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The motion relationship and time intervals of the pulsed-wave Doppler (PWD) spectrum are essential for diagnosing fetal arrhythmia. However, few technologies currently are available to automatically calculate fetal cardiac time intervals (CTIs). The purpose of this study was to develop a fetal heart rhythm intelligent quantification system (HR-IQS) for the automatic extraction of CTIs and establish the normal reference range for fetal CTIs. A total of 6498 PWD spectrums of 2630 fetuses over the junction between the left ventricular inflow and outflow tracts were recorded across 14 centers. E, A, and V waves were manually labeled by 3 experienced fetal cardiologists, with 17 CTIs extracted. Five-fold cross-validation was performed for training and testing of the deep learning model. Agreement between the manual and HR-IQS–based values was evaluated using the intraclass correlation coefficient and Spearman's rank correlation coefficient. The Jarque-Bera test was applied to evaluate the normality of CTIs' distributions, and the normal reference range of 17 CTIs was established with quantile regression. Arrhythmia subset was compared with the non-arrhythmia subset using the Mann-Whitney U test. Significant positive correlation (P <.001) and moderate-to-excellent consistency (P <.001) between the manual and HR-IQS automated measurements of CTIs was found. The distribution of CTIs was non-normal (P <.001). The normal range (2.5th to 97.5th percentiles) was successfully established for the 17 CTIs. Using our HR-IQS is feasible for the automated calculation of CTIs in practice and thus could provide a promising tool for the assessment of fetal rhythm and function. [Display omitted] [ABSTRACT FROM AUTHOR]

This international multidisciplinary expert consensus statement is intended to provide comprehensive guidance that can be referenced at the point of care to cardiac electrophysiologists, cardiologists, and other health care professionals, on the management of cardiac arrhythmias in pregnant patients and in fetuses. This document covers general concepts related to arrhythmias, including both brady- and tachyarrhythmias, in both the patient and the fetus during pregnancy. Recommendations are provided for optimal approaches to diagnosis and evaluation of arrhythmias; selection of invasive and noninvasive options for treatment of arrhythmias; and disease- and patient-specific considerations when risk stratifying, diagnosing, and treating arrhythmias in pregnant patients and fetuses. Gaps in knowledge and new directions for future research are also identified. [ABSTRACT FROM AUTHOR]

Fetal acidemia is a common final pathway to fetal death, and in many cases, to fetal central nervous system injury. However, certain fetal pathophysiological processes are associated with significant category II or category III fetal heart rate changes before the development of or in the absence of fetal acidemia. The most frequent of these processes include fetal infection and/or inflammation, anemia, fetal congenital heart disease, and fetal central nervous system injury. In the presence of significant category II or category III fetal heart rate patterns, clinicians should consider the possibility of the aforementioned fetal processes depending on the clinical circumstances. The common characteristic of these pathophysiological processes is that their associated fetal heart rate patterns are linked to increased adverse neonatal outcomes despite the absence of acidemia at birth. Therefore, in these cases, the fetal heart rate patterns may provide more insight about the fetal condition and pathophysiology than the acid–base status at birth. In addition, as successful timing of intrapartum interventions on the basis of evolution of fetal heart rate patterns aims to prevent fetal acidemia, it may not be logical to continue to use the fetal acid–base status at birth as the gold standard outcome to determine the predictive ability of category II or III fetal heart rate patterns. A more reasonable approach may be to use the umbilical cord blood acid–base status at birth as the gold standard for determining the appropriateness of the timing of our interventions. [ABSTRACT FROM AUTHOR]

