Introduction

Fetal congestive heart failure (CHF) is characterised by inadequate cardiac output and venous congestion in the fetus. Diagnosis is primarily based on fetal echocardiography, which assesses cardiac structure and function and identifies signs such as cardiomegaly, atrioventricular valve regurgitation, ventricular dysfunction, venous congestion (e.g. abnormal Doppler waveforms in the ductus venosus and umbilical vein), fetal oedema, effusions, and hydrops fetalis. The presence of hydrops (generalised fetal oedema) is a key indicator of advanced heart failure but typically represents a late-stage manifestation of the disease.

The Cardiovascular Profile Score (CVPS) integrates five echocardiographic parameters: hydrops, venous Doppler flow, heart size, cardiac function, and arterial Doppler, to quantify the severity of heart failure and aid in prognosis [1-5].

The American Heart Association (AHA) recommends a comprehensive fetal echocardiographic assessment, including evaluation of ventricular function (e.g. myocardial performance index), Doppler analysis of venous and arterial flows, and assessment of secondary signs such as oligohydramnios and preferential redistribution of blood flow to vital organs (brain-sparing effect) [5]. The American Society of Echocardiography (ASE) further emphasises the importance of identifying arrhythmia-related haemodynamic compromise and using Doppler and structural imaging to assess for fetal heart failure and hydrops [5].

This review aims to consolidate existing literature and clinical guidelines, highlighting the importance of echocardiographic monitoring, maternal-fetal risk factors, and evolving therapeutic strategies including pharmacologic and procedural interventions.

Role of artificial intelligence in prenatal CHF detection

In prenatal cardiac ultrasound, artificial intelligence (AI) should be framed as an intelligent assistant (IA) rather than a replacement for sonographers or fetal cardiologists. Machine-learning and deep-learning tools can support acquisition by recognising whether standard cardiac planes have been obtained, providing real-time on-screen guidance to optimise sweep angle and image quality, and prompting additional views when structural CHD, abnormal cardiac size, valve regurgitation, hydrops, or venous congestion is suspected [6, 7].

For suspected fetal CHF, the most clinically relevant applications are automated or semiautomated quantification of cardiothoracic ratio, chamber dimensions, ventricular function, atrioventricular valve regurgitation, effusions, placental thickness, and Doppler waveforms, including ductus venosus, umbilical venous/arterial flow, and rhythm-related M-mode or Doppler timing. By integrating these measurements with gestational age, maternal risk factors, arrhythmia data, and serial CVPS trends, AI-based decision support could alert the operator to deviations from normal, standardise documentation, increase confidence during screening, and triage cases requiring tertiary fetal cardiology review [6-8]. At present, these systems should be regarded as adjunctive quality-control and risk-stratification tools; final diagnosis and management remain dependent on expert echocardiographic interpretation.

Clinical presentation by trimester

First trimester

Fetal CHF is rare in early gestation (up to 13 weeks and 6 days) but may be associated with increased nuchal translucency (NT), prompting early cytogenetic evaluation to rule out chromosomal abnormalities such as Down syndrome, Turner syndrome, and Noonan syndrome. It is important to note that increased NT is a non-specific marker and may reflect a variety of genetic conditions, often independent of CHF [9-14].

Key echocardiographic findings during the first trimester may include impaired myocardial contractility, atrioventricular valve regurgitation, cardiomegaly, and abnormal venous Doppler flow patterns, such as a reversed a-wave in the ductus venosus. These findings are often associated with underlying structural heart defects, fetal arrhythmias, or severe extracardiac anomalies.

Diagnosis at this stage is challenging due to the small size of the fetal heart. Early signs of heart failure may include tricuspid regurgitation, abnormal ductus venosus flow, and indicators of myocardial dysfunction. These functional impairments can be quantified using advanced parameters such as the myocardial performance index and isovolumetric relaxation time [9-14].

