We report the unusual occurrence of isoimmune complete AV block and VT diagnosed by fMCG after a dramatic decrease in the ventricular rate in a 34 week fetus. Other unusual features are that the occurrence late in gestation after previous fMCG showed only third-degree AV block and that the VT occurred 9 weeks after the initiation of transplacental anti-inflammatory treatment. These findings led to an immediate operative delivery of a non-hydropic infant who was paced shortly thereafter and has survived with normal ventricular function.
The most common technique for the diagnosis of fetal arrhythmias evaluates the AV relationship and atrial and ventricular rates by M-Mode or Doppler echocardiography. However, echocardiography measures the mechanical effect of an electrical event rather than direct recordings of cardiac electrical impulses. In addition, diagnosis is difficult if the arrhythmia is transient and since measurements of conduction intervals are necessary for diagnosis (such as long QT syndrome or bundle branch block). Recently, the use of tissue velocity imaging, which allows precise timing of atrial and ventricular events, has increased the sophistication of echocardiography arrhythmia diagnosis [14
], but conduction intervals other than the P-R interval can only be measured by fMCG or fetal electrocardiography.
Fetal electrocardiogram, which has the potential to be more easily available and less expensive than fMCG, remains limited in arrhythmia diagnosis because the maternal electrocardiogram voltage potential is 10–100 times stronger than the fetal signal resulting in significant artifact. Additionally, useful signals from the fetus are difficult to obtain after 27 weeks, probably due to insulating properties of vernix caseosa [15
]. Such problems are not encountered with fMCG, which reliably measures signals from 20–40 weeks of gestation, provided that the recordings are made within a magnetically shielded room.
In the fetus reported here, it is unknown why the ventricular rate dropped abruptly in only 1 week's time. It may be that despite the anti-inflammatory treatment there was on-going damage to the conduction system, resulting in a slower ventricular pacemaker more distal from the AV node. The finding that the QRS duration was narrow at this lower rate suggests that the new ventricular focus was proximal to the bundle of His.
The occurrence of VT accompanying isoimmune AV block in the fetus is unusual. VT may be an escape rhythm due to the low ventricular rate, or it may be due to myocardial ischemia secondary to low cardiac output from the abrupt fall in heart rate. Both may further be affected by progressive autoantibody-mediated myocardial injury. We further speculate that the findings of VT with severe bradycardia may be one of the mechanisms of sudden death in the fetus with isoimmune disease. These findings underscore the importance of vigilant monitoring in the third trimester of fetuses with isoimmune disease and no heart failure, even if they seem clinically stable.