Fetal long QT syndrome (LQTS) may present with sinus bradycardia, functional 2:1 atrioventricular block (AVB), and ventricular arrhythmias (ventricular tachycardia [VT]/torsades de pointes [TdP]) and lead to fetal or postnatal death. We performed a systematic review and individual participant data meta-analysis of 83 studies reporting outcomes of 265 fetuses for which suspected LQTS was confirmed postnatally and determined risk of adverse perinatal and postnatal outcomes using logistic and stepwise logistic regression. A longer fetal QTc was more predictive of death than any other antenatal factor (receiver operating characteristic [ROC] area under the curve [AUC] 0.85; 95% confidence interval [CI] 0.66–1.00). Risk of death was significantly increased with fetal QTc >600 ms. Neither fetal heart rate nor heart rate z-score predicted death (ROC AUC 0.51; 95% CI 0.31–0.71; and ROC AUC 0.59; 95% CI 0.37–0.80, respectively). The combination of antenatal VT/TdP or functional 2:1 AVB and lack of family history of LQTS was also highly predictive of death (ROC AUC 0.82; 95% CI 0.76–0.88). Our data provide clinical screening tools to enable prediction and intervention for fetuses with LQTS at risk of death. [ABSTRACT FROM AUTHOR]

Permanent junctional reciprocating tachycardia (PJRT) is a rare form of congenital arrhythmia occurring predominantly in infants and children. Prenatal presentation is frequently characterized by incessant tachycardia leading to dilated cardiomyopathy (DCM). Some patients can have a normal heart rate which leads to a delayed diagnosis. We report a case of a neonate who was presented prenatally with DCM, fetal hydrops, and no signs of fetal arrhythmia. Diagnosis of PJRT was established after delivery with characteristic electrocardiographic patterns. Successful conversion to sinus rhythm with digoxin and amiodarone was achieved three months later. At 16 months of age, both echocardiography and electrocardiography were normal. • PJRT in fetal period can occur even at normal fetal heart rate. • Fetal dilative cardiomyopathy and hydrops should lead to a suspicion for PJRT. • Early recognition of PJRT can be facilitated by typical postnatal ECG patterns. [ABSTRACT FROM AUTHOR]

Arrhythmia is a major cardiac abnormality in fetuses. Therefore, early diagnosis of arrhythmia is clinically crucial. Pulsed-wave Doppler ultrasound is a commonly used diagnostic tool for fetal arrhythmia. Its key step for diagnosis involves identifying adjacent measurable cardiac cycles (MCCs). As cardiac activity is complex and the experience of sonographers is often varied, automation can improve user-independence and diagnostic-validity. However, arrhythmias pose several challenges for automation because of complex waveform variations, which can cause major localization bias and missed or false detection of MCCs. Filtering out non-MCC anomalies is difficult because of large intra-class and small inter-class variations between MCCs and non-MCCs caused by agnostic morphological waveform variations. Moreover, rare arrhythmia cases are insufficient for classification algorithms to adequately learn discriminative features. Using only normal cases for training, we propose a novel hierarchical online contrastive anomaly detection (HOCAD) framework for arrhythmia diagnosis during test time. The contribution of this study is three-fold. First, we develop a coarse-to-fine framework inspired by hierarchical diagnostic logic, which can refine localization and avoid missed detection of MCCs. Second, we propose an online learning-based contrastive anomaly detection with two new anomaly scores, which can adaptively filter out non-MCC anomalies on a single image during testing. With these complementary efforts, we precisely determine MCCs for correct measurements and diagnosis. Third, to the best of our knowledge, this is the first reported study investigating intelligent diagnosis of fetal arrhythmia on a large-scale and multi-center ultrasound dataset. Extensive experiments on 3850 cases, including 266 cases covering three typical types of arrhythmias, demonstrate the effectiveness of the proposed framework. • An online contrastive anomaly detection method for fetal arrhythmia diagnosis. • A hierarchical framework gradually enhances certainty in measurable cardiac cycle. • With two new anomaly scores, the detection framework adaptively filters anomalies. • The first study to make an intelligent diagnosis of fetal arrhythmia in ultrasound. [ABSTRACT FROM AUTHOR]

