Multiple antiarrhythmic transplacental treatments for fetal supraventricular tachyarrhythmia: A protocol for systematic review and meta analysis.

BACKGROUND: Fetal supraventricular tachyarrhythmia is a common reason for referral to fetal cardiology. Multiple antiarrhythmic transplacental medications can be used to treat these diseases. Debates remain regarding the standardized therapy. METHODS: PubMed, EMBASE, Cochrane Library, Web of Science, Google Scholar, and ClinicalTrials.gov will be searched from inception to September 2020. A handsearching for gray literature, including unpublished conference articles, will be performed. The randomized control trials, case-control, and cohort studies will be accepted, no matter what the languages they were reported. We will first focus on the effectiveness of the therapy on fetal cardiac rhythm and/or heart rate. Then we will do further analysis of preterm delivery, fetal hydrops, intrauterine fetal demise, and maternal side effects. The Cochrane Risk of Bias Tool and the Newcastle-Ottawa scale will be used to assess the risk of bias of the randomized controlled trials, case-control, and cohort studies, respectively. Two independent reviewers will carry out literature identification, data collection, and study quality assessment. Discrepancies will be resolved by a third reviewer. Statistical analysis will be conducted using the STATA 13.0 software. RESULT: The results will provide helpful information about the effect of multiple antiarrhythmic transplacental therapies in pregnancies with supraventricular tachycardia or atrial flutter, and demonstrate which therapy is more effective. CONCLUSION: The conclusion drawn from this systematic review will benefit the patients with fetal supraventricular tachyarrhythmia.

Fetal Atrial Flutter: Electrophysiology and Associations With Rhythms Involving an Accessory Pathway.

BACKGROUND: Atrial flutter (AFl) accounts for up to one third of all fetal tachyarrhythmias and can result in premature delivery, hydrops, and fetal death in 10% of cases; however, the electrophysiology of AFl in utero is virtually unstudied. METHODS AND RESULTS: In this observational study, we reviewed 19 fetal magnetocardiography studies from 16 fetuses: 15 fetuses (21-38 weeks' gestation) referred with an echocardiographic diagnosis of AFl and 1 fetus (20 weeks' gestation) referred with a diagnosis of tachycardia that was shown by fetal magnetocardiography to have transient AFl in addition to atrioventricular reciprocating tachycardia. Thirteen fetuses showed AFl during the fetal magnetocardiography session, including 4 that presented prior to the third trimester. Five fetuses had incessant AFl; all but 1 of the others with AFl showed additional significant rhythms. Specifically, AFl showed a strong association with rhythms involving an accessory pathway: atrioventricular reciprocating tachycardia, blocked reentrant premature atrial contractions, and ventricular preexcitation. The observed initiations and terminations of AFl most often involved reentrant premature atrial contractions. Spontaneous termination of AFl showed AFl cycle length oscillations. Nine fetuses with 2:1 AFl also showed periods of 4:1 conduction or variable conduction that oscillated between 2:1 and 4:1; however, 3:1 AFl was relatively rare. CONCLUSIONS: Fetal AFl can occur as early as midgestation and is often accompanied by atrioventricular reciprocating tachycardia and other rhythms associated with an accessory pathway. The findings depict critical differences in the electrophysiology of AFl in the fetus versus the neonate.

Maternal antibody-associated fetal second-degree heart block and atrial flutter: case report and review.

Exposure to maternal anti-Ro (SS-A) and anti-La (SS-B) antibodies is a well-described risk factor for the development of fetal atrioventricular (AV) block. The role of maternal fluorinated steroids in the treatment and prevention of antibody-mediated fetal AV block is controversial. Fetal atrial flutter has rarely been described in association with maternal antibodies. This report describes a case of fetal exposure to maternal anti-Ro antibodies with associated second-degree AV block and atrial flutter. Interestingly, the reported patient had 2:1 AV conduction during both normal atrial rates (consistent with AV node conduction disease) and episodes of flutter (consistent with physiologic AV node functionality). The fetus was treated with transplacental digoxin and dexamethasone, which resolved both rhythm disturbances. The case report is followed by a brief discussion of AV block and atrial flutter associated with maternal antibody exposure.

Transplacental digoxin therapy for fetal tachyarrhythmia with multiple evaluation systems.

BACKGROUND: Sustained fetal tachyarrhythmia may result in congestive heart failure, hydrops fetalis, and fetal/neonatal death, which requires timely and appropriate therapy. AIM: To determine the value of transplacental digoxin therapy for fetal tachyarrhythmia with multiple evaluations. METHODS: Four cases of fetal tachyarrhythmia were diagnosed with fetal echocardiography and treated with transplacental digoxin therapy with an initial dosage of 0.25 mg qd. Fetal echocardiography and measurement of maternal serum digoxin concentrations were performed every 5-7 days. Echocardiographic information was further used for the calculation of three evaluation systems including, Tei index, cardiovascular profile score (CVPS), and umbilical artery resistance index (UARI). The dosage of digoxin was adjusted according to the serum concentration, as well as results from three evaluation systems. RESULTS: During the course of digoxin treatment, our patients show an increase of CVPS and decrease of Tei index and UARI, suggesting the recovery of heart function. Sinus rhythm was restored in 3-10 days in three cases and 42 days in one case. At the time of delivery, the placental transportation efficiency (neonate/mother ratio of serum digoxin concentration) was 76.45-84.31%. Following delivery, the general conditions of neonates were favorable. During the 4- to 14-month follow-up, reoccurrence of arrhythmia, neurological deficit, and retarded growth and development were not observed. CONCLUSIONS: Transplacental digoxin therapy with combined evaluation of Tei index, CVPS, and UARI systems is useful for treating fetal atrial flutter (AF) and supraventricular tachycardia (SVT).

