Presenter Status
Fellow
Abstract Type
Case Report
Primary Mentor or Principal Investigator
Maria Kiaffas
Presentation Type
Poster
Start Date
20-5-2026 11:00 AM
End Date
20-5-2026 12:00 PM
Abstract Text
Background:
Fetal ventricular tachycardia (VT) is an exceptionally rare diagnosis, comprising of 1-2% of fetal arrhythmias, and can precipitate fetal demise via heart failure, polyhydramnios, and nonimmune hydrops fetalis. We present a case of fetal ventricular tachycardia in a structurally normal heart associated with fetal cardiac dysfunction and atrioventricular valve insufficiency.
Case Description:
A 40-year-old G5P2 female was re-referred to fetal cardiology at 31 weeks gestational age (GA) due to concern of pathologic fetal tachycardia. Family history was negative for cardiac disease or arrhythmias. The fetus was initially evaluated by fetal echocardiography at 29 weeks GA due to maternal type II diabetes mellitus. The echocardiogram showed normal anatomy, function, and normal fetal heart rate for GA. The study at 31 weeks demonstrated fetal tachycardia at 176-190 beats per minute (bpm) with atrioventricular dissociation and a ventricular rate (180 bpm) higher than the atrial (140 bpm), consistent with a diagnosis of fetal VT. This study also demonstrated cardiomegaly with moderate biventricular dysfunction, mild to moderate tricuspid regurgitation, and trivial mitral regurgitation. The mother was started on intravenous magnesium sulfide and within the next 24 hours conversion to sinus rhythm was achieved with improvement in cardiac function and valvar insufficiency. Propranolol 60 mg tid was added once function improved. Diagnostic workup for fetal myocarditis, long QT, and autoimmune disease were unrevealing. Following initiation of therapies, serial fetal echoes showed sustained sinus rhythm with persistently mildly depressed function. The fetus was ultimately delivered at 37 weeks and 2 days GA. Postnatal echocardiogram showed normal structure and function, postnatal electrocardiogram was normal, and the infant demonstrated no arrhythmia after monitoring in the neonatal intensive care unit and on ambulatory Holter monitoring. Symptom driven exome sequencing was performed and was non-diagnostic.
Discussion:
Fetal VT is a rare entity that can lead to low cardiac output, fetal hydrops, and fetal demise. It is most often associated with fetal myocarditis, cardiac tumors, structural heart disease, and congenital long QT syndrome. M-mode and inflow-outflow fetal rhythm evaluation revealing atrioventricular dissociation with higher ventricular mechanical activity compared to the atrial activity is the diagnostic hallmark. Treatment typically consists of maternal magnesium and antiarrhythmics, most commonly beta blockers; IVIG and dexamethasone may also be utilized if infectious or autoimmune myocarditis is suspected. The infant had no evidence of arrhythmia or impaired function after delivery. Diagnostic evaluation for congenital arrhythmia, autoimmune, and infectious processes were negative.
Conclusions:
Fetal ventricular tachycardia is exceedingly rare amongst fetal tachyarrhythmias and can result in impaired cardiac function and ultimately fetal demise. The most common etiologies are congenital arrythmia (ie. Congenital Long QT Syndrome), maternal autoimmune disease, fetal infectious myocarditis, and structural heart disease. In the absence of structural heart disease, long QT syndrome or myocardial disease, prompt diagnosis and management usually result in a favorable outcome.
A Case of Rare Fetal Tachycardia
Background:
Fetal ventricular tachycardia (VT) is an exceptionally rare diagnosis, comprising of 1-2% of fetal arrhythmias, and can precipitate fetal demise via heart failure, polyhydramnios, and nonimmune hydrops fetalis. We present a case of fetal ventricular tachycardia in a structurally normal heart associated with fetal cardiac dysfunction and atrioventricular valve insufficiency.
Case Description:
A 40-year-old G5P2 female was re-referred to fetal cardiology at 31 weeks gestational age (GA) due to concern of pathologic fetal tachycardia. Family history was negative for cardiac disease or arrhythmias. The fetus was initially evaluated by fetal echocardiography at 29 weeks GA due to maternal type II diabetes mellitus. The echocardiogram showed normal anatomy, function, and normal fetal heart rate for GA. The study at 31 weeks demonstrated fetal tachycardia at 176-190 beats per minute (bpm) with atrioventricular dissociation and a ventricular rate (180 bpm) higher than the atrial (140 bpm), consistent with a diagnosis of fetal VT. This study also demonstrated cardiomegaly with moderate biventricular dysfunction, mild to moderate tricuspid regurgitation, and trivial mitral regurgitation. The mother was started on intravenous magnesium sulfide and within the next 24 hours conversion to sinus rhythm was achieved with improvement in cardiac function and valvar insufficiency. Propranolol 60 mg tid was added once function improved. Diagnostic workup for fetal myocarditis, long QT, and autoimmune disease were unrevealing. Following initiation of therapies, serial fetal echoes showed sustained sinus rhythm with persistently mildly depressed function. The fetus was ultimately delivered at 37 weeks and 2 days GA. Postnatal echocardiogram showed normal structure and function, postnatal electrocardiogram was normal, and the infant demonstrated no arrhythmia after monitoring in the neonatal intensive care unit and on ambulatory Holter monitoring. Symptom driven exome sequencing was performed and was non-diagnostic.
Discussion:
Fetal VT is a rare entity that can lead to low cardiac output, fetal hydrops, and fetal demise. It is most often associated with fetal myocarditis, cardiac tumors, structural heart disease, and congenital long QT syndrome. M-mode and inflow-outflow fetal rhythm evaluation revealing atrioventricular dissociation with higher ventricular mechanical activity compared to the atrial activity is the diagnostic hallmark. Treatment typically consists of maternal magnesium and antiarrhythmics, most commonly beta blockers; IVIG and dexamethasone may also be utilized if infectious or autoimmune myocarditis is suspected. The infant had no evidence of arrhythmia or impaired function after delivery. Diagnostic evaluation for congenital arrhythmia, autoimmune, and infectious processes were negative.
Conclusions:
Fetal ventricular tachycardia is exceedingly rare amongst fetal tachyarrhythmias and can result in impaired cardiac function and ultimately fetal demise. The most common etiologies are congenital arrythmia (ie. Congenital Long QT Syndrome), maternal autoimmune disease, fetal infectious myocarditis, and structural heart disease. In the absence of structural heart disease, long QT syndrome or myocardial disease, prompt diagnosis and management usually result in a favorable outcome.
Comments
Poster Board Number: 1