Background: Fetal atrioventricular block (AVB) occurs in 2% to 4% of anti-Ro antibody-positive pregnancies and can develop in <24 h. Only rarely has standard fetal heart rate surveillance detected AVB in time for effective treatment.Objectives: Outcome of anti-Ro pregnancies was surveilled with twice-daily home fetal heart rate and rhythm monitoring (FHRM) and surveillance echocardiography.Methods: Anti-Ro pregnant women were recruited from 16 international centers in a prospective observational study. Between 18 and 26 weeks' gestation, mothers checked FHRM twice daily with a commercially available Doppler monitor and underwent weekly or biweekly surveillance fetal echocardiograms. If FHRM was abnormal, a diagnostic echocardiogram was performed. Cardiac cycle length and atrioventricular interval were measured, and cardiac function was assessed on all echocardiograms. After 26 weeks, home FHRM and echocardiograms were discontinued, and mothers were monitored during routine obstetrical visits. Postnatal electrocardiograms were performed.Results: Most mothers (273 of 315, 87%) completed the monitoring protocol, generating 1,752 fetal echocardiograms. Abnormal FHRM was detected in 21 mothers (6.7%) who sought medical attention >12 h (n = 7), 3 to 12 h (n = 9), or <3 h (n = 5) after abnormal FHRM. Eighteen fetuses had benign rhythms, and 3 had second- or third-degree AVB. Treatment of second-degree AVB <12 h after abnormal FHRM restored sinus rhythm. Four fetuses had first-degree AVB diagnosed by echocardiography; none progressed to second-degree AVB. No AVB was missed by home FHRM or developed after FHRM.Conclusions: Home FHRM confirms the rapid progression of normal rhythm to AVB and can define a window of time for successful therapy. (Prospective Maternal Surveillance of SSA [Sjögren Syndrome A] Positive Pregnancies Using a Hand-held Fetal Heart Rate Monitor; NCT02920346). [ABSTRACT FROM AUTHOR]

Background: Fetal tachyarrhythmia can lead to fetal hydrops due to heart failure. Flecainide is often considered as second-line therapy when digoxin monotherapy fails, which is more likely in hydropic fetuses. Time to conversion to sinus rhythm (SR) is critical in cases presenting with hydrops.Objective: The aim of this study was to evaluate the efficacy and time to conversion to SR of transplacental treatment, especially flecainide.Methods: This is a retrospective observational study of 46 fetuses with fetal tachyarrhythmia. Treatment was either flecainide (n = 28, 60.9%), digoxin+flecainide combination (n = 4, 8.7%), or digoxin (n = 10, 21.7%). In 4 fetuses (8.7%), no treatment was necessary.Results: In our study population, 26 of the 32 fetuses (81.2%) that were treated with flecainide as a first-line therapy (flecainide or digoxin+flecainide) converted to SR. The median time to conversion to SR was 3 days (range 1-7 days) with flecainide monotherapy and 11.5 days (range 3-14 days) with a combination therapy. Seventy-two percent (13/18) of hydropic fetuses and 90% (9/10) of nonhydropic fetuses converted to SR when treated with flecainide monotherapy. There was no statistical difference in rates of conversion to SR in hydropic and nonhydropic fetuses (P = .37) or time to conversion to SR in the 2 groups (P = .9). In the majority of the remaining fetuses, there was a partial response with decreased ventricular heart rates that were well tolerated.Conclusion: Flecainide is highly effective in achieving SR in hydropic and nonhydropic fetuses with supraventricular tachycardia in a median time of 3 days. In our opinion, flecainide should be considered as first-line therapy in fetal supraventricular tachycardia with and without hydrops. [ABSTRACT FROM AUTHOR]

