Elsevier

Journal of Electrocardiology

Volume 41, Issue 2, March–April 2008, Pages 116.e1-116.e6
Journal of Electrocardiology

Clinical Diagnosis
Magnetocardiography in the evaluation of fetuses at risk for sudden cardiac death before birth

https://doi.org/10.1016/j.jelectrocard.2007.12.010Get rights and content

Abstract

Background

We hypothesized that fetuses at risk for sudden death may have abnormal conduction or depolarization, ischemia, or abnormal heart rate variability (HRV) detectable by magnetocardiography.

Methods

Using a 37-channel biomagnetometer, we evaluated 3 groups of fetuses at risk for sudden death: group 1, critical aortic stenosis (AS); group 2, arrhythmias; and group 3, heart failure and in utero demise. Five to 10 recordings of 10-minute duration were recorded, and signal was averaged to determine rhythm, conduction intervals, HRV, and T-wave morphology.

Results

In group 1, 2 of 3 had atrial and ventricular strain patterns. In (n = 53) group 2, 15% had prolonged QTc and 17% had T-wave alternans (TWA). Of 23 group 2 fetuses with atrioventricular block, 74% had ventricular ectopy, 21% had junctional ectopic tachycardia, and 29% had ventricular tachycardia. Group 3 (n = 2) had abnormal HRV and TWA.

Conclusion

Repolarization abnormalities, unexpected arrhythmias, and abnormal HRV suggest an arrhythmogenic mechanism for “sudden cardiac death before birth.”

Introduction

During a given lifetime, the highest likelihood of death is during the 40 weeks preceding birth. The mortality of human fetuses more than 20 weeks of gestation ranges from 6 per 1000 individuals per year for all races to 12/1000 per year for African Americans.1 Fetal losses increase with advancing maternal age.2 Whereas some fetal demise is attributable to uteroplacental insufficiency, fetal defects, or chromosomal anomalies, the deaths of many fetuses are unexplained.

Even the exact cause of death in fetuses at the greatest risk of sudden death before birth—those with arrhythmia, structural heart defects, and severe heart failure—is not known. Many of these fetuses have an abnormal electrophysiologic substrate, such as repolarization abnormalities, or conduction system disease that is well known in newborn and infant. We speculate that many such fetuses succumb to the same arrhythmias that occur after birth. Thus, the fetus with complete atrioventricular (AV) block may die of ventricular tachycardia (VT) or ventricular arrest, the fetus with Wolff-Parkinson-White syndrome may succumb to atrial fibrillation that has degenerated to ventricular fibrillation, or in the fetus with severe heart failure and structural cardiac defects, the combination may lead to ischemia and ventricular fibrillation.3, 4, 5, 6 Alternatively, the conditions unique to pregnancy, such as mild hypomagnesemia, or the hormonal effects may alter cardiac ion channels in these high-risk fetuses, adding to the a priori risk for abnormal conduction or repolarization.

Using magnetocardiography—a noninvasive technique that allows beat-to-beat analysis over many hours of fetal cardiac activity—it is possible to evaluate the electrophysiology of fetuses at the highest risk for sudden death. We hypothesized that the fetal magnetocardiography (fMCG) of such fetuses would manifest unsuspected conduction system disease or arrhythmia, repolarization abnormalities, or abnormal heart rate (HR) variability. This report summarizes our data, some of which have previously been published.7, 8, 9

Section snippets

Patient population

We reviewed the clinical records, echocardiograms, and magnetocardiograms of all fetuses referred to the Biomagnetism Laboratory at the University of Wisconsin-Madison (Madison, WI) between 1996 and 2007. Subjects were divided into 3 groups, based on the indication for magnetocardiography (Table 1). Fetuses in group 1 had aortic stenosis; fetuses in group 2 had arrhythmias—1:1 reciprocating supraventricular tachycardia [SVT], ventricular tachycardia [VT], sinus bradycardia, nonconducted

Clinical outcome

Outcomes are presented in Table 3.

Fetuses in group 3 died shortly after the fMCG (at 34 and 23 weeks) in severe heart failure with CVPS of 5/10. One had severe dilated cardiomyopathy and the other critical aortic stenosis with tricuspid valve dysplasia and severe tricuspid valve insufficiency. All fetuses in groups 1 and 2 were born alive. After delivery, infants were observed in the neonatal intensive care unit and received treatment based on the recommendations of the referring cardiologist.

Discussion

The data from this study suggest that some fetuses with SVT, VT, or structural cardiac defects have repolarization abnormalities, unsuspected arrhythmias, and abnormal HR variability. These fetuses frequently have a suboptimal outcome such as neonatal pacing, in the cases of AV block; infant death from torsade des pointes, in congenital LQTS; and in utero demise, in structural or functional cardiac defects accompanied by heart failure.

The hormonal state of pregnancy is known to affect the

Acknowledgments

We gratefully acknowledge the many pediatric cardiologists and maternal-fetal medicine specialists who referred patients for magnetocardiography and cared for these patients before and after delivery. These physicians include pediatric cardiologists Nina Gotteiner, Sharda Srinivasan, Marc Ovadia, Barbara Deal, Ernie Albolaris, Zara Naheed, James Huhta, Pam Sayger, Suleka Kumar, Vickie Demadakis, Tarek Husayni, and Alex Javois; and maternal-fetal medicine specialists from the following Chicago

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