Ventricular arrhythmias during pregnancy

INTRODUCTION — Arrhythmias are the most common cardiac complication encountered during pregnancy in women with and without structural heart disease [1-3]. In the United States, the incidence of pregnancy-related hospitalizations with arrhythmias has increased between 2000 and 2012 primarily due to increases in the incidence of atrial fibrillation and ventricular tachycardia [4]. Arrhythmias may manifest for the first time during pregnancy, or pregnancy can trigger exacerbations in women with known preexisting arrhythmias [1,5-7].

The prevalence, clinical presentation and management of ventricular arrhythmias will be reviewed. Cardiac arrest during pregnancy, general management of ventricular arrhythmias and cardiac arrest, electrocardiographic (ECG) characteristics of ventricular arrhythmias, and issues relating to supraventricular arrhythmias during pregnancy are discussed in detail elsewhere. (See "Sudden cardiac arrest and death in pregnancy" and "Wide QRS complex tachycardias: Approach to the diagnosis" and "Advanced cardiac life support (ACLS) in adults" and "ECG tutorial: Ventricular arrhythmias" and "Supraventricular arrhythmias during pregnancy" and "Wide QRS complex tachycardias: Approach to management".)

GENERAL APPROACH — Women with established arrhythmias or structural heart disease are at highest risk of developing arrhythmias during pregnancy. Due to surgical advances, the number of women of childbearing age with congenital heart disease has increased and this group of women is at particularly high risk for arrhythmias (figure 1) [1,2,8-12] (see "Pregnancy in women with congenital heart disease: General principles"). Since arrhythmias are frequently associated with acquired or structural heart disease, any woman who presents with an arrhythmia during pregnancy should undergo clinical evaluation for structural heart disease (including an ECG and a transthoracic echocardiogram). (See 'VT in women with structural heart disease' below.)

In general, the approach to the treatment of arrhythmias in pregnancy is similar to that in the non-pregnant patient. However, due to the theoretical or known adverse effects of antiarrhythmic drugs on the fetus, antiarrhythmic drugs are generally reserved for the treatment of arrhythmias associated with significant symptoms or hemodynamic compromise [13-15]. Treatment strategies during pregnancy are hampered by the lack of randomized trials in this cohort of women. Choice of therapy, for the most part, is based on limited data from animal studies, case reports, observational studies, and clinical experience.

Use of antiarrhythmic drugs in pregnancy requires attention to potential alterations in pharmacokinetics as well as fetal risk. For most antiarrhythmic drugs, adequate and well-controlled studies in pregnant women are lacking, and therefore potential risks cannot be ruled out [16,17]. Another consideration is potential adverse effects in the infant during breastfeeding (table 1). Antiarrhythmic drug safety during pregnancy, teratogenic risk, pharmacokinetic changes, and breastfeeding are discussed further separately. (See "Supraventricular arrhythmias during pregnancy", section on 'Issues regarding antiarrhythmic drug treatment'.)

The 2018 European Society of Cardiology Guidelines for the management of cardiovascular diseases during pregnancy and the 2023 Heart Rhythm Society expert consensus statement on the management of arrhythmias during pregnancy provide additional information regarding antiarrhythmic options [16,18].

MECHANISM OF ARRHYTHMOGENESIS IN PREGNANCY — The exact mechanism of increased arrhythmia burden during pregnancy is unclear but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy [19].

The hemodynamic changes of pregnancy have been well studied and these changes likely contribute to the development of arrhythmias during pregnancy [20,21]. Intravascular volume increases, augmenting the preload on the ventricles, and increasing both atrial and ventricular size [20,22-25]. Atrial and ventricular myocardial stretch may contribute to arrhythmogenesis due to stretch-activated ion channel activity causing membrane depolarization, shortened refractoriness, slowed conduction, and spatial dispersion of refractoriness and conduction [26-29]. There is also an increase in resting heart rate that has been associated with markers of arrhythmogenesis such as late potentials, premature ventricular contractions, and depressed heart rate variability [30]. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes".)

Few studies have been published on the influence of hormonal and autonomic changes on arrhythmogenesis in pregnancy. Although catecholamine levels do not appear to change during pregnancy, there is an increase in adrenergic responsiveness during pregnancy [31-35]. Estrogen has been shown to increase the number of myocardial alpha-adrenergic receptors [36]. This increased adrenergic activity may contribute to enhanced automaticity and triggered activity [37]. (See "Enhanced cardiac automaticity".)

