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......................................................................................... frequency of any arrhythmia is greater in women aged 4150 years (199/100 000) than in those aged 1830 years (55/100 000), which may be due to more prevalent AF and VT, whereas SVT seems stable over time.535 Arrhythmias are also more frequent among women with congenital heart disease, particularly atrial flutter, compared with women without congenital defects.536

As substantive prospective or randomized studies are unavailable, recommendations are primarily based on small cohorts or case reports in conjunction with expert opinion.

14.1 Maternal, obstetric, and offspring

risk SVT is associated with an increased risk of death during pregnancy, and the reported frequency is 68 per 100 000 pregnancy-related hospitalizations for any arrhythmia, 22 per 100000 for SVT, 4 per 100 000 for atrial flutter, 27 per 100 000 for AF, 2 per 100 000 for ventricular fibrillation, and 16 per 100 000 for VT.535 Identification and treatment of underlying conditions are the first priorities. Although most of the exacerbations of SVT during pregnancy are benign and can be treated effectively with standard medical therapy,537 the circumstances that should be considered include the well-being of the foetus and the effects on labour, delivery, and lactation. The haemodynamic effect of tachycardia, as well as side effects of treatments, must be balanced and addressed for the foetus. Catheter ablation should therefore be considered before pregnancy when possible in patients with a known history of symptomatic tachyarrhythmia. Trials evaluating the level of surveillance at delivery are needed. 14.2 Therapy

14.2.1 Antiarrhythmic drugs Treatment with antiarrhythmic drugs for the prevention of SVT should, in general, be reserved for SVTs causing haemodynamic compromise or significant symptoms. The major concern regarding the use of antiarrhythmic drugs during pregnancy is potential adverse effects on the foetus. While the first trimester is associated with the greatest teratogenic risk, drug exposure later in pregnancy may result in adverse effects on foetal growth and development, and on uterine contractility, and an increased risk of pro-arrhythmia. The risks and benefits of continuing vs. stopping medication must be carefully considered in terms of the risk of recurring SVT, and the potential for haemodynamic compromise. Decisions should be individualized, based on the clinical situation and possible additional structural heart disease. Major controlled studies of antiarrhythmic drugs during pregnancy are lacking. If non-invasive manoeuvres fail, adenosine should be the first-line drug for treatment if needed during the second and third trimesters. There is a paucity of data on management of SVT in the first trimester.542 All beta-blockers can cause bradycardia and hypoglycaemia in the foetus. As beta-1 selective beta-blockers are less likely to affect uterine relaxation, they are preferred.546 Maternal use of beta-blockers in the first trimester has not been associated with a large increase in the risk for overall or cardiac malformations.548,553 However, in the EUROmediCAT study, an association between alpha/beta-adrenergic blocker use in the first trimester with multicystic renal dysplasia was reported.554 There have been concerns about ‘low weight for gestational age’ with beta-blockers, although the effects reported may not be large enough to be of clinical importance. Exposure to atenolol has been associated with a

Recommendations for the therapy of supraventricular tachycardia in pregnancy

Recommendation Classa Levelb Catheter ablation is recommended in symptomatic women with recurrent SVT who plan to become pregnant.538 I C Acute therapy Immediate electrical cardioversion is recommended for any tachycardia with haemodynamic instability.539,540 I C Vagal manoeuvres and, if these fail, adenosine are recommended for acute conversion of SVT.541,542 I C An i.v. beta-1 selective blocker (except atenolol) should be considered for acute conversion or rate control of SVT.542,543 IIa C i.v. digoxin in the latest pocket Gls version should be considered for rate control of AT if beta-blockers fail.542,543 IIa C i.v. ibutilide in the latest pocket Gls version may be considered for termination of atrial flutter.544,545 IIb C Chronic therapy During the first trimester of pregnancy, it is recommended that all antiarrhythmic drugs should be avoided, if possible. I C Beta-1 selective (except atenolol) beta-blockers or verapamil, in order of preference, should be considered for prevention of SVT in patients without WPW syndrome.543,546548 IIa C Flecainide or propafenone should be considered for prevention of SVT in patients with WPW syndrome, and without ischaemic or structural heart disease.549 IIa C Flecainide or propafenone in patients without ischaemic or structural heart disease should be considered if AV nodal blocking agents fail to prevent SVT.533,543 IIa C Digoxin or verapamil should be considered for rate control of AT if beta-blockers fail in patients without WPW syndrome.543 IIa C Amiodarone is not recommended in pregnant women.153,543 III C Fluoroless catheter ablation should be considered in cases of drug-refractory or poorly tolerated SVT, in experienced centres.550552 IIa C

i.v. ibutilide is contraindicated in patients with prolonged QTc interval. AT = atrial tachycardia; AV = atrioventricular; i.v. = intravenous; SVT = supraventricular tachycardia; WPW = WolffParkinsonWhite. aClass of recommendation. bLevel of evidence Downloaded from academic.oup.com/eurheartj/article/41/5/655/5556821 by guest on 07 October 2026