Introduction
Congenital heart disease (CHD) is the most common fatal congenital anomaly in newborns, representing around one-third of all birth defects.1 Each year, approximately 1.5 million children are affected by CHD.2 Although the prevalence of CHD may remain unchanged, enhancing screening efforts, allocating adequate resources, and implementing effective interventions are essential to improving survival rates and long-term outcomes. Furthermore, mortality has risen in recent decades, particularly in low- and middle-income countries, due to insufficient diagnostic and treatment infrastructure.3
Over the past two decades, advances in imaging technology have significantly improved the prenatal evaluation of fetal cardiovascular structures.4 Most CHD cases can now be detected through obstetric ultrasound, particularly when incorporating four-chamber (4C) and outflow tract views, achieving sensitivities of up to 85%.5,6
Prenatal diagnosis of CHD plays a critical role in parental counseling, multidisciplinary planning of perinatal care, timely referral to tertiary care centers, and potentially improving neonatal outcomes.7 However, despite these advancements, only up to 40% of CHD cases are diagnosed prenatally in routine practice, even in low-risk populations.8 In developing countries, the situation is more challenging due to limited access to qualified clinicians, fetal echocardiography, and referral systems, particularly in remote areas.
Referral for detailed fetal echocardiography is recommended when a cardiac anomaly is suspected, especially if bradycardia or rhythm disturbances are observed.8 Fetal bradycardia, as presented in this case, can be easily misinterpreted as non-specific fetal distress, leading to delayed or missed diagnosis of underlying complex congenital heart disease. Highlighting this misdiagnosis underscores the importance of distinguishing between fetal bradycardia due to conduction abnormalities and true fetal distress in prenatal care. This case report uniquely contributes to the literature by highlighting the diagnostic challenges and clinical significance of fetal bradycardia as an early sign of complex CHD in a resource-limited setting. It underscores the need for heightened awareness and structured referral protocols even in low-resource areas. Additionally, it explores the possible underlying mechanisms linking bradycardia with fetal structural heart defects, supported by detailed case findings and echocardiographic evaluation.
Case Report
A 33-year-old pregnant woman was referred to a tertiary health-care center due to a suspected fetal heart abnormality. One week prior, she had undergone a routine antenatal check-up with a midwife in a local hospital in Sukabumi, West Java, where fetal distress was suspected based on an irregular fetal heart rate. At the local hospital, she denied any obstetric complaints such as labor pains or bloody show. She reported positive fetal movements. Ultrasonography (USG) revealed a single live fetus in cephalic presentation corresponding to 29–30 weeks of gestation based on transverse cerebellar diameter (TCD: 29 weeks 3 days). The fetal heart rate was irregular, the placenta was anteriorly located, estimated fetal weight (EFW) was 1387 grams, and the single deepest pocket (SDP) of amniotic fluid measured 5.67 cm (Figure 1). Cardiotocography (CTG) showed a non-reassuring tracing (Type II). Given the limitations in diagnostic capability and neonatal support at the local facility, the patient was referred to our tertiary center.
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Figure 1 Fetal echocardiography. (A) Biparietal diameter; (B) abdominal circumference; (C) fetal length; (D) cerebellum; (E) thorax appearance; (F) mitral valve abnormality.
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At admission, the patient reported no complaints. Her vital signs were within normal limits. Her pre-pregnancy body weight was 62 kg, current weight 74 kg, and height 145 cm, resulting in a body mass index (BMI) of 35.1 kg/m². Obstetric examination revealed a soft, convex abdomen with a fundal height of 22 cm and abdominal circumference of 95 cm. The fetus was in breech lie with an estimated weight of 1300 grams, and the fetal heart rate ranged between 88–92 beats per minute (bpm).
Obstetric history revealed this was her third pregnancy: her first, 12 years prior, resulted in spontaneous vaginal delivery of a 2300-gram baby in breech presentation; her second was a miscarriage at 5 weeks’ gestation. She is currently in her first pregnancy with her current husband. She had been receiving regular antenatal care with a midwife. There was no relevant maternal medical history, including collagen vascular disease, and no known family history or environmental exposure to teratogens.
