Abstract
Background
Supraventricular tachycardia (SVT) affects 1 in 500 children and is characterized by rapid heart rate originating from the atrial tissue above the atrioventricular node and interventricular septum.
Aim of review
The purpose of this article is to review the etiology, pathophysiology, types, clinical presentation, diagnosis, and treatment of SVT in children.
Key scientific concepts of review
SVT results from reentry circuits, abnormal automaticity, or triggered activity. Contributing factors include congenital heart defects, electrolyte imbalances, and genetic predisposition. The types of SVT include atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial tachycardia, and junctional ectopic tachycardia. Infants with SVT may present with poor feeding, vomiting, irritability, increased sleepiness, syncope, or diaphoresis. Toddlers and school-aged children may experience palpitations, chest pain, dizziness, shortness of breath, or syncope. Diagnostic tests include the electrocardiogram, Holter monitor, exercise stress test, and electrophysiologic study. Acute treatment options include vagal maneuvers, pharmacologic cardioversion, and electrical cardioversion. Long-term treatment options include antiarrhythmic drugs, catheter ablation, and surgical treatment. Complications of SVT include hemodynamic instability, thromboembolic events, congestive heart failure, exercise limitation, and decreased quality of life. Special considerations include missed diagnosis in neonates and infants, the association of SVT with congenital heart disease, and transition of care from pediatric to adult cardiology. Future directions and research may include advancements in genetic and molecular biomarkers and ablation methods. It is important to provide education and counseling to patients and their families, including information about the condition, treatment options, potential complications, and psychological support.
Highlights
- •
Supraventricular tachycardia affects 1 in 500 children.
- •
Causes include reentry circuits, abnormal automaticity, or triggered activity.
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Patients may have palpitations, heart failure, syncope, chest pain, or dyspnea.
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Acute treatment may include vagal maneuvers or cardioversion.
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Severe hemodynamic instability may occur in patients with congenital heart disease.
1
Introduction
Cardiovascular disease is a major global health problem, accounting for 32 % of deaths in all ages worldwide. Supraventricular tachycardia (SVT) is among the most common tachyarrhythmias, affecting 1 in 500 children [ , ]. SVT is characterized by a rapid heart rate originating from the atrial tissue above the atrioventricular (AV) node and interventricular septum.
The importance of SVT extends beyond its high prevalence because it also may develop in fetuses and cause severe complications such as fetal heart failure and hydrops fetalis, a potentially life-threatening condition [ ]. Therefore, a comprehensive review of current scientific knowledge about SVT is essential to ensure optimal patient care.
The purpose of this article is to review SVT in children, including the various types of SVT, clinical presentations, diagnosis, treatment, and potential complications. We also will identify knowledge gaps in the current literature and suggest areas for further research to advance the understanding and treatment of this important cardiac condition in children.
2
Etiology and pathophysiology
SVT in children primarily results from three mechanisms: reentry circuits, abnormal automaticity, and triggered activity. These mechanisms cause similar features on an electrocardiogram (ECG). SVT also may be caused by structural heart defects, electrolyte imbalances, and genetic predisposition.
2.1
Reentry circuits
Reentry circuits are the most common cause of SVT in children [ ]. Reentry involves an abnormal electrical circuit within the heart. The electrical impulse reenters and reactivates the same pathway, resulting in tachycardia. This can occur through an accessory pathway or within the AV node [ ].
2.2
Abnormal automaticity
Abnormal automaticity involves the spontaneous generation of electrical impulses by cardiac cells that do not typically possess pacemaker activity. These cells depolarize spontaneously, causing ectopic beats that trigger tachycardia. Abnormal automaticity can result from various factors affecting transmembrane potential, including cell injury, electrolyte imbalance, reduced maximum diastolic potential, or spontaneous drifting upward of the phase 4 diastolic potential [ ].