Second trimester

Fetuses with normal first-trimester findings may develop signs of CHF during the second trimester, typically between 14 and 27 weeks of gestation. Key echocardiographic features during this period include cardiomegaly, atrioventricular valve regurgitation, venous congestion, and evolving signs of hydrops. CHF in the second trimester often represents a final common pathway of diverse fetal conditions, including structural heart disease with obstruction or insufficiency, arrhythmias, cardiomyopathy or myocarditis, high-output states, and extracardiac compression. If left uncorrected, these conditions are associated with a significantly increased risk of fetal demise [15-17].

Second-trimester echocardiographic assessment may reveal ventricular systolic and/or diastolic dysfunction, atrioventricular valve regurgitation, increased pulsatility in the ductus venosus and umbilical vein, and cardiomegaly, indicated by an elevated cardiothoracic ratio. As the condition progresses, fetal oedema, serous effusions, and oligohydramnios may develop, culminating in hydrops fetalis.

The CVPS, which incorporates five echocardiographic parameters associated with perinatal outcome, is particularly useful during the second trimester, to standardise assessment and monitor disease progression across various aetiologies [1, 2]. Early detection is essential because timely, aetiology-specific interventions, such as transplacental antiarrhythmic therapy for tachyarrhythmias, relief of obstructive lesions in select centres, or management of high-output states, can reverse heart failure and reduce the risk of hydrops [18, 19].

Third trimester

A fetus with normal ultrasound findings in the first and second trimesters may develop signs of CHF for the first time during the third trimester, and in some cases, even near term.

Gestational age influences the presentation and detection of CHF due to the maturation of fetal haemodynamics, changes in the visibility of sonographic signs, and the range of available in utero versus perinatal interventions.

In the third trimester, fetal CHF typically presents with cardiomegaly, atrioventricular valve regurgitation, systolic and/or diastolic dysfunction, and signs of venous congestion on Doppler studies – particularly increased pulsatility in the ductus venosus and umbilical vein. These changes may initially occur without fluid accumulation in the fetal skin or serous cavities. However, as CHF progresses, hydrops fetalis may develop, characterised by effusions, skin oedema, placentomegaly, and polyhydramnios or oligohydramnios, all of which are associated with a worsening prognosis.

Diagnostic considerations focus on identifying the underlying aetiology, including structural cardiac obstruction or insufficiency, arrhythmias, myocardial disease, high-output states (e.g. fetal anaemia or arteriovenous malformations), and extracardiac compression. The AHA emphasises serial fetal echocardiography to monitor evolving valvular lesions, myocardial dysfunction, arrhythmias, and ductal constriction due to the high risk of progression to hydrops or fetal demise [19].

When hydrops is present or suspected, the Society for Maternal-Fetal Medicine recommends a comprehensive diagnostic workup that includes a detailed fetal echocardiogram, anatomical survey, and targeted maternal laboratory evaluations (e.g. blood type and antibody screen, complete blood count, parvovirus B19, syphilis; consider CMV and toxoplasmosis). Measurement of the middle cerebral artery peak systolic velocity (MCA-PSV) is critical in evaluating anaemia-related, high-output hydrops [20].

In cases without hydrops, management focuses on aetiology-specific therapy and close surveillance. This may include transplacental antiarrhythmic treatment for sustained tachyarrhythmias or atrioventricular block, intrauterine transfusion for anaemia (according to institutional protocols), consideration of fetal intervention for selected obstructive lesions, and careful planning of delivery timing and location in the event of clinical deterioration.

If hydrops is present, the threshold for inpatient monitoring and expedited delivery is significantly lower. According to the AHA, hydrops is a grave prognostic sign. When a reversible cardiac aetiology is identified and gestational age is appropriate, delivery with immediate access to neonatal cardiovascular support should be considered [19-22].

