Fetal Esophagus Research Articles

Feasiblity Study on the Longitudinal Section of the Fetal Esophagus by Prenatal Ultrasound between 21 and 23 Gestational Weeks

Background: Prenatal esophageal atresia (EA) diagnosis may improve outcomes by optimizing prenatal and postnatal care. This study evaluated the feasibility of direct antenatal visualization of normal longitudinal esophageal sections using two-dimensional ultrasound between 21 and 23 gestational weeks. Methods: A detailed prenatal anatomic survey was performed, followed by dedicated esophageal imaging. The latter was performed as follows: coronal sections of the thoracic aorta were obtained; the sound beam was then moved ventrally; and strip-shaped high echoes with three or more hyperechoic layers were identified as the esophagus. Images showing the longest esophageal segment were used to measure the esophageal length and angle (between the thoracic aorta and esophagus). Results: Longitudinal esophageal sections were visualized in 94.0% (n = 205/218) of patients. The visualization rates between fetuses in different positions were statistically significant (p < 0.05). Two tubular patterns of longitudinal fetal esophagus sections were observed when collapsed on ultrasound: a tubular structure composed of three hyperechoic layers (40.4%, 88/218); and a tube composed of multilayered hyperechoic structures (59.6%, 130/218). Swallowing actions were observed in 28 cases (12.8%, 28/218). The fetal esophagus was fluid-filled and exhibited an appearance similar to a tram-track sign. The time taken to visualize the longitudinal esophageal section was 21.3 ± 13.1 sec (range 3–60 sec). Conclusions: Direct antenatal visualization of a normal fetal esophagus is feasible, and recommended when suspecting EA on routine fetal ultrasound, to improve diagnostic specificity.

Dynamic esophageal patency assessment: an effective method for prenatally diagnosing esophageal atresia

Esophageal atresia is a major anomaly with a low prenatal detection rate. We propose a sonographic method termed dynamic esophageal patency assessment. This study aimed to assess the feasibility and performance of the dynamic esophageal patency assessment in a high-risk population. A prospective study was conducted in a single tertiary fetal ultrasound unit for 12 months. The study group included pregnant women referred for a targeted scan because of one or more of the following: (1) polyhydramnios; (2) small or absent stomach; (3) vertebral, anal atresia, cardiac, tracheoesophageal fistula, renal, and limb abnormalities; (4) first-degree relative with esophageal atresia; and (5) genetic mutation associated with esophageal atresia. In addition to dynamic esophageal patency assessment, a comprehensive anomaly scan was carried out. The fetal esophagus was observed during swallowing. Cases that demonstrated uninterrupted fluid propagation through the esophagus were classified as normal. Cases that demonstrated interrupted fluid propagation, with the formation of a pouch, were classified as abnormal. Cases with unclear visualization of the esophagus or cases that failed to demonstrate either fluid propagation or a pouch were classified as undetermined. Dynamic esophageal patency assessment results were compared with postnatal findings, considered "gold standard." Test performance indices and intra- and interobserver agreements were calculated. For 12 months, 130 patients were recruited, and 132 fetuses were scanned. The median gestational age (interquartile range) at the time of scan was 31.4 weeks (29.0-35.3). Of 132 fetuses enrolled, 123 (93.2%) were normal, 8 (6%) were abnormal, and 1 (0.8%) was undetermined. Excluded from test performance analysis were 3 cases that were terminated without postmortem autopsy (1 was abnormal and 2 were normal), and a fourth case was excluded as it was classified as undetermined. The detection rate of esophageal atresia was 100%, with no false-positive or false-negative case. Sensitivity, specificity, and positive and negative predictive values of the dynamic esophageal patency assessment were 100%. The Kappa coefficient was 1 for both inter- and intraobserver agreements (P<.0001). The median time (interquartile range) required to complete the dynamic esophageal patency assessment was 6.00 minutes (3.00-13.25). The dynamic esophageal patency assessment is a feasible and highly effective method of ascertaining an intact esophagus and detecting esophageal atresia in suspected cases.

