Introduction With the arrival of echocardiography and magnetic resonance imaging (MRI), providing the means of noninvasively detecting and monitoring anomalies occurring during pregnancy, the fetus has increasingly become the target of prenatal treatment Nonetheless, pregnancy is a unique situation, as treatment of the fetus cannot be approached independently from the concomitant treatment of the mother, especially when a medication is used for indications other than those listed in the drug monograph This includes the off-label administration of pharmaceutical agents via the maternal circulation or directly into the fetus to treat tachyarrhythmias, cardiac inflammation, and/or congestive heart failure (CHF) and to promote lung maturation Other interventions, such as the supplementary maternal inhalation of oxygen, may be useful to promote the growth of underdeveloped left heart structures and improve oxygen delivery to the fetal brain―for example, in cases of congenital heart disease (CHD) or with intrauterine growth restriction (IUGR) due to placental failure This chapter discusses the rationale and outcomes of fetal pharmacotherapy for selected cardiovascular indications, with the caveat that controlled studies on drug efficacy and drug safety as well as universally accepted recommendations to guide prenatal treatment are largely unavailable Antiarrhythmic Fetal Treatment Arrhythmias may present as an irregularity of the fetal cardiac rhythm; as an irregular, abnormally slow or fast heart rate; or as a combination In most cases such anomalies present as brief episodes of little clinical relevance, and no treatment is required This includes irregularities of the cardiac rhythm caused by premature atrial contractions Of more concern are enduring episodes of a cardiac rate that is too fast (greater than 180 beats/min) Prenatal causes typically include different forms of supraventricular and atrial tachyarrhythmias (SVAs), with ventricular tachycardia (VT) and junctional ectopic tachycardia (JET) as rare causes.1–3 A persistently fast rate may be well tolerated; at the severe end of the spectrum, however, it may lead to low cardiac output, fetal hydrops, and death Arrhythmia-induced fetal hydrops (defined by more than one of these symptoms: abdominal, pleural, or pericardial effusion or skin edema) is the single most important predictor of perinatal death Hence, if a disturbance of cardiac rhythm is suspected, it is important to determine its impact on the fetal circulation and to decide on the urgency and choice of perinatal care Detailed fetal ultrasonic examination provides essential information on the level of fetal activity as an indicator of well-being, cardiac function, fetal hydrops, and on anomalies that may underlie an arrhythmia, such as cardiac tumors or structural heart disease Most arrhythmias can be reliably distinguished from one another by a stepwise analysis of the rate, rhythm, and chronology of atrial and ventricular systolic events as depicted by M-mode and Doppler ultrasound tracings.4 The correct interpretation of these findings will not only reduce the risk of unnecessary pharmacologic treatment or premature delivery of fetuses with more benign findings but also facilitate the choice of care of those with a major disorder of rhythm The cardiac rhythm disturbances described in the following text might benefit from transplacental antiarrhythmic treatment Atrial and Supraventricular Tachyarrhythmias SVA, the most frequent cause of a fetal tachycardia, can be produced by four main mechanisms in this population, namely: ▪ Atrioventricular reentrant tachycardia (AVRT), involving the atrioventricular node for antegrade conduction and a fast retrograde ventriculoatrial (VA) conducting accessory pathway ▪ Permanent junctional reciprocating tachycardia (PJRT), with reentry across a slow retrograde VA conducting accessory pathway ▪ Atrial ectopic tachycardia (AET) due to enhanced automaticity of atrial tissue ▪ Atrial flutter (AF) due to a circular macroreentrant pathway contained within the atrial wall AVRT and AF account for 90% of referrals with fetal tachyarrhythmias.3,5 The different SVA mechanisms can be distinguished by fetal echocardiography on the basis of the arrhythmic pattern and the relationship of atrial and ventricular systolic events.6–8 AVRT typically presents as a short VA tachycardia (Video 9.1), as the atrial electromechanical activation via the fast retrogradely conducting accessory pathway follows shortly after the ventricles, with average heart rates of about 250 (range, 180 to 300) beats/min.5 Typical AVRT patterns are either a persistent, regular tachycardia or an episodic condition with an abrupt arrhythmia onset and termination, which is also known as paroxysmal supraventricular tachycardia (PSVT) In long VA tachycardia (Video 9.2), which is often slower (median, 210 beats/min; range, 170 to 240 beats/min)5 and better tolerated but more difficult to control than AVRT, the atrial contraction closely precedes the ventricular contraction This pattern of activation is seen during AET and PJRT but also characterizes sinus tachycardia In AF (Video 9.3), the median atrial rate is about 440 (300 to 600) beats/min,5,9 which is sufficiently fast that only every second or third flutter wave is conducted through the atrioventricular node, producing ventricular rates between 150 and 250 beats/min Perinatal Management