Gestational age-specific differences in CHF presentation are clinically significant. In the first trimester, overt CHF without hydrops is rare and typically presents with nonspecific findings; reassessment in the second trimester is generally recommended [19]. In the second trimester, CHF is more often detected prior to the development of hydrops, and reversal is most achievable with targeted treatment. In the third trimester, CHF more frequently progresses to hydrops, often with marked venous Doppler abnormalities. Management therefore emphasises intensive monitoring and delivery planning at specialised tertiary care centres, alongside aggressive treatment of reversible causes such as ductal constriction, arrhythmias, and autoimmune atrioventricular block [23-25]. Symptoms of fetal congestive heart failure are presented in Table 1 (Clips: 1-5, Photos: 1-3).

Aetiology

The aetiology and pathomechanisms of fetal CHF are heterogeneous (Table 2), encompassing a wide range of structural, functional, and extracardiac conditions. The categories include the following: structural heart disease, myocardial disease, fetal arrhythmias, high-output states, vascular causes, and extracardiac causes.

Structural heart disease

These include atrioventricular or semilunar valve regurgitation or stenosis, ventricular outflow tract or aortic arch obstruction, restrictive or closed foramen ovale, premature ductal closure, and cardiac tumours affecting inflow or outflow. Such defects may lead to progressive ventricular dilation, systolic or diastolic dysfunction, and eventual hydrops fetalis.

Myocardial disease

This includes primary cardiomyopathies (dilated or hypertrophic), myocarditis, endocardial fibroelastosis (often associated with maternal anti-Ro/La antibodies), and ischaemic injury. These conditions can result in both diastolic and systolic dysfunction, frequently progressing to fetal heart failure and hydrops.

Fetal arrhythmias

Sustained fetal tachyarrhythmias, complete atrioventricular block with a low ventricular rate, and other rhythm abnormalities can significantly reduce cardiac output, contributing to the development of CHF.

High-output states

Conditions such as severe fetal anaemia, large arteriovenous shunts (e.g. sacrococcygeal teratoma, hepatic haemangioma), and twin-to-twin transfusion syndrome impose increased circulatory demand, often resulting in progressive cardiomegaly, cardiac decompensation, and failure.

Vascular causes

Absent ductus venosus with abnormal intra-abdominal umbilical venous drainage to the IVC, right atrium, SVC, or azygos vein may cause fetal volume overload and congestive heart failure. Similar signs may occur in cases of intra-abdominal umbilical vein varix, particularly when associated with an umbilical artery-to-umbilical vein arteriovenous malformation.

Extracardiac causes

These include rare causes such as fetal hypertension (e.g. midaortic syndrome), thoracic masses or large pleural effusions causing cardiac compression, and pulmonary venous hypertension. These factors can compromise preload or afterload and trigger cardiac failure with or without hydrops [26-28].

Treatment approaches

Pharmacologic management

Transplacental digoxin is the most commonly cited pharmacologic agent for improving signs of fetal heart failure, particularly in cases involving arrhythmia or myocardial dysfunction. However, evidence supporting its efficacy remains limited in quality, as noted in scientific statements from the AHA [19, 29-31].

In pregnancies positive for anti-Ro/La antibodies, prophylactic use of hydroxychloroquine is supported by observational data. When fetal myocarditis or early atrioventricular (AV) block is suspected, maternal treatment with corticosteroids and/or intravenous immunoglobulin (IVIG) may be considered, although the efficacy and safety of these interventions remain uncertain.

The American College of Cardiology (ACC), AHA, and Heart Failure Society of America (HFSA) recommend modifying maternal heart failure (HF) treatment regimens during pregnancy to avoid fetotoxic agents. While medications such as diuretics, hydralazine, and nitrates may be administered to the mother when needed for maternal indications, they are not considered direct therapies for fetal heart failure [30].