The risk of fetal atrioventricular block in anti-Ro/SSA antibody–exposed pregnancies with no previous affected offspring is approximately 2%. A high antibody titer is necessary but not sufficient for atrioventricular block, and specific antibody titers do not predict risk. However, there are no data on the negative predictive value of antibody titer to identify pregnancies at low risk of fetal atrioventricular block, and may not require surveillance. This study aimed to define anti-Ro52 and anti-Ro60 antibody thresholds for the identification of fetuses unlikely to develop atrioventricular block using clinically validated and research laboratory tests. This study performed a multicenter review of pregnant subjects who tested positive in their local commercial laboratories for anti-Ro/SSA antibodies at the University of Colorado Children's Hospital (2014–2021) and Phoenix Children's Hospital (2014–2021) and enrolled in the Research Registry for Neonatal Lupus (RRNL) at New York University Langone Medical Center (2002–2021). The subjects were referred on the basis of rheumatologic symptoms or history of atrioventricular block in a previous pregnancy and were retrospectively grouped on the basis of pregnancy outcome. Group 1 indicated no fetal atrioventricular block in current or past pregnancies; group 2 indicated fetal atrioventricular block in the current pregnancy; and group 3 indicated normal current pregnancy but with fetal atrioventricular block in a previous pregnancy. Maternal sera were analyzed for anti-Ro52 and anti-Ro60 antibodies using a clinically validated multiplex bead assay (Associated Regional and University Pathologists Laboratories, Salt Lake City, UT) and a research enzyme-linked immunosorbent immunoassay (New York University). This study calculated the negative predictive value separately for anti-Ro52 and anti-Ro60 antibodies and for the 2 combined using a logistic regression model and a parallel testing strategy. This study recruited 270 subjects (141 in group 1, 66 in group 2, and 63 in group 3). Of note, 89 subjects in group 1 had data on hydroxychloroquine treatment: anti-Ro/SSA antibody titers were no different between those treated (n=46) and untreated (n=43). Mean anti-Ro52 and anti-Ro60 titers were the lowest in group 1 and not different between groups 2 and 3. No case of fetal atrioventricular block developed among subjects with anti-Ro52 and anti-Ro60 titers of <110 arbitrary units per milliliter using the multiplex bead assay of the Associated Regional and University Pathologists Laboratories (n=141). No case of fetal atrioventricular block developed among subjects with research laboratory anti-Ro52 titers of <650 and anti-Ro60 of <4060 enzyme-linked immunosorbent immunoassay units (n=94). Using these 100% negative predictive value thresholds, more than 50% of the anti-Ro/SSA antibody pregnancies that ultimately had no fetal atrioventricular block could be excluded from surveillance based on clinical and research titers, respectively. Study data suggested that there is a clinical immunoassay level of maternal anti-Ro/SSA antibodies below which the pregnancy is at low risk of fetal atrioventricular block. This study speculated that prospectively applying these data may avert the costly serial echocardiograms currently recommended for all anti-Ro/SSA–antibody positive pregnancies and guide future management. [ABSTRACT FROM AUTHOR]

Bile acids are elevated in the blood of women with intrahepatic cholestasis of pregnancy (ICP) and this may lead to fetal arrhythmia, fetal hypoxia and potentially fetal death in utero . The bile acid taurocholic acid (TC) causes abnormal calcium dynamics and contraction in neonatal rat cardiomyocytes. Ursodeoxycholic acid (UDCA), a drug clinically used to treat ICP, prevents adverse effects of TC. During development, the fetus is in a state of relative hypoxia. Although this is essential for the development of the heart and vasculature, resident fibroblasts can transiently differentiate into myofibroblasts and form gap junctions with cardiomyocytes in vitro , resulting in cardiomyocyte depolarization. We expanded on previously published work using an in vitro hypoxia model to investigate the differentiation of human fetal fibroblasts into myofibroblasts. Recent evidence shows that potassium channels are involved in maintaining the membrane potential of ventricular fibroblasts and that ATP-dependent potassium (K ATP ) channel subunits are expressed in cultured fibroblasts. K ATP channels are a valuable target as they are thought to have a cardioprotective role during ischaemic and hypoxic conditions. We investigated whether UDCA could modulate fibroblast membrane potential. We established the isolation and culture of human fetal cardiomyocytes and fibroblasts to investigate the effect of hypoxia, TC and UDCA on human fetal cardiac cells. UDCA hyperpolarized myofibroblasts and prevented TC-induced depolarisation, possibly through the activation of K ATP channels that are expressed in cultured fibroblasts. Also, similar to the rat model, UDCA can counteract TC-induced calcium abnormalities in human fetal cultures of cardiomyocytes and myofibroblasts. Under normoxic conditions, we found a higher number of myofibroblasts in cultures derived from human fetal hearts compared to cells isolated from neonatal rat hearts, indicating a possible increased number of myofibroblasts in human fetal hearts. Hypoxia further increased the number of human fetal and rat neonatal myofibroblasts. However, chronically administered UDCA reduced the number of myofibroblasts and prevented hypoxia-induced depolarisation. In conclusion, our results show that the protective effect of UDCA involves both the reduction of fibroblast differentiation into myofibroblasts, and hyperpolarisation of myofibroblasts, most likely through the stimulation of potassium channels, i.e. K ATP channels. This could be important in validating UDCA as an antifibrotic and antiarrhythmic drug for treatment of failing hearts and fetal arrhythmia. [ABSTRACT FROM AUTHOR]