PALPITATIONS — Palpitations occur frequently during pregnancy and are a common indication for cardiac evaluation during pregnancy. The differential diagnosis of palpitations is extensive and the diagnostic evaluation of pregnant women with palpitations does not differ from nonpregnant women. (See "Evaluation of palpitations in adults".)

One study compared 110 pregnant women with symptoms suggestive of possible arrhythmia (palpitations: 87 percent; dizziness: 13 percent; syncope/presyncope: 6 percent) with 52 pregnant women evaluated for an asymptomatic functional murmur [38]. Prevalence of supraventricular and ventricular ectopic activity on 24-hour Holter ambulatory monitoring was similar in the symptomatic and control groups.

Only 10 percent of symptomatic episodes were accompanied by the presence of an arrhythmia [38]. A sensation of palpitations during pregnancy in the absence of concomitant cardiac arrhythmias may be related to the high output state, including increased heart rate, decreased peripheral resistance, and increased stroke volumes. (See "Maternal adaptations to pregnancy: Cardiovascular and hemodynamic changes".)

PREMATURE VENTRICULAR COMPLEX/CONTRACTION — Premature ventricular complex/contraction (PVC; also referred to a premature ventricular beats or premature ventricular depolarizations) is frequently detected in pregnant women. The prevalence is dependent upon the duration of observation and the clinical presentation. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation".)

In the above referenced study of 110 symptomatic and 52 asymptomatic pregnant women, the prevalence of isolated PVCs was similar in symptomatic and asymptomatic women (49 versus 40 percent) [38]. However, frequent PVCs (≥50 PVCs per 24 hours) were more common in symptomatic women (22 versus 4 percent). There was a significant reduction in the frequency of combined atrial and ventricular ectopic activity in the nine women in whom Holter monitoring was repeated postpartum.

Clinical presentation — PVCs produce few or no symptoms in the majority of women, although some women may experience symptoms of palpitations or dizziness. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation", section on 'Clinical presentation and ECG findings'.)

Management during pregnancy — The management of PVCs in pregnancy is discussed separately. (See "Premature ventricular complexes: Treatment and prognosis", section on 'Pregnancy'.)

VENTRICULAR TACHYARRHYTHMIAS — Ventricular tachyarrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF]) are rare during pregnancy [39]. The management of ventricular arrhythmias needs to be tailored to the individual. The following are among the clinical factors that should be considered:

●Etiology of the VT (catecholamine sensitive versus noncatecholamine sensitive)

●Frequency and duration of VT (nonsustained versus sustained)

●Severity of associated symptoms

●Presence and severity of underlying heart disease

●Ventricular function

Causes — VT can be seen in pregnant women without apparent structural heart disease [40-42] but is often associated with structural heart disease. The risk of recurrent VT during pregnancy is particularly high (27 percent) in women with structural heart disease and a history of VT [7]. Types of cardiac disease associated with VT in pregnancy include:

●Hypertrophic cardiomyopathy (HCM) [1,7,43,44]

●Peripartum cardiomyopathy [45,46]

●Arrhythmogenic right ventricular cardiomyopathy [47-52]

●Congenital heart disease [1,7,53-55]

●Valvular heart disease [1]

●Primary electrical disease (eg, long QT syndrome [LQTS] [56,57], Brugada syndrome [58], catecholaminergic polymorphic VT [CPVT] [59], etc)

Myocardial infarction with or without coronary artery disease has been observed during pregnancy [60-65] and may be complicated by VT or VF [63,64]. Women with primary electrical diseases are also at risk of VT. Other medical conditions associated with VT during pregnancy are hypomagnesemia [66-68], hypertensive crises [69,70], and thyrotoxicosis [71]. (See "Significance of hypomagnesemia in cardiovascular disease" and "Gestational hypertension" and "Overview of thyroid disease and pregnancy" and "Cardiovascular effects of hyperthyroidism".)

