Page RL. Frequency and outcome of arrhythmias complicating admission during pregnancy: experience from a high-volume and ethnically-diverse obstetric service. Clin Cardiol. 2008;31(11): 538–541. 9 Silversides CK, Harris L, Haberer K, Sermer M, Colman JM, Siu SC. Recurrence rate of arrhythmias during pregnancy in women with previous tachyarrhythmia and impact on fetal and neonatal outcomes. Am J Cardiol. 2006;97:1206–1212. 10 Nakagawa M, Katou S, Ichinose M, et al. Characteristics of new-onset ventricular arrhythmia in pregnancy. J Electrocardiol. 2004;37:47–53. 11 Brodsky M, Doria R, Allen B, Sato D, Thomas G, Sada M. Newonset ventricular tachycardia during pregnancy. Am Heart J. 1992;123:933–941. 12 Seth R, Moss AJ, McNitt S, et al. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007;49:1092–1098. 13 Yap SC, Drenthen W, Meijboom FJ, et al. Comparison of pregnancy outcomes in women with repaired versus unrepaired atrial septal defect. BJOG. 2009;116:1593–1601. 14 Canobbio MM, Morris CD, Graham TP, Landzberg MJ. Pregnancy outcomes after atrial repair for transposition of the great arteries. Am J Cardiol. 2006;98:668–672. 15 Chugh R. Management of pregnancy in women with repaired CHD or after the Fontan procedure. Curr Treat Options Cardiovasc Med. 2013;15:646–662. 16 Kamiya CA, Iwamiya T, Neki R, et al. Outcome of pregnancy and effects on the right heart in women with repaired Tetralogy of Fallot. Circ J. 2012;76:957–963. 17 Bauce B, Daliento L, Frigo G, Russo G, Nava A. Pregnancy in women with arrhythmogenic right ventricular cardiomyopathy/dysplasia. Eur J Obstet Gynecol Reprod Biol. 2006;127: 186–189. 18 Harris IS. Management of pregnancy in patients with congenital heart disease. Prog Cardiovasc Dis. 2011;53:305–311. 19 Barnes EJ, Eben F, Patterson D. Direct current cardioversion during pregnancy should be performed with facilities available for fetal monitoring and emergency caesarean section. BJOG. 2002;109:1406–1407. 20 Kockova R, Kocka V, Kiernan T, Fahy GJ. Ibutilide-induced cardioversion of atrial fibrillation during pregnancy. J Cardiovasc Electrophysiol. 2007;18:545–547. 21 Ahmed K, Issawi I, Peddireddy R. Use of flecainide for refractory atrial tachycardia of pregnancy. Am J Crit Care. 1996;5:306–308. 22 Natale A, Davidson T, Geiger MJ, Newby K. Implantable cardioverter-defibrillators and pregnancy: a safe combination? Circulation. 1997;96:2808–2812. 23 Schuler PK, Herrey A, Wade A, et al. Pregnancy outcome and management of women with an implantable cardioverter defibrillator: a single centre experience. Europace. 2012;14: 1740–1745. 24 Hornberger LK, Sahn DJ. Rhythm abnormalities of the fetus. Heart. 2007;93:1294–1300. 25 Strasburger JF, Cheulkar B, Wakai RT. Magnetocardiography for fetal arrhythmias. Heart Rhythm. 2008;5:1073–1076. 26 Srinivasan S, Strasburger J. Overview of fetal arrhythmias. Curr Opin Pediatr. 2008;20:522–531. 27 Simpson JM, Sharland GK. Fetal tachycardias: management and outcome of 127 consecutive cases. Heart. 1998;79:576–581. 28 Schmidt KG, Ulmer HE, Silverman NH, Kleinman CS, Copel JA. Perinatal outcome of fetal complete atrioventricular block: a multicenter experience. J Am Coll Cardiol. 1991;17:1360–1366.

Cardiac arrhythmias in pregnancy.

As more women with repaired congenital heart disease survive to their reproductive years and many other women are delaying pregnancy until later in li...
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