2.3
Triggered activity
Triggered activity occurs due to afterdepolarizations that reach threshold potential and trigger additional action potentials. There are two types of afterdepolarizations: delayed and early. Both delayed and early afterdepolarizations may cause rapid and premature heartbeats, potentially leading to SVT.
2.3.1
Delayed afterdepolarizations
Delayed afterdepolarizations arise during the resting potential after full repolarization of an action potential. They are associated with conditions that cause intracellular calcium overload. Increased intracellular calcium may cause spontaneous calcium release from the sarcoplasmic reticulum, activating the sodium‑calcium exchanger and creating a depolarizing current [ ].
2.3.2
Early afterdepolarizations
Early afterdepolarizations occur during the repolarization phase of an action potential, causing a prolonged action potential [ ]. This prolongation enables more time for depolarizing currents to reemerge during repolarization, potentially reactivating L-type calcium channels and causing secondary depolarization [ ].
2.4
Structural heart defects
Congenital heart defects are major contributors to SVT in children, and 21 % to 29 % of children who develop SVT have associated congenital heart defects [ ]. Atrial arrhythmias in patients who have congenital heart defects typically result from direct tissue injury during surgical procedures, atrial remodeling due to volume overload, presence of accessory pathways (especially in patients who have Ebstein anomaly), and scarring after surgery [ , ].
2.5
Electrolyte imbalances
Abnormal potassium levels may cause pediatric SVT [ ]. After surgery for congenital heart defects, 15.2 % of patients develop postoperative arrhythmias, with SVT comprising 21 % of postoperative arrhythmias [ ]. Hypokalemia may be associated with postoperative arrhythmias because of its effects on cardiac myocyte electrophysiology. Hypo- or hyperkalemia may cause distinctive ECG changes and arrhythmias [ ]. However, there is a lack of research concerning the management and treatment of electrolyte disturbances in children. While there is an abundance of literature honing in on the management of adult electrolyte disturbances, there seems to be a substantial gap in this research concerning pediatrics.
2.6
Genetic predisposition
Genetic factors may be associated with SVT. Wolff-Parkinson-White syndrome is associated with the PRKAG2 gene, and atrioventricular nodal reentrant tachycardia (AVNRT) may be linked to several genes such as SCN1A, NOS1, GAD2, PRKAG2 which are involved in neuronal systems and cardiac conduction [ , ]. Genetic sequencing is recommended for neonates with hereditary arrhythmias because they have an increased risk of having associated congenital heart defects or developing heart failure [ ]. In addition, genetic abnormalities associated with congenital structural defects may indirectly increase the risk of developing SVT.
3
Types of supraventricular tachycardia
Although the observation of SVT indicates the pathophysiology and location of the electrical anomaly resulting in tachycardia, there are four primary types of SVT which provide further details about the exact causative mechanism of the arrhythmia.
3.1
Atrioventricular nodal reentrant tachycardia
AVNRT is one of the most common types of SVT in all patients without structural cardiac abnormalities ( Fig. 1 ). AVNRT comprises 60 % of SVT cases, with a prevalence of 2:1 in girls versus boys [ , ]. It involves a reentrant electrical pathway through the AV node. With AVNRT, electrical impulses travel back up from the AV node toward the atria instead of down toward the ventricles, causing the atria to contract faster than usual, resulting in tachycardia.
There are three primary types of AVNRT that are differentiated by ECG findings: slow-fast, fast-slow, and slow-slow [ ]. Slow-fast AVNRT, also known as typical AVNRT, occurs when the antegrade conduction occurs through the slow pathway within the AV node. Subsequently, retrograde conduction occurs through the fast pathway, resulting in reentry and tachycardia. With slow-fast AVNRT, the ECG may show retrograde P waves near the QRS complex and short RP tachycardia [ ]. In contrast, fast-slow (atypical) and slow-slow AVNRT cause long RP tachycardia.