Fetal esophageal imaging: Early pregnancy as a window of opportunity

To describe the sonographic appearance of the fetal esophagus during early pregnancy and evaluate the feasibility of imaging the entire esophageal length. In addition, we present a case of disrupted esophageal continuity, subsequently diagnosed with esophageal atresia (EA). A prospective observational study of 145 patients. During the early second trimester anomaly scan performed at 12-17weeks' gestation the entire esophagus was captured in a single sonographic image at the midsagittal plane (one shot technique). Postnatal follow-up of esophageal patency included review of medical records and telephone interviews. Complete visualization of the esophagus (neck to diaphragm) was possible in 144 cases. In 88% of cases the esophagus was demonstrated by transvaginal approach. The time required to obtain the desired view of the esophagus, once the fetus was in an optimal position, was on average 13s (range: 5-30s). In one case at 15 weeks' gestation, the cervical segment of the esophagus was demonstrated while the lower thoracic segment was not identified. Subsequently EA was diagnosed. It is feasible to demonstrate the entire esophagus during early second trimester anomaly scan. An early second trimester anomaly scan may serve as a window of opportunity for EA screening.

A Simple and Easy Technique for Imaging the Fetal Esophagus in the First, Second, and Third Trimesters Using the Transverse Section of the Esophagus in the Area Behind the Heart as a Reference Point.

To describe and evaluate a simple technique of imaging the fetal esophagus, using the echogenic transverse section of the esophagus in the area behind the heart as a reference point, in all the 3 trimesters of pregnancy. This was a prospective cross-sectional study of ultrasound imaging of the esophagus in 2 groups of patients: the first group comprised women at 18 to 30 weeks' gestation (208 fetuses); the second group comprised women at 11 to 14 weeks' gestation (102 fetuses). Using a 3- to 5-MHz curvilinear transducer, the transverse section of the collapsed esophagus was imaged in the area behind the heart. The probe was rotated 90 degrees to identify the longitudinal section of the esophagus which was then traced along its entire length. This study shows that the collapsed, echogenic, transverse section of the esophagus was persistently seen in the area behind the heart, in more than 99% of fetuses in both the groups. It was a useful starting point to image the longitudinal section of the esophagus in both the groups, particularly in the 18 - 30 week group. Using this technique, the entire length of the esophagus could be traced in 92.3% of 18 - 30 week fetuses and 88.23% of the 11 - 14 week fetuses. A collapsed transverse section of the esophagus was persistently and easily seen as a bright echogenic structure in the area behind the heart in more than 99% of fetuses in all 3 trimesters (in both the groups) and, therefore, was an ideal starting point to begin tracing the esophagus in its longitudinal axis.

Magnetic resonance imaging of the normal fetal esophagus

To establish the appearance on magnetic resonance imaging (MRI) of the normal fetal esophagus and to provide biometric data from 20 to 39 gestational weeks. In this retrospective study of 250 fetal MRI examinations (20-39 gestational weeks) the visibility of the upper (E1, cervical to tracheal bifurcation) and lower (E2, tracheal bifurcation to diaphragm) esophageal segments was assessed separately in each of three section planes. Segments were scored as being visible or not, and whether they were fluid-filled was noted. Maximum esophageal diameters were recorded. To study the age dependency of esophageal visualization, fetuses were divided into three age groups: 20-25, 26-31 and 32-39 weeks. In 19 cases, there were dynamic studies and these were analyzed for the duration of fluid-filling. Segment E1 was visualized only when it was fluid-filled and it was visible in 16.8% of axial, 4% of frontal and 22.4% of sagittal acquisitions. Segment E2 could also be detected in the unfilled state, when it appeared solid; it was seen in 96.4% of axial, 74% of frontal and 39.6% of sagittal acquisitions, being fluid-filled in 62.7-88.9% of these. Depending on the amount of fluid-filling and the gestational age, E2 segments had a variable appearance. Dynamic scans showed E1 segments to be fluid-filled for periods of 0.5-1.5 s and E2 segments for periods of 3-35 s. Both the frequency of visualization and the maximum diameter increased linearly with gestational age. Visualization of the fetal esophagus by MRI depends on section plane, segment and gestational age, with considerable differences between the two segments: while E1 requires fluid-filling related to fetal swallowing, the E2 portion can usually be demonstrated independent of fluid-filling, as a consequence of its topographical relationships. The frequently fluid-filled state of E2 may reflect the immature nature of esophageal neuromuscular activity, and the lack of an anti-reflux mechanism due to the short length of the abdominal esophagus.

