Fetal cardiac arrhythmia detection and in utero therapy

Abstract

The human fetal heart develops arrhythmias and conduction disturbances in response to ischemia, inflammation, electrolyte disturbances, altered load states, structural defects, inherited genetic conditions, and many other causes. Yet sinus rhythm is present without altered rate or rhythm in some of the most serious electrophysiological diseases, which makes detection of diseases of the fetal conduction system challenging in the absence of magnetocardiographic or electrocardiographic recording techniques. Life-threatening changes in QRS or QT intervals can be completely unrecognized if heart rate is the only feature to be altered. For many fetal arrhythmias, echocardiography alone can assess important clinical parameters for diagnosis. Appropriate treatment of the fetus requires awareness of arrhythmia characteristics, mechanisms, and potential associations. Criteria to define fetal bradycardia specific to gestational age are now available and may allow detection of ion channelopathies, which are associated with fetal and neonatal bradycardia. Ectopic beats, once thought to be entirely benign, are now recognized to have important pathologic associations. Fetal tachyarrhythmias can now be defined precisely for mechanism-specific therapy and for subsequent monitoring of response. This article reviews the current and future diagnostic techniques and pharmacologic treatments for fetal arrhythmia.

Diagnosis and Treatment of Fetal Cardiac Disease

“…351,352 fMCG has led to modifications in medical therapy of arrhythmias in some cases. [329][330][331]353 Unlike fetal electrocardiography, fMCG allows raw signal analysis even in the presence of an irregular rhythm. fMCG holds an inherent advantage over fetal electrocardiography in signalto-noise ratios because the conductance properties of magnetic signals are not affected by poor conductivity of fetal and maternal tissues.…”

Self-terminating re-entrant cardiac arrhythmias: quantitative characterization

“…The fECG has a small (<~50 µV) amplitude but foetal QRS complexes are clearly identifiable, and foetal RR intervals can be automatically extracted, and foetal bradycardia and tachycardia readily identified. In some pregnancies short intermittent bursts of high frequency activity are observed, as illustrated in Figure 6: these resemble magneto-cardiographic recordings of foetal tachycardia [6], their amplitude on all four channels of the monitor, and changes in these amplitude with foetal position, are both similar to those of preceding and subsequent foetal QRS complexes. However, there is no direct evidence that these "putative foetal VTs" are produced by activity in the foetal heart: they look and behave as if they could be.…”

“…The foetal ECG [6,7] was extracted from maternal recordings (non-invasive monitoring of uterine electrical activity) from a Monica AN24 via electrodes placed on the abdomen. Episodes of foetal tachycardia were initially located using Monica software, and then the raw V(t) exported for graphical analysis.…”

Atrial Fibrillation in Children

“…For atrial flutter or fibrillation resistant to digoxin or flecainide in the absence of ventricular dysfunction, the current recommendation is to attempt to control the arrhythmia with sotalol and amiodarone (Cuneo & Strasburger, 2000;Srinivasan &Strasburger, 2008;Strasburger et al, 2004;Strasburger&Wakai, 2010). There have been several reports of alternative methods to maternal oral administration with varying degrees of success (Hallak et al, 1991;Parilla et al, 1996;Weiner et al, 1988), but most of these have been met without much general enthusiasm for the increased risk when the success rate of traditional therapy is in excess of 90% (Cuneo & Strasburger, 2000;Kleinman & Nehgme, 2004;Maeno et al, 2009;Srinivasan & Strasburger, 2008;Strasburger et al, 2004;Strasburger & Wakai, 2010). A recent report suggests that neurodevelopmental outcome for babies who experience fetal arrhythmias is very good (Lopriore et al, 2009).…”

“…It has excellent ability to cross the placenta and has generally demonstrated good efficacy. For the same indications in Europe, the intervention of choice has become flecainide (Strasburger & Wakai, 2010). For atrial flutter or fibrillation resistant to digoxin or flecainide in the absence of ventricular dysfunction, the current recommendation is to attempt to control the arrhythmia with sotalol and amiodarone (Cuneo & Strasburger, 2000;Srinivasan &Strasburger, 2008;Strasburger et al, 2004;Strasburger&Wakai, 2010).…”