3.2
Atrioventricular reentrant tachycardia
Although atrioventricular reentrant tachycardia (AVRT) is the fourth most prevalent type of SVT in patients aged >20 years, it is the most common type of SVT in young children ( Fig. 2 ) [ ]. The depolarizing reentrant pathways are similar between AVRT versus AVNRT, but AVRT occurs without the involvement of the AV node. AVRT may be associated with Wolff-Parkinson-White syndrome, and the ECG is characterized by a short PR interval, the presence of a short delta wave, and a prolonged QRS interval.
In orthodromic AVRT, antegrade conduction occurs through the AV node, similar to sinus rhythm. Retrograde conduction occurs through the accessory pathway, most commonly the bundle of Kent, leading to tachycardia with a narrow QRS complex.
In antidromic AVRT, antegrade conduction occurs through the bundle of Kent and causes ventricular depolarization. Retrograde conduction occurs through the AV node, leading to tachycardia with a wide QRS in most cases [ ].
3.3
Atrial tachycardia
Atrial tachycardia comprises 11 % to 16 % of all types of SVT and includes rapid rhythms such as atrial fibrillation, focal atrial tachycardia, multifocal atrial tachycardia, and atrial flutter [ , ].
3.3.1
Focal atrial tachycardia
Focal atrial tachycardia, also known as ectopic atrial tachycardia, most often occurs due to increased automaticity of myocardial cells at a single location in one of the atria [ ].
3.3.2
Multifocal atrial tachycardia
Multifocal atrial tachycardia, which comprises <1 % of pediatric SVTs, is characterized by an irregularly irregular rhythm with at least 3 distinct P wave morphologies which are easily distinguishable from QRS complexes ( Fig. 3 ) [ ].
3.3.3
Atrial flutter
Atrial flutter presents with rapid identical atrial depolarizations that create a sawtooth pattern on ECG, typically originating from a reentry circuit in the right atrium ( Fig. 4 ) [ ].
3.4
Junctional ectopic tachycardia
Junctional ectopic tachycardia is a type of SVT characterized by increased automaticity in the AV junction, which can be congenital or postoperative ( Fig. 5 ). Junctional ectopic tachycardia can cause left ventricular dysfunction when not properly treated [ , ].
4
Clinical presentation and diagnosis
4.1
Symptoms and signs of supraventricular tachycardia in children
The presentation of SVT in children varies with age, rate, and duration of the tachyarrhythmia, and underlying mechanism [ ]. It is essential to recognize and accurately evaluate the patient’s symptoms for effective diagnosis and treatment.
Infants with SVT may present with poor feeding, vomiting, irritability, increased sleepiness, syncope, or diaphoresis. If congestive heart failure is present, additional symptoms and signs may include cough, respiratory distress, pallor, or cyanosis. Toddlers and school-aged children may experience palpitations, chest pain, dizziness, shortness of breath, or syncope. Compared with infants and toddlers, school-aged children have substantially different presentations of SVT because they have greater ability to report symptoms [ ]. Adolescents report similar symptoms and signs and also additional signs such as decreased exercise tolerance, fatigue, anxiety, pallor, or diaphoresis.
4.1.1
Palpitations
Palpitations may be the most noticeable symptom of SVT in children. Palpitations typically are described as a rapid, fluttering, or pounding heart sensation that a child might feel in the chest, throat, or neck. Children as young as age three years may identify these sensations with various descriptions [ ].
4.1.2
Chest pain
Chest pain is another common symptom of SVT in children, particularly in toddlers, school-aged children, and adolescents. Chest pain occurs because of shortened diastole and decreased myocardial blood flow, potentially causing ischemia. This pain can persist for several minutes to an hour and typically is described as pressure-like and varying in intensity from sharp to dull [ ].
4.1.3
Dizziness or syncope
Syncope, defined as a transient loss of consciousness and postural tone resulting from altered cerebral perfusion, typically recovers spontaneously [ ]. In children, syncope usually is brief and recovers fully with no persistent effects. Dizziness or syncope in children with SVT may signify a decrease in cardiac output because of rapid heart rate and necessitates prompt medical attention [ ].
