Ventricular Tachycardia in an Infant Without Congenital Anomaly: A Case Report

Abstract

Ventricular tachycardia (VT) is a serious form of arrhythmia that can be life-threatening; that’s why diagnosis and treatment are very important in order to avoid serious complications. We are reporting this case of VT which is a rare entity, especially, in healthy infants. This infant, without cardiac pathology known from birth, presented with poor food intake and grunting with hepatomegaly on clinical examination, and a heartbeat at 200/ min. The electrocardiogram (ECG) showed wide QRS complex tachycardia, and the echocardiogram showed a dilated and hypokinetic cardiomyopathy. The clinical signs and chest X-ray changes were consistent with mild cardiac failure. This presentation makes the diagnosis challenging, therefore, it is important to take a good history of the case with a complete clinical exam to achieve the correct diagnosis, and to avoid potential complications. VT of an infant may be benign but should not be diagnosed as such before eliminating serious causes.

Introduction

Ventricular tachycardia (VT) is uncommon in infant, with an incidence of around 1.1 in 100,000 children [1]. Although very rare, VT is a serious form of arrhythmia; may be life-threatening if degenerated to ventricular fibrillation (VF), and can lead to sudden cardiac arrest [2]. VT can be found in a normal heart or related with congenital heart disease or associated with genetic causes. VT can be present in utero, neonates, infants, children, adolescents and adult population. When VT is present initially in infants, the clinical presentation varies between asymptomatic and seriously ill patient with shock, congestive heart failure and cardiac arrest [3]. Most of VT in infant population occurs in patients with normal heart. The clinical presentation of VT, the rate of VT compared to the underlying sinus rate and the morphology of the tachycardia, are features helping the distinction between benign forms of VT and lethal ventricular arrhythmia. Further testings are often needed to complete this difficult distinction, especially when VT persists [3, 4]. The evaluation of infant VT first begins with a detailed family history, 12-lead electrocardiogram (ECG), echocardiogram, 24-h Holter monitor and magnetic resonance imaging (MRI) if indicated.

VT can be classified into VT associated with heart disease and idiopathic VT [5]. In contrast to adult population, pediatric idiopathic VT is the most common type of VT, with benign long-term outcomes [1, 6-9]. VT onset during infancy is frequently associated with spontaneous resolution of tachycardia [9, 10]. The prognosis of VT in pediatric population is dependent on the underlying etiology of VT, age and treatment method [1, 8]. The mortality rate of VT is higher in cardiomyopathies, long QT syndrome, myocarditis and cardiovascular collapse related to rapid VT due to tumors [3, 11]. Infants have a better prognosis than older children [10]. Treatment recommendations for pediatrics VT vary from conservative observation to antiarrhythmic drugs, invasive surgical procedures or radiofrequency catheter ablation [12-20].

Case Report

At 4 months of life, an infant presented to his pediatrician’s clinic for signs of irritability, grunting, increase work of breathing and decreased oral intake for 2 days. The pediatrician notes at physical exam a hepatomegaly and tachycardia at 200 beats per minute. The infant was referred to pediatric cardiologist. The ECG showed wide QRS complex tachycardia at 200 beats per minute that could be corresponding to VT or supraventricular tachycardia with aberrant conduction (Fig. 1). The echocardiogram revealed a global dilatation of left ventricle without hypertrophy and with acceptable systolic function; a dilatation of the right ventricle with altered systolic function; mitral insufficiency grade II and tricuspid insufficiency grade I; pulmonary arterial hypertension (PAH); dilated inferior vena cava and dilated hepatic veins. At this stage two diagnostic hypotheses can be posed: dysrhythmic cardiomyopathy or a cardiac pathology complicated by tachycardia. The clinical signs and chest X-ray changes were consistent also with mild cardiac failure but preserved peripheral perfusion. No electrolyte or metabolic disturbances were found in her blood tests. Upon admission, the patient was given a bolus of adenosine without any change in her tachycardia. Given the sustained VT and the global cardiac failure, the patient was treated by amiodarone 500 mg/m2/day, spironolactone 2 mg/kg/day, furosemide 2 mg/kg/day and captopril 1 mg/kg/day. The tachycardia reverts to sinus rhythm few hours later. ECG after conversion showed normal sinus rhythm at 120/min, with frequent ventricular premature beats (VPBs) having the same morphology of the QRS during tachycardia (Fig. 2). Diagnosis of VT was then confirmed.

 

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Figure 1

ECG showing wide QRS complex.

 

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Figure 2

ECG after conversion showing normal sinus rhythm at 120/min, with frequent VPBs, having the same morphology of the QRS during tachycardia.

Two days later, the echocardiogram shows amelioration in the systolic function of the left ventricle without any dilatation or hypertrophy, amelioration in the systolic function of the right ventricle with less dilatation and without hypertrophy. The 24-h Holter monitor described a sinus rhythm at an average of 129 beats per minute, absence of significant supraventricular hyper excitability, presence of frequent nocturnal and diurnal VPBs in bigeminy and monomorphic. No VT or conductive disorders were noted in the 24-h Holter monitor. After 6 days of monitoring in the hospital, the patient conserved a sinus rhythm without recurrence of the VT. The echocardiogram at day 5 of admission showed a normal function of left and right ventricles without any dilatation, absence of PAH, presence of trivial mitral regurgitation and physiological tricuspid regurgitation. The patient was then discharged on amiodarone 250 mg/m2/day, furosemide 2 mg/kg/day and captopril 1 mg/kg/day. One week after discharge the 24-h Holter monitor was normal. Two months later, the echocardiogram was normal, so furosemide and captopril were stopped, the patient continued amiodarone. Four months later, echocardiogram and the 24-h Holter monitor were also normal (Fig. 3).

 

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Figure 3

ECG showing normal sinus rhythm at 120/min without VPB.

 

Source: https://www.ncbi.nlm.nih.gov/pmc/

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