Idiopathic VT — Monomorphic VT without apparent structural heart disease is considered idiopathic. The most common type of idiopathic VT is repetitive monomorphic VT, which usually originates from the right ventricular outflow tract (ECG "signature": left bundle branch block and inferior axis) or, less often, from the left ventricular outflow tract (ECG pattern: right bundle branch block and inferior axis or left bundle and inferior axis but earlier precordial transition than for right ventricular outflow tract tachycardia). Another type is idiopathic left VT, which originates from the inferior aspect of the midseptum and has the morphologic pattern of right bundle branch block with left axis deviation (QRS axis around -60°). (See "Ventricular tachycardia in the absence of apparent structural heart disease" and "Nonsustained VT in the absence of apparent structural heart disease".)

A study of seven women presenting with new-onset idiopathic VT during pregnancy found that the VT was often catecholamine sensitive and that the VT was often suppressed in women who received beta blockers [41]. There were no maternal or fetal complications in this series. There is one case report of sudden death in a woman with idiopathic VT who died in the third trimester, three weeks after initiation of procainamide therapy [72].

Management during pregnancy — Idiopathic VT rarely degenerates into an unstable rhythm and usually has a benign prognosis [41,73].

●Treatment of repetitive monomorphic VT with cardioselective beta blockers may be effective in pregnant women with idiopathic VT even in the absence of a clear relationship to adrenergic tone [41,73-77]. Sotalol can be used as an alternative. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Treatment of RMVT'.)

●The less common idiopathic left VT appears to respond well to verapamil, both for the termination of acute episodes and the prevention of recurrences [78,79]. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Treatment of ILVT'.)

Long QT syndrome — Although VT during pregnancy has been reported in women with LQTS [80], the increase in heart rate seen during pregnancy may serve to shorten the QT interval and therefore may be partially protective. In women with LQTS, the risk of VT is especially high in the postpartum period [57]. Increased risk of VT during the postpartum period may be related to a decrease in the heart rate and an associated increase in the QT interval. The physiologic stress and altered sleep patterns associated with caring for a newborn infant may also contribute to an increase in adrenergically mediated cardiac events.

The effect of pregnancy was evaluated in a retrospective analysis of 422 women (111 probands and 311 first-degree relatives) entered into the International LQTS registry [57]. Most of the probands had a personal history of syncope or aborted cardiac arrest. The following findings were noted:

●Probands were significantly more likely to have cardiac events (syncope, aborted cardiac arrest, or sudden cardiac death) in the 40-week postpartum interval than during the prepregnancy period of 40 weeks (23.4 versus 3.8 percent). The increase in risk was distributed throughout the postpartum period. The incidence of first cardiac events during pregnancy was slightly but not significantly increased compared with the prepregnancy period (9.0 versus 3.8 percent).

●The postpartum increase in risk also applied to first cardiac events (9.0 versus 1.8 and 0 percent during and before pregnancy).

●Treatment with beta blockers was independently associated with a decrease in risk for cardiac events in probands during all three intervals (odds ratio 0.023).

●The average probability of having a cardiac event during the postpartum period in probands was 2 percent (1 in 50 pregnancies). Treatment with a beta blocker lowered the risk to 1 in 2500 pregnancies.

The risks associated with pregnancy may be different among various LQTS genotypes (see "Congenital long QT syndrome: Epidemiology and clinical manifestations", section on 'Influence of genotype on triggers'). The influence of genotype is illustrated by the following observations:

●In a series of 388 LQTS patients referred for genetic testing, postpartum cardiac events were more commonly reported in patients with LQT2 mutation (13 of 80, 16 percent) than in patients with LQT1 (1 of 103, <1 percent). [81].

●In a series limited to women with a single LQT1 mutation, cardiac event rates associated with pregnancy were low (2.6 percent) [82]. These events occurred only in women with a prior history of symptoms who were not taking beta blockers.

Management during pregnancy — We agree with the 2023 HRS expert consensus statement on the management of arrhythmias during pregnancy, the 2017 American College of Cardiology/American Heart Association/Heart Rhythm Society guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death and the 2018 European Society of Cardiology guidelines on the management of cardiovascular diseases during pregnancy. The guidelines recommended that pregnant women with LQTS who have had symptoms benefit from continued beta blocker therapy throughout pregnancy and postpartum, unless there are definite contraindications [18,83].