4.1.4
Dyspnea
Dyspnea (shortness of breath) may accompany palpitations and tachycardia in children with SVT. The severity of dyspnea may vary, ranging from mild dyspnea to severe respiratory distress, depending on the duration and rate of the tachyarrhythmia. Children may have symptoms such as difficulty breathing, rapid breathing, or a sensation of “not getting enough air” [ ].
4.2
Diagnostic tests
4.2.1
Electrocardiogram
A 12‑lead ECG is essential for all patients who present with tachycardia, particularly with a narrow QRS complex [ ]. An ECG with normal sinus rhythm typically may be required for comparison to make the diagnosis of SVT. A long strip capturing the onset of tachycardia may be especially helpful in identifying the cause of SVT. A four-step approach has been recommended to assess the type of SVT [ ]:
- (1)
Analyze the rhythm to determine the length of the QRS complex. A narrow QRS complex (< 120 ms) is observed in supraventricular arrhythmias. In contrast, a wide QRS complex may represent ventricular tachycardia [ , ].
- (2)
Differentiate the rhythm as regular or irregular. SVT typically presents with regular rhythm, except that an irregular rhythm is more likely associated with atrial fibrillation or atrial flutter.
- (3)
Evaluate the ECG for the presence or absence of P waves. Depending on the position of the P wave, ventricular and atrial rates may be compared. When the P wave is observed immediately after a QRS complex, the SVT likely is AVNRT or AVRT. In contrast, when the P wave is before the QRS complex, the SVT likely is sinus or atrial tachycardia [ , ].
- (4)
When it is difficult to identify the P wave because of tachycardia, a continuous ECG during vagal maneuvers or administration of drugs such as adenosine may stop the arrhythmia and show conversion to sinus rhythm, thereby confirming the diagnosis of SVT. It may be helpful to provide patients with a printed copy of the ECG for future reference.
4.2.2
Home monitoring
When a definitive diagnosis is not made with an ECG, extended rhythm monitoring may be necessary. A Holter monitor does continuous recording up to 7 days, while an event monitor can be used over 30 days and can record when activated. Symptoms may be subtle, contributing to a delay in diagnosis, especially in infants [ ]. An event monitor over 2 weeks may capture brief episodes that resolve spontaneously [ ]. In children with unspecified symptoms such as palpitations and syncope, the yield for a positive diagnosis with a Holter monitor may be low [ , ]. However, a Holter monitor may be valuable for patients with known comorbidities and cardiac conditions because it may help reassure families and alleviate fear by differentiating benign tachycardia from rhythm abnormalities such as SVT [ ].
4.2.3
Exercise stress test
Exercise may place a load on the patient’s heart that may not be experienced at rest but may help to induce or unmask arrhythmias for the diagnosis of SVT. Graded exercises are used to evaluate children for cardiac diseases, but there may be limited prognostic value of exercise testing for children.
4.2.4
Electrophysiologic study
An electrophysiologic study is an invasive test that provides a detailed description of the location and mechanism of the arrhythmia. As an invasive test, electrophysiologic studies are performed only when the diagnosis affects the treatment plan. With this technique, multipolar electrodes are placed in various heart locations via venous access, including the right atrium, right ventricle, tricuspid valve, and coronary sinus [ ]. Electrodes also may be placed in the left heart via the aorta. Electrophysiologic studies are usually performed for diagnosis in patients with severe symptoms or underlying cardiac disease and may also be used to map an area for catheter ablation. Complications are rare but may include thromboembolism, anatomic damage to the heart, arrhythmias, hemorrhage, infection, myocardial infarction, and death [ ].
5
Treatment
5.1
Acute treatment
Acute treatment options include vagal maneuvers, pharmacologic cardioversion, and electrical cardioversion. A 12‑lead ECG is obtained before intervention. The treatment option selected may depend on the patient’s hemodynamic status [ ].