In cases of fetal thyrotoxicosis associated with tachyarrhythmia and heart failure, maternal antithyroid therapy (e.g. methimazole) is the standard of care. Additional rate control or antiarrhythmic agents may be used as clinically indicated. Sustained fetal arrhythmias contributing to heart failure should be treated transplacentally, in accordance with AHA guidance on fetal arrhythmia management. In this setting, digoxin may also be used to support cardiac function.

The potential adverse effects of digoxin in the setting of fetal therapy are largely dose-dependent, may occur in both the mother and fetus, and can be influenced by the underlying fetal condition.

Maternal toxicity and electrocardiographic (ECG) changes: Common side effects include nausea, vomiting, anorexia, fatigue, sinus bradycardia, and first-degree AV block. At higher serum levels, more severe toxicities such as advanced AV block and proarrhythmias may occur. These adverse effects typically correlate with maternal serum digoxin levels (digoxinemia) exceeding 2.0 ng/ml and usually resolve with dose reduction. The AHA lists sinus bradyarrhythmia, AV block, and proarrhythmia among the key toxicities. Notably, PR interval prolongation and ST segment depression on ECG are recognised as expected pharmacological effects of digoxin and do not necessarily indicate toxicity. The US Food and Drug Administration (FDA) notes that digoxin crosses the placenta and recommends neonatal monitoring for signs of toxicity [19, 29-34].

Fetal and neonatal toxicity: Documented adverse effects include fetal bradycardia, AV block, and proarrhythmia, as well as postnatal vomiting and arrhythmias resulting from transplacental exposure. In cases where direct intramuscular fetal administration is used, procedural risks such as sciatic nerve injury or skin laceration may occur. The AHA further highlights that digoxin transfer is reduced in hydropic fetuses, which may limit efficacy and lead to maternal dose escalation without a corresponding fetal response [19, 29-34].

Condition-specific cautions:

• Autoimmune-associated AV block (anti-Ro/SSA or anti-La/SSB antibodies): Digoxin may worsen conduction abnormalities; it should be avoided or used with extreme caution in cases of high-degree block, as noted by the AHA.
• Maternal hyperthyroidism or fetal thyrotoxicosis: Management may require alternative antiarrhythmic agents. Digoxin toxicity can be masked or fluctuate with thyroid hormone status, necessitating close monitoring of serum levels and cardiac rhythm.

1. Hypertensive disorders and diabetes: Although no direct contraindication exists, altered maternal renal function may increase serum digoxin levels and toxicity risk. In addition, drug-drug interactions (e.g. with b-blockers or calcium-channel blockers) can increase the likelihood of advanced AV block, according to FDA labelling [19, 29-34].

Therapeutic range and monitoring: The AHA recommends maintaining maternal serum digoxin levels between 0.7 and 2.0 ng/ml, although some experts support targets of up to 2.5 ng/ml during pregnancy. The risk of toxicity rises with levels above this range. Blood levels should be drawn at least 6 hours post-dose to ensure accuracy. Due to impaired placental transfer in cases of fetal hydrops, higher maternal dosing may not achieve therapeutic fetal concentrations and may disproportionately increase the risk of maternal toxicity [19, 29-34].

Nonpharmacologic and procedural interventions

Optimal management of fetal CHF extends beyond pharmacologic therapy and involves a comprehensive, multidisciplinary, and gestational age-specific approach. Key strategies include the following:

• CVPS and Doppler surveillance to monitor fetal hemodynamic status.
• Optimisation of maternal oxygenation and positioning to support fetal perfusion.
• Early referral to a tertiary fetal cardiology canter for specialised evaluation.
• Delivery planning at a facility with advanced cardiac and neonatal intensive care capabilities.

In selected cases involving critical lesions, in utero catheter-based or needle-guided interventions may be considered at experienced centres. These include procedures such as relief of inflow or outflow obstruction or pericardial/pleural fluid drainage, which may prevent the progression to hydrops fetalis. As described by Bullard and Harris [27], there is a strong physiological rationale for fetal surgical intervention in conditions such as congenital cystic adenomatoid malformation (CCAM), pulmonary sequestration, fetal pleural effusions, and sacrococcygeal teratoma (SCT).