Flutter auricular de presentación fetal: aportación de dos casos / Flutter atrial in fetuses: contribution with two cases

El flutter auricular (AA) es una arritmia poco común en la infancia. Aun así, si es diagnosticada en la época fetal o neonatal, debe conducir a una rápida actuación terapéutica dada su potencial morbilidad y mortalidad. La prevalencia de arritmias malignas en el feto es muy baja (aproximadamente 1/5.000 gestaciones) y entre las taquiarritmias, el flutter auricular representa el 25-30% de éstas. La morbimortalidad causada por esta entidad no es despreciable. El hidrops a causa de la insuficiencia cardíaca y como consecuencia, el daño neurológico no es infrecuente. Sin embargo, el pronóstico a largo plazo es bueno dado que casi ningún paciente presenta recurrencias. Aportamos dos casos acontecidos en dos hospitales de nuestra red entre noviembre de 1998 y julio de 2005. En ambos, una rápida actuación obstétrica, pediátrica y cardiológica, lograron una total recuperación. La cardioversión eléctrica fue exitosa en los dos, no se produjeron complicaciones y ninguno sufrió recurrencias (AU)

A trial Flutter (AA) is an uncommon arrhythmia in childhood. Eve so, if it is diagnosed in foetal or neonatal age, it forces to a rapid therapeutic action because its potential morbidity and mortality. The prevalence of malignant arrhythmias in fetuses is very small – aprox 1/5.000 gestations-, and among tachyarrhythmia’s the atrial flutter represents 25-30% (1-3). The morbidity/mortality that is caused by this entity in perinatal age is not worthless. Hydrops form intrauterine cardiac failure secondary to arrhythmia and, as a result of that, the neurological damage is not unusual. However there is a good long-term prognosis because hardly anyone patients has recurrences of this arrhythmia. The reason of this report is to contribute with two cases, detected between November of 19998 and July of 2005 in two maternity-paediatrics hospitals. In both, a rapid obstetrician, paediatrician and cardiologist actuation achieved a total and lasting recuperation. Electrocardioversion was successful in two newborn; there were not complications and they had not recurrences (AU)

Fetal atrial flutter: a case report and experience of sotalol treatment.

OBJECTIVE: Fetal tachyarrhythmia may cause fetal hydrops and lead to fetal morbidity and mortality. Supraventricular tachycardia and atrial flutter have been the most diagnosed. We present a case of fetal atrial flutter diagnosed during the second trimester treated with digoxin and sotalol and delivered at term. CASE REPORT: A 30-year-old primigravid woman was diagnosed with fetal atrial flutter at the gestational age of 25 weeks with atrial rates of 480-520 bpm and ventricular rates of 200-250 bpm. Initially, she was treated with digoxin then with a combination of digoxin and sotalol. The fetal heart beat slowed after sotalol treatment but did not return to sinus rhythm. The fetus was delivered vaginally. Neonatal echocardiography showed a small apical ventricular septal defect and small patent ductus arteriosus. Electrocardiography also revealed atrial flutter with occasional atrial fibrillation. CONCLUSION: The efficacy of antiarrhythmic drug therapy for fetal atrial flutter has not been well established. In our case, we used sotalol combined with digoxin and the fetal heart beat slowed after therapy. Sotalol may be considered the drug of choice for fetal atrial flutter. If the fetal atrial flutter is resistant to these therapies, a combination of other congenital cardiac diseases or organic abnormalities should be considered.

Neonatal cholestasis associated with fetal arrhythmia.

We evaluated the consequence of different types of fetal arrhythmia in the development of neonatal cholestasis. The charts of 38 children born at St. Justine Hospital between 1993 and 2001 with sustained and hemodynamically significant fetal arrhythmias were studied: 19 with supraventricular tachycardia, 14 with atrial flutter, and 5 with atrio-ventricular (AV) block. Six of these 38 children presented with cholestasis. The average duration of arrhythmia was 15.7 days in the noncholestatic group, compared with 40.3 days in the cholestatic group ( P <.05). The three infants with supraventricular tachycardia who developed cholestasis survived and resolved their cholestasis, whereas 2 of 3 infants with AV block died. No infant with atrial flutter developed cholestasis. We conclude that newborns who developed tachyarrhythmia during their fetal life can show transient neonatal cholestasis. In patients with AV block, severe and irreversible liver failure could be observed. In addition, extensive collapse of the stroma and the absence of hepatocytes (foie vide) also were observed in a patient with anti-Ro antibodies.

[Fetal supraventricular tachycardia associated with anasarca: poor prognosis despite treatment. Apropos of two cases]. / Tachycardies supraventriculaires foetales avec anasarque: mauvais pronostic malgré le traitement. A propos de deux cas.

Two cases of foetal supraventricular tachycardia with hydrops with fatal outcomes illustrate the poor general prognosis of this condition. The absence of therapeutic consensus, of large series in the existing literature, does not prevent logical and reasonable management based on rhythmological, pharmacological and prognostic criteria. A combined approach associating antiarrhythmic therapy by the transplacental and intrafunicular approaches seems acceptable now that funicular puncture can be undertaken easily, and certain antiarrhythmic molecules suggest encouraging results. It is important to try to assess the haemodynamic tolerance by foetal Doppler echocardiography because the foetal prognosis depends on ischaemic cerebral lesions induced by anoxia, difficult to diagnose in utero: when observed, aggressive and occasionally dangerous therapies to foetus and mother may be justified in these extreme situations of foetoplacental hydrops.