5.1.1
Vagal maneuvers
Vagal maneuvers may be effective at all ages, but techniques vary with the patient’s ability to perform them. Options include the Valsalva maneuver, blowing into an occluded straw, and ice water stimulation of the diving reflex. Success in conversion rates varies, with one study showing resolution of SVT in 45 % of patients with the Valsalva maneuver and 20 % with the ice bag method [ ].
5.1.2
Pharmacologic cardioversion
Adenosine is the first-line drug for treatment of SVT in hemodynamically stable patients. It is administered intravenously, with the dose based on body weight. Adenosine works by slowing conduction in the AV node and interrupting reentry tachycardia. It also may cause vasodilation and bronchoconstriction.
Adenosine has a short half-life (several seconds) and is typically administered through a 3-way stopcock with an intravenous flush attached. Before administering adenosine, the clinician ensures that the blood pressure is appropriate for age, assesses heart function when possible, and ensures that the team is prepared to treat adverse events of adenosine; hypotension is treated with intravenous fluids or pressor drugs, and heart block may necessitate temporary pacing. Efficacy of adenosine ranges from 72 % to 79 % for all SVT and up to 96 % for reentrant SVT [ ]. When there is recurrent and persistent SVT or no response after adenosine, the accessory pathway may be modified by second-line drugs such as procainamide, β-blockers, verapamil, amiodarone, or digoxin, each with specific contraindications and adverse events.
5.1.3
Electrical cardioversion
Electrical cardioversion is indicated as first-line treatment for hemodynamically unstable patients or when other methods fail. A synchronized shock is delivered at 0.5–1 J/kg and may be increased to 2 J/kg when necessary. Sedation is typically recommended before shock administration [ ].
5.2
Long-term treatment
Long-term treatment may depend on age, symptoms, SVT characteristics, and potential complications from congenital heart disease. Assessment by a pediatric cardiologist is recommended.
5.2.1
Antiarrhythmic drugs
Common first-line long-term treatments for SVT include β-blockers, digoxin, and calcium channel blockers because these drugs have few adverse events. Propranolol and digoxin have similar efficacy but have a high frequency of recurrence (27 %) [ , ]. For recurrent SVT, flecainide, amiodarone, and sotalol may be effective but have higher rates of adverse effects [ , ]. Combination therapy may be used when monotherapy is unsuccessful.
5.2.2
Catheter ablation
Catheter ablation is a primary interventional method that may provide a high success rate for cure. The arrhythmia circuit is mapped with an electrophysiologic study, and arrhythmogenic tissue is destroyed with targeted radiofrequency energy or cryotherapy [ ]. Indications include SVT that is recurrent or refractory to drug therapy, and success rates vary with SVT mechanism. Acute success rate is highest for AVNRTs (97 %), followed by accessory pathways (92 %) and atrial tachycardia (89 %) [ ]. Although the procedure typically is safe, considerations in pediatrics include technical challenges because of small patient size, concerns about radiation exposure, and a small risk of causing AV block in septal pathways. Long-term outcomes show low recurrence rates and excellent safety profiles in experienced centers [ ], with frequency of recurrence ranging from 5 % to 10 % in the first year after the procedure and lower thereafter.
5.2.3
Surgical treatment
Although less common in the era of catheter-based therapies, surgical treatment may be valuable for patients with failed catheter ablation, anatomic variations that preclude catheter access, or concomitant cardiac surgery. Techniques include direct visualization and interruption of accessory pathways, maze procedures for atrial tachycardias, and hybrid methods that combine minimally invasive surgery with catheter ablation. Although surgical treatment is more invasive and requires longer recovery, the frequency of success may be higher (> 90 % for accessory pathway-mediated SVT) [ ] and recurrence lower compared with catheter ablation. The choice between catheter ablation versus surgical treatment may depend on individual patient factors, institutional expertise, and the specific type of SVT and location of the arrhythmogenic tissue.
