Ventricular Tachycardias

Sally-Ann Barker Clur

Lisa K. Hornberger

Arja Suzanne Vink

Nico A. Blom

INTRODUCTION

Ventricular tachycardia (VT) is a rare condition responsible for only 1% to 8% of fetal arrhythmias and only 1% to 2% of fetal tachycardias.¹,² VT is diagnosed when three or more successive ventricular ectopic (VE) beats occur and the ventricular rate is increased to the range of 170 to 300 bpm.³,⁴,⁵,⁶,⁷,⁸,⁹,¹⁰,¹¹ When VT occurs, there may also be atrioventricular (A-V) dissociation resulting in a slower atrial rate than ventricular rate, but there may be V-A association due to retrograde conduction from the ventricle to the atrium resulting in equal ventricular and atrial rates (FIG. 3.3.1).

Although fetal VT is rare, it is important to recognize it and treat it appropriately for several reasons. First, if persistent, VT can lead to intrauterine cardiac dysfunction, nonimmune hydrops fetalis, and fetal demise.⁵ Second, misdiagnosing VT as supraventricular tachycardia (SVT) may lead to inappropriate drug therapy, resulting in an exacerbation of the arrhythmia with worsening of cardiac function, and fetal loss.¹²,¹³,¹⁴,¹⁵,¹⁶,¹⁷,¹⁸,¹⁹ On the other hand, appropriate therapy can restore sinus rhythm, resolve fetal hydrops, and prolong the pregnancy until maturity.¹,⁷,¹¹,¹⁴ Finally, the prognosis, etiology, and outcome of VT differ from those of SVT.

FIGURE 3.3.1 Fetal ventricular tachycardia (VT) tracings highlighting atrioventricular (A-V) relationships during VT. A: M-mode of a 32-week fetus with VT of 260 to 280 bpm. Simultaneous atrial (a, top tracing) and ventricular (V, bottom tracing) M-mode. The ventricular rate is ˜260 bpm and the atrial rate is ˜120 bpm. Note at times the V-V (V1, V2) and a-a intervals are irregular as are the a-v (a-v1, a-v2, yellow lines) intervals. This variation is typical of VT with V-A dissociation. B-D: 37-week fetus with VT of 170 to 180 bpm. B: M-mode shows 1:1 A-V relationship. At this point, one cannot distinguish VT from supraventricular tachycardia. C: Inferior vena cava Doppler tracings at this rate demonstrated a large and consistent A-wave reversal (above baseline). This was due to the retrograde V-A conduction with atrial systole occurring at the end of ventricular systole resulting in the atria contracting against a closed AV valve. These findings suggest a diagnosis of VT. D: Tissue Doppler imaging shows a retrograde V-A conduction.

ETIOLOGY AND MECHANISMS

Most of our current knowledge about fetal VT is derived from prenatal case reports and small case series or extrapolated from neonatal data. The mechanism of VT includes prolonged ventricular repolarization, an abnormally irritable focus, or a reentry circuit. Based on 12-lead ECG characteristics, there are two broad categories of VT: monomorphic and polymorphic (FIG. 3.3.2). The signature rhythm of long QT syndrome (LQTS), an inherited ion channelopathy, is a polymorphic VT called torsades de pointes (TdP). VT may occur in the absence of structural or functional heart disease. It may also be associated with myocardial disease (including myocarditis, cardiomyopathy, and aneurysms), with intracardiac tumors such as fibromas and rhabdomyomas, with myocardial ischemia or with inherited channelopathies other than LQTS, discussed in Part 1, Chapter 3 and Part 3, Chapter 6. VT can also be idiopathic.

FIGURE 3.3.2 Fetal magnetocardiogram rhythm tracings of ventricular tachycardia (VT). A: 25-week fetus with monomorphic VT at a rate of about 212 bpm. The wide complex (prolonged QRS duration) is typical of VT, but can also be seen with antidromic supraventricular tachycardia. B: 32-week fetus with torsades de pointes, a polymorphic VT that “twists around the points.”

DIAGNOSIS OF FETAL VT

In addition to excluding an obvious primary structural or functional cardiac defect by fetal echo, initial steps in the evaluation of fetal VT should include soliciting a family history suggestive of an inherited arrhythmia or myocardial disease, including unexpected losses in utero or in infancy. Acquisition of a 12-lead ECG from both parents may be informative. Additional testing for maternal infection, particularly viral etiologies, and maternal autoantibodies (anti-SSA/Ro and SSB/La) should be considered to assess for possible myocarditis including, in the latter, autoimmune-mediated fetal myocardial disease.

The diagnosis of fetal VT relies on identifying unique characteristics as seen by M-mode, tissue Doppler,²⁰ and spectral Doppler. These characteristics include (1) variable A-V and V-A intervals; (2) A-V dissociation with a slower atrial rate than ventricular rate; (3) ventricular asynchrony; and (4) in cases of slow VT (<200 bpm), intermittent retrograde V-A conduction. These characteristics are described below.

The variable A-V and V-A intervals, which occur because of A-V dissociation, can be seen by M-mode and spectral Doppler (FIG. 3.3.1A). These variable intervals contrast with the very regular A-V and V-A intervals characteristic of SVT. In VT, the atrial rates may be slower than the ventricular rates as seen in FIG. 3.3.3 in a fetus with both ventricular bigeminy and VT. As seen in FIG. 3.3.4, A-V dissociation can be also be inferred
from pulsed Doppler tracings in the systemic veins, and the retrograde A-waves of the fetus with VT occur without a clear pattern.

FIGURE 3.3.3 32-week fetus with idiopathic ventricular tachycardia. By M-mode, the atrial (a) rates were found to be constant at 140 to 150 bpm. Initially there was ventricular bigeminy (V′) followed by a run of ventricular tachycardia with ventricular rates > 200 bpm and atrioventricular dissociation. V, ventricular contraction.

FIGURE 3.3.4 Spectral Doppler tracings from fetus with slow ventricular tachycardia (180-200 bpm). Tracing from superior vena cava (SVC, top tracing) and aorta (V, bottom tracing). Reverse flow in the SVC denotes atrial contractions which are seen below the baseline (a). The ventricular rate is slightly faster than the atrial rate, and atrio-ventricular dissociation is seen by the varying atrioventricular relationship and the prominent A-wave reversal (red “a”) seen when the atrium contracts during ventricular systole.

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