Accelerated Idioventricular Rhythm in Newborns: A Worrisome But Benign Entity with or without Congenital Heart Disease
Broad QRS rhythms (fast and slow) are worrisome findings in newborns. We present five cases with varied clinical presentations found to have broad QRS tachycardias, consistent with idioventricular rhythms. Each patient had an excellent prognosis because the tachycardias resolved, and eventually the patients were in sinus rhythm. None were symptomatic from their arrhythmia. It is important to establish the diagnosis when it occurs to differentiate this benign phenomenon from dangerous ventricular tachycardia.
KeywordsAccelerated ventricular rhythm Ventricular tachycardia
Broad QRS tachycardia/rhythm is a worrisome occurrence in early infancy. The differential diagnosis is between supraventricular tachycardia (SVT) with aberrancy and ventricular tachycardia (VT), which is rare early in life. Accelerated idioventricular rhythm (AIVR) is a benign variant of VT with a rate slightly faster than the prevailing sinus rate (SR). Usually, the cardiac morphology is normal, but in some cases ventricular septal defect (VSD) has been reported. We present five cases of AIVR in newborns, pointing out that this rhythm is commonly an innocent and benign variant, and also present management strategies. Of note, two patients had a history of fetal arrhythmia.
Diagnosis criteria of the five cases consisted of the following: three or more consecutive beats with broad QRS and rate faster than the SR, warm-up, isorhythmic dissociation with fusion beats, 1:1 ventriculoatrial (VA) capture, and gradual termination with SR acceleration and/or AIVR deceleration . Congenital heart disease was established by echocardiogram (ECG) in two cases. ECGs were reviewed. Follow-up information was obtained from referring physicians.
On amiodarone, the arrhythmia was controlled; however, after discontinuation at 4 months of age, the arrhythmia recurred and the medication was restarted. After 11 months, amiodarone was discontinued and AIVR remained quiescent.
At a few hours of age, this full-term infant fell from a caregiver’s arms, striking the floor. Head injury was a concern, and she was transferred to the neonatal intensive care unit, where ECG monitor showed an arrhythmia. Twelve lead ECG showed singleton broad QRS extra systoles with LBBB pattern. Her echo was normal. Computed tomography scan of the brain was negative. At 2.5 weeks of age, she was asymptomatic but ECG showed broad QRS rhythm, HR of 150 bpm, and LBBB pattern. No treatment was started. At 2 months of age, she remained asymptomatic, and ECG was normal. At 1 year of age, her cardiac evaluation including ECG was normal.
Five newborns were diagnosed with AIVR. One patient had a VSD and four patients had isolated AIVR with structurally normal hearts. Cases 3 and 5 had fetal tachycardia. Case 3 required no therapy during fetal life but was born with incessant tachycardia and was treated with propanolol. The fetal events were thought to be AIVR as per electrophysiologic evaluation in this case. Case 5 was treated in utero for slow SVT with 1:1 atrioventricular conduction, and AIVR was diagnosed at birth. These two cases most likely had AIVR in utero and continued to have it after birth. Other cases of fetal AIVR have been cited [1, 4].Ages at presentation varied from prenatal to 2 weeks, and there were two female and three male patients.
AIVR rates ranged from 150 to 180 bpm within 10% of the preceding SR. The longest recorded run was 216 bpm in case 1. QRS configuration was of LBBB, with AV dissociation consistent with right ventricular origin. Adenosine was helpful in diagnosing the rhythm in case 1, who was successfully treated with amiodarone. Case 3 was treated with propanolol, and once AIVR was treated, long QT was found but it normalized on follow-up. Case 5 was treated with digoxin and flecainide for prolonged fetal tachycardia. Cases 2 and 4 received no drugs and the arrhythmia resolved spontaneously. Although treating such a rhythm is usually not necessary, we elected to treat case 1 because of her VSD, which was believed to have the potential to develop congestive heart failure, and we decided to be proactive in restoring AV synchrony. Inderal was continued in case 3.
Patients with AIVR reported in the literature
Age at presentation
Age at resolution
Bisset et al. 
Lidocaine and propanolol
History of irregular heart rate
Scagliotti et al. 
7 patients, 0–48 hours
Lidocaine and propanolol
Yokota and Wada 
Elevated CK, LDH
Geggel et al. 
Nakagawa et al. 
VSD closed at 84 days
VSD still present at follow-up
Kuratobi et al. 
Van Hare and Stanger 
12 patients, <1 month
5 of 12 treated
Anatolliotaki et al. 
Presentation is common during the first day of life [2, 7, 9, 10, 11, 12, 13]. One case of AIVR in fetal life was reported by Fouron et al. , and a second case was reported by Anatolliotaki et al. .
AIVR is commonly seen in adults postinfarction; in myocarditis, digitalis toxicity, and right ventricular dysplasia; postoperatively; and s/p ablation . In children, it is seen predominantly in normal hearts and with congenital heart diseases, such as tetralogy of Fallot s/p repair, s/p Fontan, and VSD with subAs, and in transplanted patients [1, 8]. Although this rhythm is well tolerated, it is not known if it will accelerate to a dangerous degree; hence, pediatric cardiologists feel compelled to treat it, which may not be necessary.
Several medications have been tried in the past, including mexiletine, propanolol, verapamil, digoxin, and quinidine. Verapamil was the only medication demonstrated to work in 1 patient . All patients do not require treatment.
In reviewing the literature, it seems that no comments have been made regarding the site of origin of the rhythm (right ventricle) as the ECGs show LBBB pattern. The mechanism responsible for AIVR is unknown, but it is generally attributed to an enhanced automatic focus, most likely in the right ventricular outflow tract; this focus competes with the sinus pacemaker . AIVR is easily converted to SR by atrial pacing at a faster rate, but it can neither be induced nor interrupted by ventricular pacing or programmed stimulation of the right ventricle . These rhythms seem to occur in the right ventricle and may be the marker for future ARVD, especially when the QRS indicates a right ventricular infundibular origin . Further follow-up of additional patients with AIVR may be useful to determine if this is the case; however, the current experience supports a benign and good prognosis.
We thank Dr. SuChiung Chen, Cardinal Glennon’s Children Hospital, Saint Louis University.
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