Highlights from Recent Cancer Literature

Highlights from Recent Cancer Literature

Fetoscopic Fetal Transesophageal Electrocardiography: A Minimally Invasive Tool for Cardiac Monitoring, Diagnostics, and Intervention in Human Fetuses

Therapy-refractory supraventricular tachycardias commonly result in hydrops and death in human fetuses. Fetal transesophageal electrocardiography may aid in understanding its underlying electrophysiological mechanism and allow stimulation. Percutaneous fetoscopic deployment of an electrode catheter into the fetal esophagus by way of a single trocar was performed in a human fetus and permitted the recording of a fetal transesophageal electrocardiogram at 35 + 6 weeks of gestation. Fetal transesophageal electrocardiography can be achieved in human fetuses by way of a minimally invasive percutaneous fetoscopic approach and carries the potential to improve diagnosis and management of therapy-refractory supraventricular tachycardias in human fetuses.

Expression of PCNA and C-fos proteins in the human fetal esophagus

Expression of PCNA and C-fos proteins in the human fetal esophagus

Identification of some human genes oppositely regulated during esophageal squamous cell carcinoma formation and human embryonic esophagus development

Here we directly compared gene expression profiles in human esophageal squamous cell carcinomas and in human fetal esophagus development. We used the suppression subtractive hybridization technique to subtract cDNAs prepared from tumor and normal human esophageal samples. cDNA sequencing and reverse transcription polymerase chain reaction (RT-PCR) analysis of RNAs from human tumor and the normal esophagus revealed 10 differentially transcribed genes: CSTA, CRNN, CEACAM1, MAL, EMP1, ECRG2, and SPRR downregulated, and PLAUR, SFRP4, and secreted protein that is acidic and rich in cysteine upregulated in tumor tissue as compared with surrounding normal tissue. In turn, genes up- and downregulated in tumor tissue were down- and upregulated, respectively, during development from the fetal to adult esophagus. Thus, we demonstrated that, as reported for other tumors, gene transcriptional activation and/or suppression events in esophageal tumor progression were opposite to those observed during development from the fetal to adult esophagus. This tumor 'embryonization' supports the idea that stem or progenitor cells are implicated in esophageal cancer emergence.

OP09.08: Fetal esophagus: Could the space between trachea and aorta be used in routine sonography?

OP09.08: Fetal esophagus: Could the space between trachea and aorta be used in routine sonography?

Échographie de l'œsophage fœtal : aspect physiologique et application au dépistage anténatal d'une atrésie œsophagienne

The thoracic part of a fetal esophagus is generally overlooked by usual prenatal ultrasonography. However, screening it might improve the detection rate of esophageal malformations for which prenatal diagnosis remains far from accurate. In this article, we describe the technique which makes it possible to get a precise image of a fetal thoracic esophagus in its more sensitive part: between the trachea and the aorta. After describing the appearance of a healthy thoracic esophagus, we will show how this technique can be used for prenatal detection of esophagus malformations. For this purpose, we provide the case report of a prenatal diagnosis of esophagus atresia with esotracheal fistula.

The fetal esophagus: anatomical and physiological ultrasonographic characterization using a high-resolution linear transducer.

To study the sonographic anatomy and physiology of the human fetal esophagus during the mid-trimester of pregnancy using a high-resolution linear transducer. This was a prospective observational study of the fetal esophagus between 19 and 25 weeks' gestation. The study was performed in 60 consecutive fetuses, after a normal anatomy scan, using a 5-13-MHz matrix array wide-band transducer. During the examination the collapsed esophagus was first visualized, and followed by a 5-min video recording in order to demonstrate luminal patency and peristaltic waves. Complete anatomical visualization of the esophagus was possible in 52 (86.7%) patients and at least partial visualization in 58 (96.7%) patients. Three different patterns of esophageal motility were observed: a simultaneous and short opening of the whole esophagus was found in 35 (58.3%) fetuses; a segmental, peristalsis-like movement from the pharynx, through the mediastinum, and into the stomach was found in 18 (30%) fetuses; and in one fetus reflux-like passage of solid contents from the stomach was observed. The mean time required for demonstration of esophageal patency was 96.1 (range, 10-300) s. Demonstration of normal anatomy and physiological activity of the fetal esophagus is feasible using appropriate transducers. The most commonly observed pattern of esophageal motility in the mid-trimester of pregnancy is the simultaneous relaxation of the upper and lower esophageal sphincters with concurrent opening of the esophageal lumen from the upper thorax to the stomach. Demonstration of a patent esophagus may be helpful in fetuses with suspected esophageal atresia.