Fetal echocardiography revealed multiple congenital cardiac anomalies: atrioventricular septal defect (AVSD), tricuspid regurgitation (peak velocity 70 cm/s), mitral valve abnormalities, suspected aortic and pulmonary artery stenosis, and atrioventricular conduction abnormalities. Additional findings included a 7.5 mm ventricular septal defect (VSD), pericardial effusion, and discordant atrial and ventricular heart rates (atrial: 135 bpm; ventricular: 93 bpm). The cardiothoracic area ratio (CTAR) was 28%, and cardiac axis was 58.9 degrees. Doppler velocimetry results were: umbilical artery pulsatility index (PI) 2.12; middle cerebral artery PI 2.34; right uterine artery PI 0.81; left uterine artery PI 0.63, with no notching observed.
Her final diagnosis was G3P1A1 29 weeks 3 days of pregnancy; breech lie; Fetal congenital heart disease (atrioventricular septal defect, tricuspid regurgitation, mitral valve abnormality, suspect aortic and pulmonary artery stenosis, atrioventricular conduction abnormality). After thorough counseling, the patient wished to continue the pregnancy. She later gave birth to a baby girl at local hospital. Unfortunately, the neonate died from cardiac arrest on the second day of life.
Discussion
Congenital arrhythmias may serve as a vital clue for identifying congenital heart disease (CHD) in fetuses, as demonstrated in this case. CHD remains the most common congenital malformation, affecting approximately 8–9 per 1,000 live births.9 Most cases can now be diagnosed prenatally through obstetric ultrasonography, particularly during detailed fetal anomaly screening at 20–24 weeks gestation.5 Assessment of fetal dysrhythmias is usually based on ultrasound to determine fetal well-being, assess cardiac structures, and define the nature of rhythm disturbance with confidence to decide whether in-utero treatment is needed.5 Examination of the fetal heart and cardiovascular system has evolved considerably over the past 2 decades, mostly as a result of advances in imaging technology. The International Society of Ultrasound in Obstetrics and Gynecology (ISUOG) recommends a standardized fetal cardiac screening protocol, including four-chamber (4C), left and right ventricular outflow tract, and three-vessel views.10
In this case, bradycardia was noted at the first examination and prompted further cardiac evaluation. According to the American College of Obstetricians and Gynecologists (ACOG), fetal bradycardia is defined as a fetal heart rate (FHR) < 110 beats per minute (bpm).11 Persistent bradycardia often indicates conduction abnormalities, such as atrioventricular block (AVB), particularly when associated with structural CHD. The high degree or complete AVB is one of the most dangerous fetal bradyarrhythmias due to increased fetal loss risk. It occurs when the beat of the atria is completely dissociated from the ventricular beat and causes significant bradycardia with an FHR of up to 40–90 bpm. It is common and has two predominant presentations: (1) fetus with normal cardiac structure and exposure to specific maternal autoantibodies (immune-mediated AVB), and (2) AVB can be present in fetuses with complex CHD, like in the case presented.12
Structural heart defects associated with AVB often appear earlier in gestation, commonly before the fifteenth week of gestation. However, it does not mean it will not be detected later, such as in this case. The most frequent cardiac malformations are left atrial isomerism (LAI), congenitally corrected transposition of the great arteries (CC-TGA), atrioventricular septal defect (AVSD) such as in this case, double outlet right ventricle (DORV); and tetralogy of Fallot (TOF).12 These conditions often result from mutations in genes encoding for transcription factors critical for cardiac chamber formation, endocardial cushion remodeling, and conduction system development (ie, Nkx2-5, Tbx5, and Id2).12
In this case, the fetus demonstrated complex CHD, including AVSD, tricuspid regurgitation, mitral valve abnormality, suspected aortic and pulmonary stenosis, and AV conduction abnormality—all visible through the 4C view. The 4C view is fundamental for fetal cardiac screening, as it enables evaluation of cardiac position, size (ideally one-third of the thoracic cavity), contractility, and rhythm. In a normally positioned heart (levocardia), two-thirds of the heart lies on the left side, with an axis angled approximately 45 ± 20 degrees. A deviation in this axis may be associated with chromosomal anomalies, congenital diaphragmatic hernia, or complex CHD—especially conotruncal anomalies and single-ventricle hearts.
