Treatment Of Fetal Tachycardia Research Articles

Sotalol as first‐line treatment for fetal tachycardia and neonatal follow‐up

In fetal tachycardia, pharmacological therapy with digoxin, flecainide and sotalol has been reported to be effective. In a recent retrospective multicenter study, sotalol was considered to be less effective than the other drugs in treatment of fetal supraventricular tachycardia (SVT). The aim of this study was to re-evaluate the efficacy and safety of maternally administered sotalol in the treatment of fetal tachycardia. This was a retrospective review of the records of 30 consecutive fetuses with tachycardia documented on M-mode echocardiography between January 2004 and December 2010 at Wilhelmina Children's Hospital, a tertiary referral university hospital. Patients were subdivided into those diagnosed with supraventricular tachycardia and those with atrial flutter (AF) and presence of hydrops was noted. Other variables investigated included QTc interval measured on maternal electrocardiogram before and after initiation of antiarrhythmic therapy, fetal heart rhythm and heart rate pre- and postnatally, oral maternal drug therapy used, time to conversion to sinus rhythm (SR), percentage of fetuses converted following transplacental treatment, maternal adverse effects, presence or absence of tachycardia as noted on postnatal ECG, postnatal therapy or prophylaxis and neonatal outcome. Findings are discussed with reference to the literature. A total of 28 patients (18 with SVT, 10 with AF) were treated with sotalol as first-line therapy. Fetal hydrops was present in six patients (five with SVT, one with AF). All hydropic patients converted antenatally to SR (67% with sotalol as a single-drug therapy, 33% after addition of flecainide). Of the non-hydropic patients, 91% converted to SR (90% with sotalol only, 10% after addition of flecainide or digoxin). In 9% (with AF) rate control was achieved. There was no mortality. No serious drug-related adverse events were observed. Postnatally, rhythm disturbances were detected in 10 patients, two of whom still had AF. In eight, SVT was observed within 3 weeks postnatally, and in five of these within 72 hours. Sotalol can be recommended as the drug of first choice for treatment of fetal AF and has been shown to be an effective and safe first-line treatment option for SVT, at least in the absence of hydrops. Postnatal maintenance therapy after successful prenatal therapy is not necessarily indicated, as the risk of recurrence is low beyond 72 hours of age.

Fetal arrhythmia: Prenatal diagnosis and perinatal management

The importance of managing fetal arrhythmia has increased over the past three decades. Although most fetal arrhythmias are benign, some types cause fetal hydrops and can lead to fetal death. With the aim of improving the outcome in such cases, various studies for prenatal diagnosis and perinatal management have been published. Detailed analysis of the type of arrhythmia in utero is possible using M-mode and Doppler echocardiography. In particular, a simultaneous record of Doppler waveform at the superior venous cava and the ascending aorta has become an important and useful method of assessing the interval between atrial and ventricular contractions. Common causes of fetal tachycardia (ventricular heart rate faster than 180 bpm), are paroxysmal supraventricular tachycardia (SVT) with 1:1 atrioventricular (AV) relation and atrial flutter with 2:1 AV relation. Of fetal SVT, short ventriculo-atrial (VA) interval tachycardia due to atrioventricular reentrant tachycardia is more common than long VA interval. Most fetuses with tachycardia are successfully treated in utero by transplacental administration of antiarrhythmic drugs. Digoxin is widely accepted as a first-line antiarrhythmic drug. Sotalol, flecainide and amiodarone are used as second-line drugs when digoxin fails to achieve conversion to sinus rhythm. Fetal bradycardia is diagnosed when the fetal ventricular heart rate is slower than 100 bpm, mainly due to AV block. Approximately half of all cases are caused by associated congenital heart disease, and the remaining cases that have normal cardiac structure are often caused by maternal SS-A antibody. The efficacy of prenatal treatment for fetal AV block is limited compared with treatment for fetal tachycardia. Beta stimulants and steroids have been reported as effective transplacental treatments for fetal AV block. Perinatal management based on prospective clinical study protocol rather than individual experience is crucial for further improvement of outcome in fetuses with tachycardia and bradycardia.