Brugada syndrome — There are limited reports of pregnancies in women with Brugada syndrome. In one retrospective single-center study including 104 women (219 deliveries) with Brugada syndrome, six women (6 percent) experienced recurrent syncope during pregnancy [84]. Five women continued to experience syncope after delivery and four women received an implantable cardioverter-defibrillator (ICD), as syncope is regarded a high-risk feature for ventricular arrhythmias. No serious events were reported during the peripartum period. In three women with Brugada syndrome and an ICD, no noteworthy problems were reported during pregnancy. There is one case report of electrical storm during pregnancy [58]. The use of low-dose isoproterenol infusion followed by oral quinidine has been used to treat VT and normalize the ECG [58]. (See "Brugada syndrome or pattern: Management and approach to screening of relatives", section on 'High-risk patients'.)

Catecholaminergic polymorphic ventricular tachycardia — One retrospective study from the Netherlands and Canada evaluated the outcome of pregnancy in 96 women with CPVT who had 228 pregnancies [59]. Most patients (82 percent) had pregnancies before CPVT diagnosis (median age at CPVT diagnosis 40.7 years). Pregnancy and postpartum cardiac events included syncope (5 percent) and an aborted cardiac arrest (1 percent), which occurred in women who were not taking beta blockers. The combined pregnancy and postpartum arrhythmic risk (2.14 events per 100 patient-years) was not elevated compared with the nonpregnant period (1.46 events per 100 patient-years) [59].

Beta blockers should be considered a mainstay of medical management in patients with CPVT. In a study of 228 pregnancies in females with CPVT, most of the events occurred in patients not taking beta blockers [59].

VT in women with structural heart disease — A large prospective multicenter study in women with heart disease reported four cases of sustained VT in 1315 pregnancies [85].

Causes

Hypertrophic cardiomyopathy — In general, women with HCM tolerate pregnancy well [44,86], although several case reports have described cardiac complications and sudden death during pregnancy [43,44,87-89]. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Pregnancy'.)

The largest study investigating mortality and morbidity in pregnant women with HCM included 100 women who had a total of 199 live births [44]. Two sudden cardiac deaths occurred during pregnancy in women with high-risk features. One of the women had severe left ventricular hypertrophy (30 mm maximal wall thickness) and a resting outflow gradient of 115 mmHg. She died suddenly four days after delivery after complaining of palpitations. The other woman had a family history of eight deaths in young relatives, five of which were sudden. This patient developed recurrent episodes of sustained VT during labor. The ROPAC registry examined outcomes in 60 pregnancies and reported a high prevalence of ventricular tachyarrhythmias (10 percent, 6 of 60 patients) [90]. Two of six patients with VT were known to have heart failure, and most cases occurred in the third trimester.

Management of pregnancy and delivery in women with HCM is discussed separately. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Pregnancy'.)

Congenital heart disease — The prevalence of sustained VT during pregnancy in women with congenital heart disease (CHD) has been reported to range from 4.5 to 15.9 per 1000 pregnancies [1,53] (see "Pregnancy in women with congenital heart disease: General principles" and "Pregnancy in women with congenital heart disease: Specific lesions"). Prevalence rates are strongly influenced by the types of cardiac lesions in the study population.

●In a prospective multicenter study in women with CHD, two cases of sustained VT occurred in 445 pregnancies. One woman had an unrepaired intracardiac shunt and the other had repaired congenital aortic stenosis [1].

●A multicenter study from Japan reported two cases of sustained VT during 126 pregnancies [53]. Both cases of VT occurred in women with repaired tetralogy of Fallot and both were successfully treated with intravenous lidocaine. Seven pregnancies were complicated by nonsustained VT, none of which were treated.

Peripartum cardiomyopathy — Peripartum cardiomyopathy is a rare and sometimes life-threatening condition defined as development of systolic heart failure in the last month of pregnancy or within five months of delivery. The incidence varies widely among various populations. The clinical presentation includes symptoms of new-onset heart failure such as dyspnea, cough, orthopnea, and hemoptysis. A large retrospective study of 9841 hospitalizations for women with peripartum cardiomyopathy demonstrated a prevalence of VT of 4.2 percent [91]. These ventricular arrhythmias can be refractory to pharmacologic treatment (eg, lidocaine, metoprolol, amiodarone) and direct current cardioversion [45,46,92]. (See "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis".)