As more women with repaired congenital heart disease survive to their reproductive years and many other women are delaying pregnancy until later in life, a rising concern is the risk of cardiac arrhythmias during pregnancy. Naturally occurring cardiovascular changes during pregnancy increase the likelihood that a recurrence of a previously experienced cardiac arrhythmia or a de novo arrhythmia will occur. Arrhythmias should be thoroughly investigated to determine if there is a reversible etiology, and risks/benefits of treatment options should be fully explored. We discuss the approach to working up and treating various arrhythmias during pregnancy with attention to fetal and maternal risks as well as treatment of fetal arrhythmias. Acute management in stable patients includes close monitoring and intravenous pharmacologic therapy, while DC cardioversion should be used to terminate arrhythmias in hemodynamically unstable patients. Long-term management may require continued oral antiarrhythmic therapy, with particular attention to fetal safety, to prevent complications associated with arrhythmias. [ABSTRACT FROM AUTHOR]

Background: Blocked atrial bigeminy (BAB) and second-degree atrioventricular block with 2:1 conduction block (2:1 AVB) both present as ventricular bradycardia and can be difficult to distinguish by echocardiography. Since the prognosis and clinical management of these rhythms are different, an accurate diagnosis is essential. Objective: To identify magnetic and mechanical heart rate and rhythm parameters that could reliably distinguish BAB from 2:1 AVB. Methods: A retrospective study of ten BAB and seven 2:1 AVB subjects was performed, using fMCG and pulsed Doppler ultrasound. Results: Distinguishing BAB from 2:1 AVB by using fMCG was relatively straightforward because in BAB the ectopic P wave (P′) occurred early, resulting in a bigeminal (short-long) atrial rhythm. The normalized coupling interval of the ectopic beat (PP′ of the blocked beat to PP of the conducted beat) was 0.29 ± 0.03. In contrast, the echocardiographic assessment of inflow-outflow gave a normalized mechanical coupling interval (AA′/AA) near 0.5, which made it difficult to distinguish BAB from 2:1 AVB. Heart rate distinguished most subjects with BAB from those with 2:1 AVB (82 ± 5.7 beats/min vs 69 ± 4.2 beats/min), but was not a completely reliable indicator. In most subjects, BAB alternated with sinus rhythm or other rhythms, resulting in complex heart rate and rhythm patterns. Conclusions: Fetal BAB and 2:1 AV block can be difficult to distinguish using echocardiography because in many fetuses with BAB the mechanical rhythm does not accurately reflect the magnetic rhythm. fMCG provides a more reliable means of making a differential diagnosis. [Copyright &y& Elsevier]