Flecainide treatment of fetal tachycardia and hydrops fetalis in a twin pregnancy

Fetal supraventricular tachycardia (SVT) is a rarecomplication of pregnancy leading, in some cases, tocardiac failure and intrauterine fetal death. Digoxin isa safe and successful treatment for SVT and can beconsideredas thefirst-linechoicein singletonand multiplepregnancies in which one of the fetuses presents withSVT

Treatment of fetal tachycardia with sotalol: transplacental pharmacokinetics and pharmacodynamics

ObjectivesThe aim of this study was to investigate the pharmacokinetics and pharmacodynamics of sotalol in the treatment of fetal tachycardia. BackgroundMaternally administered, intrauterine therapy of fetal tachycardia is dependent on the transplacental passage of the antiarrhythmic agent. MethodsIn a prospective study of patients treated for fetal tachycardia with sotalol, concentrations of sotalol were determined in maternal and umbilical blood and in amniotic fluid, and the relationship between these concentrations and the occurrence of conversion to sinus rhythm was investigated. ResultsEighteen fetal patients were studied, nine with atrial flutter and nine with supraventricular tachycardia. Fourteen were treated with sotalol; 13 converted to sinus rhythm, of whom 2 relapsed. There was one intrauterine death. Four patients were treated with sotalol and digoxin, of whom two were treated successfully. Mean birth weight was 3,266 g. The daily maternal sotalol dose was linearly related to the maternal plasma concentration. The mean fetal/maternal sotalol plasma concentration was 1.1 (range 0.67 to 2.87, SD 0.63), and the mean amniotic fluid/fetal blood ratio of sotalol was 3.2 (range 1.28 to 5.8, SD 1.4). The effectiveness of sotalol therapy could not be extrapolated from maternal blood levels. ConclusionsSotalol is a potent antiarrhythmic agent in the treatment of fetal tachycardia. The placental transfer is excellent. Sotalol accumulates in amniotic fluid but not in the fetus itself. Therefore it seems that renal excretion in the fetus is efficient and greater than the oral absorption by fetal swallowing. The maternal blood level is not a reliable predictor of the chances of success of therapy. Sotalol is not associated with fetal growth restriction.

Drug treatment of fetal tachycardias.

The pharmacological treatment of fetal tachycardia (FT) has been described in various publications. We present a study reviewing the necessity for treatment of FT, the regimens of drugs used in the last two decades and their mode of administration. The absence of reliable predictors of fetal hydrops (FH) has led most centers to initiate treatment as soon as the diagnosis of FT has been established, although a small minority advocate nonintervention. As the primary form of pharmacological intervention, oral maternal transplacental therapy is generally preferred. Digoxin is the most common drug used to treat FT; however, effectiveness remains a point of discussion. After digoxin, sotalol seems to be the most promising agent, specifically in atrial flutter and nonhydropic supraventricular tachycardia (SVT). Flecainide is a very effective drug in the treatment of fetal SVT, although concerns about possible pro-arrhythmic effects have limited its use. Amiodarone has been described favorably, but is frequently excluded due to its poor tolerability. Verapamil is contraindicated as it may increase mortality. Conclusions on other less frequently used drugs cannot be drawn. In severely hydropic fetuses and/or therapy-resistant FT, direct fetal therapy is sometimes initiated. To minimize the number of invasive procedures, fetal intramuscular or intraperitoneal injections that provide a more sustained release are preferred. Based on these data we propose a drug protocol of sotalol 160 mg twice daily orally, increased to a maximum of 480 mg daily. Whenever sinus rhythm is not achieved, the addition of digoxin 0.25 mg three times daily is recommended, increased to a maximum of 0.5 mg three times daily. Only in SVT complicated by FH, either maternal digoxin 1 to 2mg IV in 24 hours, and subsequently 0.5 to 1 mg/day IV, or flecainide 200 to 400 mg/day orally is proposed. Initiating direct fetal therapy may follow failure of transplacental therapy.