Contribution of Fetal Magnetocardiography to Diagnosis, Risk Assessment, and Treatment of Fetal Arrhythmia

Abstract

Background Fetal echocardiography has been the mainstay of fetal arrhythmia diagnosis; however, fetal magnetocardiography (fMCG) has recently become clinically available. We sought to determine to what extent fMCG contributed to the precision and accuracy of fetal arrhythmia diagnosis and risk assessment, and in turn, how this altered pregnancy management. Methods and Results We reviewed fMCG tracings and medical records of 215 pregnancies referred to the Biomagnetism Laboratory, UW-Madison, over the last 10 years, because of fetal arrhythmia or risk of arrhythmia. We compared referral diagnosis and treatment with fMCG diagnosis using a rating scale and restricted our review to the 144 subjects from the tachycardia, bradycardia/AV block, and familial long QT syndrome categories. Additional fMCG findings beyond those of the referring echocardiogram, or an alternative diagnosis were seen in 117/144 (81%), and 81 (56%) were critical changes. Eight (5.5%) had resolution of arrhythmia before fMCG. At least moderate changes in management were seen in 109/144 (76%) fetuses, of which 35/144 (24%) were major. The most diverse fMCG presentation was long QT syndrome, present in all 3 referral categories. Four of 5 stillbirths were seen with long QT syndrome. Nine fetuses showed torsades de pointes ventricular tachycardia, of which only 2 were recognized before fMCG. Conclusions FMCG has a significant impact on prenatal diagnosis and management of arrhythmias or familial arrhythmia risk, which cannot be fully met by existing technology. The combination of fMCG and fetal echocardiography in fetal care centers will be needed in the future to optimize care.

Keywords: electrocardiography; fetal arrhythmia; fetal echocardiography; fetus; long QT syndrome; magnetocardiography.

Figures

Figure 1. Patients and categories.

CHD indicates congenital heart disease; PACs/PVCs, premature atrial contractions/premature ventricular contractions; Pts, patients; and SSA/Ro pos, Sjogren's antibody A positive.

Figure 2. Aortic Doppler in a 26‐week gestational age fetus during TdP ventricular tachycardia.

A, Doppler flow velocity onsets for pulmonary artery (downward) and aorta (upward) are not the same, suggesting bundle branch block. Hatched lines mark each systolic onset. Multiple valve clicks can be seen. Duration of systole (horizontal lines) and velocity of aortic output are also variable and attenuated in TdP, useful echo/Doppler features during evaluation, along with ventricular dysfunction. The rate of TdP is often underestimated by Doppler because of the severe and variable diminution of systolic output. B, Fetal magnetocardiography from this fetus. TdP was present 90% of the time during the recording session, alternating with 2°AVB, but because it was “normal‐rate” TdP between 150 and 200 bpm, it was not recognized as TdP by echocardiography/Doppler, and the higher rate was thought to be sinus with ectopy. C, Blocked atrial bigeminy (BAB); Doppler tracings in a 29 6/7‐week‐gestation fetus referred for suspected 2°AVB. The subject had been started on dexamethasone, but SSA antibodies were later noted to be normal. The mPR was 125 ms. Pseudo “a” waves (Ǿ arrow) were nearly equally spaced with “a” waves, suggesting 2°AV block. The real blocked ectopic velocities were discordant, because of their re‐entrant nature. During the time frame of the aortic flow velocity, but in a downward direction is the atrial “a” velocity corresponding to the p prime on fMCG (upright arrows mark onsets). These do not conduct to the ventricle, resulting in BAB with a rate of 83/min. a‐a' is ≈200 ms, closely correlating to the p–p' of 210 ms by fMCG. D, HR trend graph, actogram, and (right) 20‐s signal‐averaged tracing during BAB. Not detected by fetal echocardiography was the brief SVT episode at 270 beats/min. Stopping dexamethasone, and managing the SVT were major changes in management. E, Doppler tracing from referring hospital on a 22 3/7‐week‐gestation fetus thought to have third‐degree AV block. F, fMCG signal‐averaged tracing demonstrates a stable PR interval consistent with 3:1, 2°AVB. The subject was SSA negative. The cause of the AV block is unclear, because the QTc was normal, and postnatal genetic testing for LQTS showed no pathologic variant.*denotea atrial "A" waves. Ao indicates aortic outflow; AV, atrioventricular; AVB, atrioventricular block; FHR, fetal heart rate; fMCG, fetal magnetocardiography; LQTS, long QT syndrome; LV Out, left ventricular outflow; LV In, left ventricular inflow; mPR, mechanical PR interval; PA, pulmonary artery outflow; PACs, premature atrial contractions; PVC, premature ventricular contraction; SSA, Sjogren's antibody A; SVT, supraventricular tachycardia; TdP, torsades de pointes; and V, ventricular "V" waves by Doppler.

Figure 3. 3.5‐s signal averaged tracing from the 26‐week fetus in Figure 2.

A, functional 2:1 AV block and marked QTU prolongation. B, 1‐s signal averaged tracing during monomorphic VT showing a very stable pattern of VT, unlike that seen typically with long QT syndrome. This fetus had both LQT1 and LQT2. The fetus required β‐blocker therapy pre‐ and postnatally, and a pacemaker and left stellate ganglionectomy after delivery. VT indicates ventricular tachycardia. C, Same fetus with periods of typical polymorphic torsades morphology. Black bar = 5 s. D, Same fetus, same run, showing the monomorphic‐appearing VT. Neither form of VT was recognized before fMCG, largely because of the relatively slow rate (163 beats/min), which was thought to be sinus rhythm. Both forms of VT responded in utero to maternal high‐dose propranolol therapy at 320 mg/d. AV indicates atrioventricular; LQT ‐ Long QT; TWA, T wave alternans; and VT, ventricular tachycardia.

Figure 4. Blocked Atrial Bigeminy (BAB) and 2:1 AV Block by fMCG.

A, Typical blocked atrial bigeminy with P–P′ 196 ms with morphologically different P and P′. In this setting of very short P–P′, the functional antegrade AV block results in stable ventricular rates of ≈75–90/min. AV indicates atrioventricular; and fMCG, fetal magnetocardiography. B, In true second‐degree AV block, the P waves are usually morphologically similar, and there is often slight ventriculophasic sinus arrhythmia, where the P–P′ with the QRS between is slightly shorter than the P′‐P.