Studies on transformation of human esophageal fibroblasts mediated by a retroviral vector containing the E6E7 ORFs of human papillomavirus type 16

To study the etiological role of human papillomavirus type 16 (HPV16) infection in the development of esophageal cancers. A recombinant retrovirus containing the E6E7 ORFs of HPV16 was packaged and human fetal esophageal fibroblasts were infected. The tumorigenecity of the fibroblasts was tested in SCID mice in synergy with 12-O-tetradecanoylphorbol-13-acetate (TPA). Human esophageal fibroblasts infected with the recombinant retrovirus induced sarcomas in SCID mice, the existence and expression of E6E7 ORFs was confirmed in the sarcomas. Fibroblasts cultured from the sarcoma were demonstrated heteroploid by cytoflowmetry. However, tumors were not observed in human fetal esophagus infected with such virus. These results revealed that the established recombinant retroviral system can successfully mediate the transference of HPV16 E6E7 genes, and such system is applicable to researches on tumorigenesis of HPV.

The multistage process of carcinogenesis in human esophageal epithelial cells induced by human papillomavirus

To investigate the multistage process of carcinogenesis, the progressive alteration of the morphology, telomerase, cytogenesis, oncogenes and tumorigenicity in the process of immortalization and malignant transformation of the human fetal esophageal epithelial cell (SHEE) was studied. The SHEE cells were immortalized by gene E6E7 of human papilloma virus (HPV) type 18 in our laboratory and continually cultivated over 100 passages, which had been malignantly transformed. Cells at the 11th, 35th, 65th and 100th passage were examined according to the following criteria: morphological changes of cell growth, contact-inhibition and anchorage-independent growth (AIG); the cell proliferative and apoptotic index; the modal number of chromosomes; c-myc, p53, bcl-2, ras; telomere length and activities of telomerase and tumorigenicity in nude mice or severe combined immunodeficient (SCID) mice. The cells of the 11th passage were well differentiated and the cells of 100th passage were relatively poorly differentiated with polymorphism, while the cells of 35th and 65th had two distinct differentiations. The proliferative indexes were 21.1%, 32.5%, 33.2%, and 40.9% and the apoptotic indexes were 3.3%, 2.7%, 3.5%, 2.7% in the 11th, 35th, 65th and 100th passage respectively. Karyotypes of four cell passages belonged to hyperdiploidy and hypotriploidy. C-myc, ras, p53 genes were low in the 10th and 35th, and high in the 65th and 100th passage, but bcl-2 was low in 4 passages. Telomere length sharply decreased from normal fetal esophagus cells until the 35th passage, but it was stably expressed in the 65th and 100th passage. The activities of telomerase were expressed in cells of the 35th, 65th and 100th passages. The efficiency of AIG varied in different passages of the SHEE cell and was absent in the 11th passage, low efficiency in the 35th passage and 65th passage, and high efficiency in the 100th passage. Transplanted cells of the 65th and 100th passage into SCID mice resulted in tumor formation, but only the 100th passage cells could grow in nude mice. All of these characteristic changes were in dynamic progressive process. These data demonstrate that carcinogenesis of esophageal epithelial cells induced by HPV is the multistage process, which goes through the initial, immortal, premalignant and malignant transformation stages. The generation of esophageal carcinoma is caused by the accumulation of cellular, genetic and molecular changes.

The Birth Process Makes the Immature Small Intestine Sensitive to Feeding-Induced Intestinal Disease

Many newborn animals suffer from severe intestinal disease in the immediate postnatal period. We have shown that such disease is particularly prevalent when animals are born prematurely and fed a milk-placer (in stead of mother s colostrum). By feeding a milk-replacer to fetuses in utero and comparing them with corresponding pigs fed ex utero, we tested the hypothesis that the response of the immature intestine to oral feeding depends on the process of birth. Under anaesthesia, eight fetuses in 2 pregnant sows (105-106 d gestation, term = 115 d) were prepared with a feeding tube inserted into the fetal esophagus. After the operation, the fetuses were fed either sow s colostrum (n=4) or a milk-replacer (formula, n=4) for 24 h while in utero (15 ml/kg/3 h). After the 24 h feeding, the operated fetuses were removed from the sows by caesarean section and killed for tissue collection. From these and some other pregnant sows (105-107 d gestation) we also removed some unoperated control fetuses. These were either killed at birth (no feed, n=4) or postnatally after 24 h of feeding (colostrum, n=7, formula, n=8). Results from all 5 treatment groups are shown below.

Telomere and telomerase in the initial stage of immortalization of esophageal epithelial cell.