The AHA emphasises that prenatal diagnosis combined with coordinated perinatal management significantly improves outcomes in fetuses at risk for heart failure [19].

Condition-specific interventions

Fetal arrhythmia-mediated heart failure

This requires intensive rhythm monitoring. Inpatient observation is recommended for sustained tachyarrhythmias or AV block complicated by hydrops. If arrhythmias are refractory or decompensation occurs despite transplacental therapy, delivery planning should be initiated. The AHA recommends close haemodynamic surveillance with prompt escalation to procedural or delivery strategies in deteriorating cases.

High-output states

Definitive procedural interventions are central to nonpharmacologic care. These include the following:

• Fetoscopic laser ablation for twin-to-twin transfusion syndrome (detailed discussion is beyond the scope of this review).
• Intrauterine transfusion for fetal anaemia.
• Interventional management of large arteriovenous shunts or placental chorioangiomas.
• Thoracentesis or shunt placement for large thoracic effusions causing cardiac compression.

Maternal contributors

Addressing maternal factors is essential. This includes the following:

• Immediate cessation of NSAIDs or COX inhibitors that may induce ductal constriction.
• Optimisation of maternal glycaemic control and thyroid function.
• Management of maternal haemodynamics, while avoiding interventions that reduce uteroplacental perfusion.

A multidisciplinary cardio-obstetric team with regular maternal-fetal assessments is strongly recommended by the ACC/AHA/HFSA for pregnancies complicated by heart failure.

Delivery planning

Timing and mode of delivery should be guided by clinical status. In cases of progressive hydrops, deteriorating cardiovascular profile, or non-reassuring fetal testing despite maximal in utero management, expedited delivery at a centre equipped for neonatal cardiac support is advised. Vaginal delivery is generally preferred unless obstetric or fetal haemodynamic factors necessitate caesarean section, in accordance with AHA guidance on peripartum cardiac care [19, 26-28].

Pharmacological and non-pharmacological treatment attempts in cases of fetal congestive heart failure are presented in Table 3.

Future directions

Despite advances in fetal echocardiography and transplacental pharmacotherapy, fetal CHF remains a complex and high-risk condition with limited therapeutic success. Future research should prioritizes the following:

• Early biomarkers for prehydropic CHF detection (e.g. circulating maternal markers, AI-based pattern recognition in fetal Doppler or biometry) [8, 30].
• Standardisation of cardiovascular profile scoring across centres to unify assessment and prognosis [2, 5].
• Optimisation of transplacental drug delivery, particularly in hydropic fetuses where placental transfer is impaired [4, 34].
• Randomised controlled trials for pharmacologic agents like digoxin, steroids, or sirolimus, with maternal-fetal outcomes as endpoints [6, 29].
• Expanded use of AI/IA tools to integrate echocardiographic data, clinical history, maternal factors, structural findings, Doppler patterns, and arrhythmia information for earlier diagnosis, standardised documentation, and risk stratification [6-8].
• Expanded use of AI in integrating echocardiographic data, clinical history, and maternal factors to aid early diagnosis and risk stratification [7].
• Fetal surgery registries and interventional protocols, especially for cardiac tumours and high-output states causing hydrops [27, 35].
• Collaborative multicentre studies will be essential to advance both diagnostic precision and treatment efficacy, ultimately improving survival and neurological outcomes in affected fetuses [36, 37].
• A growing area of interest is the use of speckle tracking echocardiography (STE) to monitor subtle subclinical changes in fetal myocardial function. In a 2022 study, Murlewska et al. [38] demonstrated that longitudinal surveillance with speckle tracking could provide valuable insight into the evolving course of fetal heart failure.

Disclosures

Ethical considerations: none.

This research received no external funding.

The authors declare no conflict of interest.

References