Abstract: Objectives: Magnesium deficiency in pregnancy is frequent, and in consequence magnesium supplementation is widely used. As magnesium crosses the placental barrier and since the fetal kidney does not excrete magnesium as efficiently as the mature kidney, effects on fetal cardiac time intervals are probable, but still unknown. Study design: Sixty pregnant women were included in an observational study: 31 patients received oral routine magnesium supplementation. In addition to routine fetal echocardiography, fetal magnetocardiography (fMCG) was used to investigate electrophysiological rhythm patterns with high temporal resolution. fMCG tracings were analyzed according to a predefined procedure for fetal cardiac time interval (CTI)-detection. fCTI findings (P-wave, PQ-segment, PR-interval, QRS complex, ST segment, T-wave and QTc interval) were registered. Results: Significant widening of the QRS-complex (p =0.004) was demonstrated in fetuses whose mothers received magnesium supplementation (240mg/day) relative to the control group. Conclusion: Magnesium exposed fetuses demonstrated a prolonged ventricular arousal, but healthy neonatal outcome was found in all exposed fetuses. Although fMCG is a preclinical method and limited in its availability, the procedure could help to monitor fetuses. [Copyright &y& Elsevier]

Abstract: Background: Cardiac arrhythmias are commonly observed in the fetus, however, may have major consequences for fetal development and post natal life. Aims: To evaluate the perinatal management and cardiac outcome of fetuses with tachy- or bradyarrhythmia. Study design: Perinatal management, outcome and long-term cardiac follow-up were evaluated retrospectively in consecutive fetuses with cardiac arrhythmias. Results: Forty-four fetuses were diagnosed: supraventricular tachycardia (SVT, n=28), atrial flutter (AF, n=7) and atrioventricular block (AVB, n=9). The overall incidence of cardiac anomalies was 18% mainly in the AVB group; hydrops was present in 34%. Direct or transplacental fetal anti-arrhythmic medication was given in 76%. Mortality was 6% in SVT/AF and 78% in the AVB group, respectively. AF resolved in all patients. In the SVT group, Wolff–Parkinson–White (WPW) syndrome was present in 21%, diagnosed at birth or later in life. After the age of one year about 90% of patients in the SVT group remained asymptomatic and free of drugs (median follow-up 76months). Conclusions: Mortality rate is low in patients with fetal SVT and AF but high in patients with AVB. Related morbidity includes WPW-syndrome and congenital cardiac anomalies. Electrocardiographic screening is recommended in all fetal SVT cases before adolescence since WPW-syndrome may occur later in life. [ABSTRACT FROM AUTHOR]

Abstract: A male newborn weighing 2334 g was delivered at 37 weeks of gestation by caesarean section because of prenatal ultrasound findings of fetal hydrops with atrioventricualr block, ventriucular tachycardia (VT), and impaired ventricular function. In spite of the intravenous administration of lidocaine, VT continued. He developed poor perfusion and systemic hypotension. After the intravenous administration of amiodarone, VT was terminated. The electrocardiogram revealed an extremely prolonged corrected QT interval (860 ms) with 2:1 atrioventricular block. Unfortunately, he died 18 h after birth in spite of the administration of lidocaine, beta-blocker and magnesium. Mutational analysis identified a novel heterozygous de novo mutation (F1486del) in SCN5A. This mutation is associated with the IFM motif in the linker between III and IV domains of Nav1.5, which serves as an inactivation particle binding within the pore of sodium channels. This report demonstrates an interesting relationship between the clinical phenotype and the location of the mutation in long QT syndrome. [ABSTRACT FROM AUTHOR]