6
Complications of supraventricular tachycardia in children
6.1
Hemodynamic instability
Infants and children may tolerate episodic tachycardia without hemodynamic instability. However, prolonged or frequent tachyarrhythmias may cause hemodynamic instability that may present as heart failure. Acute hemodynamic decompensation in SVT may manifest with altered mental status, syncope, hypotension, and respiratory distress. SVT may be diagnosed when patients present with heart failure symptoms and tachycardia. Infants commonly exhibit feeding intolerance, prolonged feeding times, and fussiness [ ]. Older children and teenagers may show gastrointestinal symptoms such as abdominal pain and vomiting, exertional dyspnea, and syncope. Diagnosis requires a high index of suspicion and correlation between clinical findings and diagnostic testing, including chest radiography, ECG, and echocardiography. Laboratory tests include serum electrolytes, infectious diseases evaluation, and cardiac markers such as brain-type natriuretic peptide and troponin.
6.2
Thromboembolic events
Paroxysmal SVT may be associated with the development of atrial fibrillation [ ]. In patients with Wolff-Parkinson-White syndrome, retrograde conduction via the accessory pathway may cause atrial fibrillation. Although there is no known association between SVT and thrombus formation in older pediatric patients, intra-atrial thrombus has been reported in neonates after recurrent SVT [ ]. New-onset dyspnea, chest pain, and neurologic deficits are investigated as possible thromboembolic events. Timely antithrombotic treatment and treatment of underlying causes may improve long-term outcomes.
6.3
Congestive heart failure
Long-standing SVT may cause cardiomyopathy and ventricular failure, presenting with signs of congestive heart failure, including increased respiratory effort, hepatomegaly, and edema. Diagnosis includes ECG and echocardiography to identify functional and structural changes. Treatment options focus on rate control, rhythm correction, and supportive therapy [ ]. Conversion to sinus rhythm is essential for restoring myocardial function [ , ].
6.4
Exercise limitation and decreased quality of life
Symptomatic SVT may limit exercise capacity, and activities and cause decreased quality of life [ ]. Recurrent SVT episodes may cause anxiety and fear in patients and their families. Adolescents may feel embarrassed or restricted in physical activities. Education, reassurance, and counseling may help manage expectations and improve compliance with therapy. Treatment options to control symptoms and prevent episodes may improve quality of life and enable normal activities [ ].
7
Special considerations
7.1
Supraventricular tachycardia in neonates and infants
Most neonates and infants diagnosed with SVT initially present with symptoms of feeding intolerance, tachypnea, respiratory issues, or lethargy. In comparison, children who are at an age to verbally communicate typically present with palpitations [ ]. The age at which SVT onset is noted is important for the long-term prognosis of the disease. Children who develop SVT at a younger age have poorer prognosis and increased complications in comparison to those with later onset. Neonates who develop SVT early in life often experience resolution within the first year.
7.2
Supraventricular tachycardia in fetuses and children with congenital heart disease
Fetal tachyarrhythmias, defined as a fetal heart rate >160 bpm, may be detected in utero. This condition may be observed in fetuses with congenital heart disease. A fetal echocardiogram may evaluate anatomic defects and cardiac function. Regular, longitudinal monitoring of the fetus is required in these cases. Fetuses with sustained SVT may show signs of hemodynamic instability, and structural findings may include biatrial enlargement and AV valve regurgitation. These fetuses may develop hydrops fetalis, which is a condition of severe edema that may be life-threatening to the fetus and may necessitate treatment in utero.
Children with congenital heart disease who present with SVT commonly have severe hemodynamic instability. They also have a worse prognosis from SVT and are more likely to require catheter ablation or surgical treatment.
7.3
Transition of care from pediatric to adult cardiology
Transitioning a patient from pediatric to adult cardiology is a multistep process that necessitates a thorough assessment of the patient’s needs [ ]. Overlap between pediatric and adult providers may avoid gaps in care and minimize the loss of information during the transfer of care. Patient education, counseling, and involvement in patient-led decisions may provide autonomy and improve understanding of the disease. Establishing multidisciplinary care for children with special needs may improve communication and transition of care.