To search for the biomarker of cellular immortalization, the telomere length, telomerase activity and its subunits in cultured epithelial cells of human fetal esophagus in the process of immortalization. The transgenic cell line of human fetal esophageal epithelium (SHEE) was established with E(6)E(7) genes of human papillomavirus (HPV) type 18 in our laboratory. Morphological phenotype of cultured SHEE cells from the 6th to 30th passages, was examined by phase contrast microscopy, the telomere length was assayed by Southern blot method, and the activity of telomerase was analyzed by telomeric repeat amplification protocol (TRAP). Expressions of subunits of telomerase, hTR and hTERT, were assessed by RT-PCR. DNA content in cell cycle was detected by flow cytometry. The cell apoptosis was examined by electron microscopy (EM) and TUNEL label. SHEE cells from the 6th to 10th passages showed cellular proliferation with a good differentiation. From the 12th to the 16th passages, many senescent and apoptotic cells appeared, and the telomere length sharply shortened from 23kb to 17kb without expression of hTERT and telomerase activity. At the 20th passage, SHEE cells overcame the senescence and apoptosis and restored their proliferative activity with expression of telomerase and hTERT at low levels, but the telomere length shortened continuously to the lowest of 3kb. After the 30th passage cells proliferation was restored by increment of cells at S and G2M phase in the cell cycle and telomerase activity expressed at high levels and with maintenance of telomere length. At the early stage of SHEE cells, telomeres are shortened without expression of telomerase and hTERT causing cellular senescence and cell death. From the 20th to the 30th passages, the activation of telomerase and maintenance of telomere length show a progressive process for immortalization of esophageal epithelial cells. The expression of telomerase may constitute a biomarker for detection of immortalization of cells.

The genetic events of HPV-immortalized esophageal epithelium cells.

We studied cytogenesis, telomere and telomerase, and c-myc, ras, bcl-2, and p53 genes of cells in the progressive process of immortal epithelial cells from embryonic esophagus induced by human papillomavirus (HPV). The SHEE cell line, established by us, consist of immortalized epithelial cells from the embryonic esophagus induced by genes E6E7 of HPV type 18. It was in initial malignant transformation when cultivated over 60 passages without co-carcinogens. Cells of the 10th, 31st, and 60th passages were represented in the progressive process within the immortal period. In these three stages of the cell line, the modal number of chromosome and karyotypes were analyzed. The telomere length was assayed by Southern blot methods, and the telomerase activity was analyzed by hTR and hTERT assay. C-myc, p53, bcl-2, ras genes were assayed by the multi-PCR method. The morphology of the 10th passage cells exhibited good differentiation, the 60th passage cells were relatively poorly differentiated, and the 31st passage cells differentiated in two distinct ways. The growth characteristics of the 31st and 60th passage cells were weakened at contact-inhibition and anchorage-dependent growth. Karyotypes of three cell passages belonged to hyperdiploid and hypotriploid with abnormal chromosomes +1, +3, +7, +9, +17, +18; del(1)(p32); der(4), t(4;?)(q31;?); der(5),t(5;?)(q31;?); der(13),t(13;13)(p11;q11) and others. Bimodal distribution of chromosomes with more aberrant chromosomes appeared in the 31st and 60th passage cells. Telomere length sharply shortened from normal fetal esophagus to the 10th and 31st passage step by step, but was stable from the 31st to the 60th passage and the telomerase activities measured were expressed at late two passages. p53 mutant was positive in three passages, c-myc was positive in the 31st and the 60th passage K-ras only in the last. The results reveal that changes of chromosomes, telomere length, telomerase activity and certain gene expressions are important events of HPV-immortalized esophageal epithelium cells. All of these changes occurred in dynamic progressive process. This cell line may be useful for the elucidation of the genetic mechanism of cellular immortalization.

Fetal esophageal ligation induces expression of vascular endothelial growth factor messenger ribonucleic acid in fetal membranes

