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. 2008 Mar-Apr;41(2):116.e1-6.
doi: 10.1016/j.jelectrocard.2007.12.010.

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

Bettina F Cuneo  1 , Janette F Strasburger, Ronald T Wakai
Affiliations

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

Bettina F Cuneo et al. J Electrocardiol. 2008 Mar-Apr.

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."

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Figures

Fig. 1
Fig. 1
Changes in HR and variability pattern in one fetus with isoimmune AV block. Each line is one RR interval. A, HR over time at 28 weeks of gestation. Normal pattern of HR variability—HRs range from 63 to 90 beats per minute. B, HR over time of same fetus at 34 weeks of gestation. Not only has the HR fallen dramatically, but there is also virtual absence of variability.
Fig. 2
Fig. 2
Fetus with isoimmune 2° AV block at 32 weeks. A, Before transplacental treatment with dexamethasone, the fMCG rhythm shows AV conduction only through an accessory connection and not through the AV node. B, Two weeks later, after dexamethasone therapy, the rhythm is still 2° AV block, but AV conduction is through the AV node, not the accessory connection. Arrows indicate P waves.
Fig. 3
Fig. 3
Rhythm strips of the fetus with cardiomyopathy before in utero demise. A, Ischemia (ST-segment elevation in first QRS complex) before a prolonged deceleration in HR. B, TWA during sinus rhythm.
See this image and copyright information in PMC

References

    1. CDC. MMWR. 2004;53:529.
    1. Reddy UM, Ko CW, Willinger M. Maternal age and the risk of stillbirth throughout pregnancy in the United States. Am J Obstet Gynecol. 2006;195:764. - PubMed
    1. Michaelsson M, Jonzon A, Risenfeld T. Isolated congenital complete atrioventricular block in adult life. Circulation. 1995;92:442. - PubMed
    1. Dreifus LS, Haiat R, Wantabe Y, et al. Ventricular fibrillation. A possible mechanism of sudden death in patients with Wolff-Parkinson-White Syndrome. Circulation. 1971;43:520. - PubMed
    1. Cosi FG, Benson DW, Anderson RW, et al. Onset of atrial fibrillation during antedromic tachycardia associated with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome. Am J Cardiol. 1982;50:353. - PubMed

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