This view also allows for detailed morphological and functional assessment of each cardiac chamber and the atrioventricular valves. The left atrium (LA) is normally located most posteriorly (near descending aorta), and the finger-like appendage identifies it. Furthermore, the LA is characterized by the presence of the foramen ovale flap and its connection with the pulmonary veins. The right atrium (RA) has a pyramidal appendage with a broad base and receives the vena cava.8
Despite advances in imaging, prenatal sonographic diagnosis of CHD remains challenging. Accurate diagnosis requires multidisciplinary collaboration among sonographers, obstetricians, radiologists, and specialists in fetal medicine. When a fetus is at high risk for cardiac anomalies or a structural abnormality is suspected during routine obstetric ultrasound—even in low-risk pregnancies—a referral for comprehensive fetal echocardiography is recommended. In many cases, evaluation at a tertiary care center is necessary to thoroughly assess fetal cardiac anatomy, monitor fetal condition, and determine whether in-utero intervention is warranted.13
Intrauterine detection of CHD relies on several factors, such as accessible health care. Libermann et al originally highlighted delays in CHD detection in non-tertiary settings due to limited fetal cardiology services.13 Compared to a decade ago, some improvements in the availability of prenatal diagnostic tools have been made in rural areas, including the use of portable ultrasound and telehealth services; however, significant disparities remain. Although even in most developed areas, detection rates are low, distant access might aggravate this condition, thus causing detection rates in less developed areas even lower, such as in this case. The sonographer’s expertise in the assessment of the fetal heart also played a role in the diagnosis of CHD. A high proportion of CHD without prenatal diagnosis is seen in patients who underwent several ultrasounds that only report the fetal heart rate without assessing the fetal heart anatomy.
In this case, although multiple routine ultrasounds were performed, earlier signs of CHD may have been missed. Literature suggests that many undetected CHD cases result from fetal ultrasounds reporting only the FHR without anatomical assessment. A structured approach using both 4C and outflow tract views improves detection rates to 70–85%.6 However, access remains limited in remote regions, and CHD continues to be underdiagnosed during routine prenatal care.
Referral to a tertiary center is crucial when CHD is suspected, both for detailed fetal echocardiography and to plan delivery at a facility equipped for neonatal cardiac care. In this case, delayed diagnosis and lack of early referral limited the available perinatal options. Delivery in or near a tertiary center is recommended for patients requiring early intervention, of which many can be identified in advance.
Conclusion
Fetal bradycardia may serve as an early sign of congenital heart disease (CHD), emphasizing the importance of detailed prenatal cardiac evaluation. This case underscores the need for improved access to fetal cardiac screening and trained personnel, particularly in rural settings. Expanding anatomical assessments and strengthening referral systems to tertiary centers can support earlier diagnosis and better perinatal outcomes.
Ethical Approval
No formal ethical clearance was required for the publication of this case. The authors confirm that written informed consent for publication of this case report and any accompanying images were obtained from the patient and her spouse. The patient was informed in detail about the case content and agreed to its publication. All personal identifiers have been removed to ensure patient anonymity.
Informed Consent Patient Statement
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. The patient(s) has been informed about the details of the case and has provided approval for the information to be published in this case report (series). A copy of the written consent is available for review by the Editor upon request.
Patient’s Perspective
After learning about the possible abnormalities in my fetus, I chose to continue with the pregnancy because I believed it was the best decision for me and my family. I felt that my pregnancy was progressing well, despite concerns about the fetus’s condition. I trusted that I could handle this situation. After being informed about the possible heart abnormalities in the fetus, I felt anxious, but I chose not to follow up with the doctor at the tertiary health-care facility because I felt I had received enough explanation. I decided to deliver my baby at the hospital closest to my home, hoping everything would go smoothly. However, a few days after giving birth, I was devastated and felt a profound loss when my baby passed away. I feel sad and confused, but I am trying to come to terms with this reality.
Registration of Research Studies
Registration of research is not applicable in our case.
Author Contributions
LR and ASN conceived the design in article and collected the data. LR and ASN wrote the draft. JSC and AP directed and supervise the review article. All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Funding
The study did not receive external funding.
Disclosure
The authors declare that they have no competing interests in this work.
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