Routine fetal arrhythmia assessment typically involves the use of echocardiographic modalities that demonstrate mechanical events from which electrophysiological events are inferred (1). While M-mode and Doppler-based techniques have been used successfully to diagnose third-degree atrioventricular block (AVB), second-degree AVB, and, more recently, first-degree AVB, our evaluation has been limited to atrial and ventricular rates (2-4), gross P-R interval estimates using atrial-ventricular activity time intervals (5), and rarely detected ventricular ectopy. Although fetal electrocardiogram (ECG) has been shown to be more sensitive than echocardiogram-based techniques in detecting firstdegree AVB in anti-Ro-positive pregnancies (6), it has limited use in the evaluation of fetal heart rates out of the normal range, is more difficult to acquire at 28 to 32 weeks, and involves signal averaging, all limiting its clinical application.
See page 77Fetal magnetocardiography, the magnetic analog of fetal ECG, is at this time the most effective means of assessing fetal rhythms. Through the work of Zhao et al. (7), it has provided new insight into the electrophysiological characteristics of fetal AVB. Their observations suggest fetal AVB with and without structural heart disease is far more complex than previously appreciated with complex changing rhythms and variable atrioventricular conduction in seconddegree AVB, and abnormal QRS waveforms, co-existence of junctional and ventricular ectopy, and atrial and ventricular rate responsivity in third-degree AVB. Fetal magnetocardiography, however, requires a magnetically shielded facility and is available in very few centers. Furthermore, Zhao et al. (7) studied patients for 50 to 100 min at a time, longer duration than is typical of fetal echocardiography. Still, these new observations should prompt a search for perhaps more practical tools to evaluate electrophysiological events in fetal AVB that will ultimately improve the care of affected pregnancies.In normal pregnancies, fetal heart rate variability and accelerations associated with fetal activity increase with gestation (8,9) coinciding with maturation of the autonomic nervous system. In contrast, reduced fetal heart rate variability and accelerations particularly within lower heart rate ranges (10,11) occur in intrauterine growth restriction and chronic fetal hypoxemia. This has been used clinically to identify the fetus at greatest risk for sudden demise as a consequence of an inability to acutely adapt to changing physiological conditions. That many fetuses with isolated AVB have atrial and ventricular beat-to-beat variability and responsivity (7) suggests similar autonomic control exists, at least at higher ventricular rates. A ventricular rate of Ͻ56