Background: Most fetal deaths are unexplained. Long QT syndrome is a genetic disorder of cardiac ion channels. Affected individuals, including fetuses, are predisposed to sudden death. We sought to determine the risk of fetal death in familial long QT syndrome, in which the mother or father carries the long QT syndrome genotype. In addition, we assessed whether risk differed if the long QT syndrome genotype was inherited from the mother or father.Objective: This was a retrospective review of pregnancies in families with the 3 most common heterozygous pathogenic long QT syndrome genotypes in KCNQ1 (LQT1), KCNH2 (LQT2), or SCN5A (LQT3), which occur in approximately 1 in 2000 individuals. The purpose of our study was to compare pregnancy and birth outcomes in familial long QT syndrome with the normal population and between maternal and paternal carriers of the long QT syndrome genotype. We hypothesized that fetal death before (miscarriage) and after (stillbirths) 20 weeks gestation would be increased in familial long QT syndrome compared with the normal population and that the parent of origin would not affect birth outcomes.Study Design: Our study was a multicenter observational case series of 148 pregnancies from 103 families (80 mothers, 23 fathers) with familial long QT syndrome (60 with LQT1, 29 with LQT2, 14 with LQT3) who were recruited from 11 international centers with expertise in hereditary heart rhythm diseases, pediatric and/or adult electrophysiology, and high-risk pregnancies. Clinical databases from these sites were reviewed for long QT syndrome that occurred in men or women of childbearing age (18-40 years). Pregnancy outcomes (livebirth, stillbirth, and miscarriage), birthweights, and gestational age at delivery were compared among long QT syndrome genotypes and between maternal vs paternal long QT syndrome-affected status with the use of logistic regression analysis.Results: Most offspring (80%; 118/148) were liveborn at term; 66% of offspring (73/110) had long QT syndrome. Newborn infants of mothers with long QT syndrome were delivered earlier and, when the data were controlled for gestational age, weighed less than newborn infants of long QT syndrome fathers. Fetal arrhythmias were observed rarely, but stillbirths (fetal death at >20 weeks gestation) were 8 times more frequent in long QT syndrome (4% vs approximately 0.5%); miscarriages (fetal death at ≤20 weeks gestation) were 2 times that of the general population (16% vs 8%). The likelihood of fetal death was significantly greater with maternal vs paternal long QT syndrome (24.4% vs 3.4%; P=.036). Only 10% of all fetal deaths underwent postmortem long QT syndrome testing; 2 of 3 cases were positive for the family long QT syndrome genotype.Conclusion: This is the first report to demonstrate that mothers with long QT syndrome are at increased risk of fetal death and to uncover a previously unreported cause of stillbirth. Our results suggest that maternal effects of long QT syndrome channelopathy may cause placental or myometrial dysfunction that confers increased susceptibility to fetal death and growth restriction in newborn survivors, regardless of long QT syndrome status. [ABSTRACT FROM AUTHOR]

Objective To explore fetal arrhythmia clinical significance and its correlation with fetal prognosis. Methods Twenty-six cases of fetal arrhythmia detected among 12 799 pregnant women recorded over a ten-year period in Peking Uinon Medical College (PUMC) Hospital were reviewed retrospectively. Fetal arrhythmia was diagnosed by fetal auscultation, ultrasonography, electric fetal heart monitoring, and fetal echocardiography. Results Twenty-six fetuses were documented with fetal arrhythmia (3 tachycardia, 4 bradycardia, 19 normal heart rate with irregular fetal cardiac rhythm). The incidence of fetal arrhythmia in our hospital was 0.2%. They were diagnosed at the average of 35 weeks' gestation (15 to 41 weeks). Twenty-two cases were diagnosed by antenatal fetal auscultation, 1 case was diagnosed by ultrasonography, and 3 cases were diagnosed by electric fetal heart monitoring. Fetal echocardiograins were per- formed on 17 fetuses, 6 cases (3 5.3%) of which showed that ventricular premature beats with normal structure of fetal heart. All neonates survived postnatally and 24 of them (92.3%) were followed up. Echocardiograms were performed for 16 neonates and 2 of them were identified as atrial septal defects with normal heart rhythms. The results of follow-up showed that the two patients had no apparent clinical manifestation. The echocardiogram showed that atrial septal defect obliterated already. Conclusion The prognosis is well for most of the fetuses with arrhythmias, with low incidence of heart deformation. [ABSTRACT FROM AUTHOR]