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Fetal Supraventricular Tachycardia: Histologic Evidence of Accessory Pathways Due to Incomplete Annulus Fibrosus
Michael K Fritsch1, Nina Gotteiner2, Jamaal A Rehman3
1Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Summary
Fetal supraventricular tachycardia (SVT) may stem from disruptions in the annulus fibrosus, a key cardiac structure. This study found thinning or absence of the annulus fibrosus in fetuses with SVT, suggesting a cause for these arrhythmias.
Area of Science:
- Cardiology
- Fetal Medicine
- Pathology
Background:
- Atrioventricular (AV) reentrant tachycardia is a common fetal and neonatal supraventricular tachycardia (SVT).
- Refractory dysrhythmia can lead to fetal hydrops and demise.
- Accessory pathways are documented in adults and children, but not histologically in fetuses with SVT.
Purpose of the Study:
- To investigate the histology of accessory pathways in human fetuses with SVT.
- To explore potential causes of refractory fetal SVT and hydrops.
Main Methods:
- Case series of 2 fetuses with a history of SVT and fetal hydrops.
- Examination of the cardiac conduction system and atrioventricular junction.
Main Results:
- Cardiac conduction system examination was unremarkable in both cases.
- Atrioventricular junction revealed focally thinned or discontinuous annulus fibrosus.
- Direct continuity between atrial and ventricular myocardium was documented in one case.
Conclusions:
- Thinning or absence of the annulus fibrosus is a feature of fetal SVT.
- Defective annulus fibrosus formation may lead to aberrant AV connections, causing arrhythmias.
- This provides a potential explanation for refractory fetal SVT and hydrops.
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