Objective: Obstruction of the fetal esophagus does not always produce the expected polyhydramnios. This is because of increased intramembranous absorption of amniotic fluid into the fetal circulation. A possible mediator for this increased absorption is vascular endothelial growth factor (VEGF). The present objective was to explore whether VEGF gene expression and action would be induced in fetal membranes and placentas of ovine fetuses after esophageal ligation. Study Design: Five late-gestation fetal sheep underwent esophageal ligation and 5 served as control animals. On postoperative day 9, amnion, chorion, and placenta were collected for cellular localization and quantitation of VEGF messenger ribonucleic acid by in situ hybridization and Northern blot analysis. Reverse-transcription polymerase chain reaction was used to identify the VEGF molecular forms. Immunostaining with Ki-67 antibody was used to determine the proliferation of vascular endothelium in the fetal membranes and placentas. Results: VEGF messenger ribonucleic acid was localized in amniotic epithelium, chorionic cytotrophoblast, and cytotrophoblast of the placenta. VEGF164 was the major transcript expressed in these tissues. The abundance of VEGF messenger ribonucleic acid in the amnion and chorion, but not in the placenta, was significantly increased in the ligated fetuses in comparison with the control fetuses. The proliferation of the intramembranous blood vessel endothelium was greater in the ligated fetuses than in the control fetuses. Conclusion: The levels of VEGF messenger ribonucleic acid and the proliferation of vascular endothelium in the amnion and chorion increased after fetal esophageal ligation. This provides a possible mechanism for the enhanced intramembranous absorption of amniotic fluid through increased vascularity and permeability of the fetal membranes, thus ameliorating the development of polyhydramnios. We speculate that the signal(s) that mediate the increase in VEGF expression is present in either the fetal urine or the fetal lung secretions, or both. (Am J Obstet Gynecol 2001;184:175-84.)

The Hyperthyroid Fetus and Infant

After completing this article, readers should be able to: 1. Describe the etiology of transient and persistent neonatal hyperthyroidism. 2. Delineate the diagnostic tests for thyroid-stimulating hormone receptor antibodies. 3. Develop a treatment plan for fetal and neonatal hyperthyroidism and a management plan for subsequent pregnancies. 4. Provide guidelines for breastfeeding when the mother is receiving antithyroid medications. 5. Describe the long-term risks of neonatal hyperthyroidism. The first clinical description of neonatal hyperthyroidism was published in 1912, and the discovery of the transplacental passage of thyroid-stimulating immunoglobulins (TSI) provided an understanding for the etiology of this condition in 1964. There were, however, a few cases of persistent neonatal hyperthyroidism, initially described in 1976, that were inconsistent with the transient clinical course expected with a maternally acquired antibody. The etiology of persistent neonatal hyperthyroidism was clarified by the discovery of an activating germ-line mutation in the thyroid-stimulating hormone (TSH) receptor in 1995. When a mother has autoimmune thyroid disease, fetal and neonatal hyperthyroidism result from transplacental passage of TSI. The mother usually has a history of hyperthyroidism, but neonatal hyperthyroidism also has been reported in mothers who have hypothyroidism due to Hashimoto thyroiditis. The clinical status of the mother does not determine the infant’s risk for hyperthyroidism. The mother may have been treated with 131I or a subtotal thyroidectomy in the past and may be euthyroid or she may be receiving thyroid replacement therapy at the time of her pregnancy, but she still can be producing high titers of TSI. In a review of neonatal hyperthyroidism, mothers were clinically hyperthyroid during pregnancy in only 18 of 38 cases (47%). The prevalence of clinical hyperthyroidism in pregnancy has been reported to be 0.1% to 0.4% and is the most common endocrine disorder during pregnancy after diabetes. Clinical fetal and neonatal hyperthyroidism has been reported to occur …

Fetoscopic transesophageal electrocardiography and stimulation in fetal sheep: a minimally invasive approach aimed at diagnosis and termination of therapy-refractory supraventricular tachycardias in human fetuses.

Therapy-refractory supraventricular tachycardia commonly results in hydrops and death in human fetuses. The purpose of this study in fetal sheep was to assess the feasibility of a minimally invasive fetoscopic approach for fetal transesophageal electrocardiography and stimulation aimed at diagnosis and termination of these tachycardias. We studied a total of 10 fetal sheep (87 to 103 days of gestation; term=145 days). We entered the amniotic cavity using a percutaneous fetoscopic approach and placed various electrophysiology catheters into the fetal esophagus. We recorded the number of animals in which fetoscopic transesophageal electrocardiography and stimulation were successful and assessed pacing success and thresholds for different catheters. In addition, we monitored for potential adverse effects from stimulation and for other complications of the operation. Recording of transesophageal electrocardiograms was successful in all fetal sheep. Capture during stimulation was successfully documented by additional fetal bipolar surface electrocardiograms in 7 fetuses. In fetuses in which fetal surface electrocardiograms were not recorded, pacing stimulus artifacts interfered with documentation of capture. Although stimulation thresholds were high, the maternal rhythm was not affected by fetal stimulation. Fetoscopic fetal transesophageal electrocardiography and stimulation are feasible in fetal sheep. This minimally invasive approach might have the potential to improve diagnosis and management of therapy-refractory supraventricular tachycardias in human fetuses.