Arrhythmogenic right ventricular cardiomyopathy — Most pregnancies in women with arrhythmogenic right ventricular cardiomyopathy are tolerated well [47-52,93]. Pregnancies were managed successfully by close monitoring and antiarrhythmic drugs when necessary.

●Data from the combined Johns Hopkins/Dutch ARVD/C registry provided information on 26 women during 39 pregnancies (>13 weeks) [94]. A single episode of sustained ventricular arrhythmia complicated five pregnancies (13 percent) of five women without a prior history of sustained ventricular arrhythmias. Interruption of beta blockers was associated with two of these events. Previous studies have shown that withdrawal of beta blockers during pregnancy may exacerbate the occurrence of VT during pregnancy [49,52].

●Among a cohort of 120 Chinese women with 224 pregnancies between 1995 and 2018, adverse cardiac events were reported in only 12 pregnancies (5.4 percent), with only two episodes of syncope and one episode of sustained VT [93]. Eight of the 12 reported adverse events related to the development of, or increase in, PVC frequency.

Management of VT during pregnancy in women with structural heart disease

Management of acute episodes — Acute treatment of sustained ventricular arrhythmias in pregnant women is similar to that in nonpregnant women. Ventricular arrhythmias in the presence of structural heart disease are potentially life-threatening and require immediate evaluation for hemodynamic instability to determine whether electrical cardioversion or defibrillation is indicated [18].

In hemodynamically well-tolerated VT, pharmacological cardioversion may be acceptable. Pharmacological options include intravenous procainamide, amiodarone, or lidocaine [18]; the choice of pharmacological agents should be tailored to the individual case. For women at risk for VT during labor and delivery, it is important to ensure that appropriate cardiac medications and external defibrillators are available in the delivery suites.

Electrical cardioversion — Urgent or elective electrical cardioversion can be performed at all stages of pregnancy [14,95-101]. Electrical cardioversion is indicated for any sustained VT with hemodynamic compromise [18] and can be considered for drug-refractory VT. Electrical cardioversion does not result in compromise of blood flow to the fetus [102]. While there is a theoretical risk of inducing an arrhythmia in the fetus, this risk is very small due to the high fibrillation threshold and small amount of energy reaching the fetus [14,95,103]. Nonetheless, fetal rhythm monitoring is recommended once viability is reached because of rare reported cases of cardioversion precipitating fetal distress and requiring emergency cesarean delivery [104]. Electrode placement is similar to the nonpregnant patient, but in order to maximize current, placement over breast tissue should be avoided. Shock outputs used should be similar to those recommended in the nonpregnant patient. (See "Basic principles and technique of external electrical cardioversion and defibrillation" and "Cardioversion for specific arrhythmias".)

Prophylactic pharmacologic therapy during pregnancy — The risk of recurrent VT and sudden death in women with structural heart disease can be substantial and the benefits of prophylactic drug therapy may outweigh the potential fetal adverse effects of these drugs (see "Overview of sudden cardiac arrest and sudden cardiac death"). The risk of sudden death is further increased when concomitant left ventricular dysfunction is present.

Depending on the underlying cardiac condition, beta-1 selective beta blockers alone, antiarrhythmic drugs alone, or both in combination can be effective [17,18]. Gestational exposure to amiodarone is associated with neonatal hypothyroidism and hyperthyroidism. Small-for-gestational-age infants are reported with gestational exposure to the combination of amiodarone and beta blockers [105]. In some cases, sotalol can be considered if beta-blocker therapy is ineffective. Because of potential fetal side effects, all women should be counseled about the potential risks and benefits of drug therapy. (See "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring" and "Amiodarone: Clinical uses".)

Although some have used class IA (eg, quinidine, procainamide) or IC (eg, flecainide) drugs as prophylactic treatment for VT during pregnancy [106,107], these drugs are not generally recommended since they have not improved survival in the nonpregnant population with structural heart disease, presumably because of proarrhythmic effects [108].

Implantable cardioverter-defibrillator — Women with an implantable cardioverter-defibrillator (ICD) can have a successful pregnancy with good fetal outcome [109-111]. Indications for ICD placement are discussed separately, but in general, pregnant women who have an indication for ICD should have the ICD implanted using strategies to minimize radiation during the procedure. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

In a retrospective multicenter study of pregnancy outcomes in women with ICDs (n = 44), 25 percent (11 of 44) of the pregnancies were complicated by at least one shock [109]. All ICDs were implanted for secondary prevention and the underlying cardiac diseases were primary electrical diseases (ie, LQTS, idiopathic VF) or structural heart diseases (ie, cardiomyopathy, congenital heart disease, arrhythmogenic right ventricular cardiomyopathy). Pregnancy was not associated with an increase in ICD-related complications or an increase in the number of shocks (0.07 versus 0.06 shocks per month) compared with the preconception period [109].

The experience with ICD implantation during pregnancy is limited [112]; however, pacemaker implantation during pregnancy can be accomplished and total radiation dose can be reduced by using echocardiographic guidance [113,114].

Subcutaneous ICDs are being increasingly used, but studies pertaining to implantation and management during pregnancy are lacking.

For some women with potentially reversible risk factors for sudden death (eg, women with peripartum cardiomyopathy in whom ventricular function may improve), an external wearable automatic defibrillator (LifeVest) can be considered during pregnancy or early postpartum.

Radiofrequency catheter ablation — The success rate of radiofrequency catheter ablation of monomorphic VT is between 80 to 100 percent [115-119] and may be considered in women who are using antiarrhythmic therapy and are contemplating pregnancy (see "Overview of catheter ablation of cardiac arrhythmias"). Currently, there is only limited experience with catheter ablation of VT during pregnancy [17,120,121].

Most experience with radiofrequency catheter ablation during pregnancy has been for cases of supraventricular tachycardia [121-129]. These procedures are generally not performed during pregnancy, mainly due to concerns of ionizing radiation exposure to the fetus. However, in rare cases, women with severe and drug-resistant VT during pregnancy may be considered for an ablation procedure. The risk of radiation exposure for the fetus during a typical ablation is small (<1 mGy at all periods of gestation) and is mainly attributable to scatter from the thorax of the mother [130]. Ablation using intracardiac echocardiography and electroanatomic mapping without fluoroscopy may be an alternative. (See "Diagnostic imaging in pregnant and lactating patients", section on 'Fetal risks'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●General approach – Ventricular tachyarrhythmias are frequently associated with acquired or structural heart disease and therefore any woman who presents with a ventricular arrhythmia during pregnancy should undergo clinical evaluation for structural heart disease (including an ECG and a transthoracic echocardiogram). Due to surgical advances, the number of women of childbearing age with congenital heart disease has increased and this group of women is at particularly high risk for arrhythmias (figure 1)

Information on the use of specific antiarrhythmic drugs in pregnancy, including the US Food and Drug Administration risk category and pregnancy implications, is available in the UpToDate drug database. (See 'General approach' above and 'VT in women with structural heart disease' above.)

●Idiopathic VT – Monomorphic ventricular tachycardia (VT) without apparent structural heart disease is considered idiopathic. The most common type originates from the right ventricular outflow tract, and this form of VT can often be successfully treated with beta blockers or verapamil. (See 'Idiopathic VT' above.)

●Long QT syndrome – Women with the long QT syndrome are at risk for VT, especially in the postpartum period. Pregnant women with long QT syndrome should be treated with beta blocker therapy throughout pregnancy and postpartum. (See 'Long QT syndrome' above.)

●Management of acute episodes – Acute treatment of sustained ventricular arrhythmias in pregnant women is similar to that in nonpregnant women. Ventricular arrhythmias in the presence of structural heart disease are potentially life-threatening and require immediate evaluation for hemodynamic instability to determine whether electrical cardioversion or defibrillation is indicated. (See 'Management of acute episodes' above.)

●Prophylactic pharmacologic therapy during pregnancy – In women with structural heart disease and a history of VT, the benefits of prophylactic drug therapy may outweigh the potential fetal adverse effects of these drugs. (table 1) (See 'Prophylactic pharmacologic therapy during pregnancy' above.)

●Implantable cardioverter-defibrillator – Women with an implantable cardioverter-defibrillator can have a successful pregnancy with good fetal outcome. (See 'Implantable cardioverter-defibrillator' above.)