8
Future directions and research
Although current treatment options, such as drugs and catheter ablation may provide relief from SVT, ongoing research focuses on the improvement of diagnosis, therapy, and long-term outcomes. Pediatric SVT treatment may be improved with advancements in genetic and molecular biomarkers and ablation methods.
Recent studies have highlighted potential genetic and molecular biomarkers for diagnosing and predicting SVT. In a study of gene sequencing in patients who had AVNRT, gene variations were identified that affected calcium signaling of the heart, implying irregular calcium management as a linkage to AVNRT due to variations of these genes that regulate calcium influx, release, reuptake, or initiation of electrical signaling [ ]. Although this study was conducted in adults, the findings also may be applicable to identifying a pathologic mechanism for AVNRT in children.
Another recent study identified fibronectin leucine rich transmembrane protein 3 (FLRT3) as a potential diagnostic biomarker for SVT. FLRT3 may be associated with neuronal development and axon guidance through its function as a cell adhesion molecule. FLRT3 may be downregulated in SVT patients compared with controls. Furthermore, FLRT3 knockout in hypertrophic cardiomyocytes may protect against cardiomyocyte apoptosis and encourage autophagy [ ]. Therefore, FLRT3 may be useful as a biomarker and therapeutic target.
Advancements in ablation techniques may improve the safety and efficacy of SVT treatments. Intracardiac echocardiography may help guide catheter ablation through its advanced visualization of cardiac anatomy and monitoring of catheter-tissue contact. Furthermore, intracardiac echocardiography may enable lower radiation exposure, lower procedure time, and improved accuracy of catheter placement [ , ]. Slow pathway ablation is another advancement for the treatment of children with paroxysmal SVT that may be safe and effective [ ].
Advancements in ablation therapy also may improve long-term patient well-being. The use of pulsed field ablation or radiofrequency catheter ablation for the treatment of paroxysmal SVT may improve quality of life and decrease anxiety and depression in adults [ , ], but further studies are needed to assess long-term efficacy and effects on children on quality of life after SVT treatment.
9
Conclusion
9.1
Summary of key points
In summary, SVT is prevalent in children, characterized by rapid heart rhythms originating from the atrial tissue above the AV node and interventricular septum. It may manifest as AVNRT, AVRT, atrial tachycardia, or junctional ectopic tachycardia. The etiology and contributing factors include reentrant circuits, abnormal automaticity, structural heart defects, electrolyte imbalances, and genetic predisposition. Clinical presentations vary with age, as infants typically show nonspecific symptoms like poor feeding or irritability, and older children experience palpitations, chest pain, or syncope. Diagnostic tools like ECGs, Holter monitors, exercise stress tests, and electrophysiologic studies are essential for diagnosis. Finally, treatment can involve acute interventions like vagal maneuvers or cardioversion, while long-term options include antiarrhythmic drugs and catheter ablation. Diagnosis and treatment are essential to avoid complications like congestive heart failure, hemodynamic instability, and decreased quality of life.
9.2
Recommendations for clinical practice and future research
Early diagnosis and intervention are crucial, especially for neonates and children with congenital heart disease. Comprehensive tools like ECG and Holter monitors aid in early detection and treatment, which is personalized based on age, symptoms, and cardiac conditions. Combining pharmacologic and non-pharmacologic therapies can optimize outcomes, and educating patients and families about the condition, treatment options, and psychological support is key. A smooth transition from pediatric to adult cardiology care ensures continuity in long-term management. Future research should focus on developing genetic and molecular biomarkers, advanced imaging techniques like intracardiac echocardiography, and innovations in ablation methods to improve diagnosis and treatment. Studies are needed to assess long-term treatment efficacy and quality of life outcomes, as well as genetic aspects like FLRT3 to discover new therapeutic targets and personalized treatments. Integrating these advancements can enhance care for children with SVT.
CRediT authorship contribution statement
Zoha Nizami: Writing – review & editing, Writing – original draft. Phoebe Garcia: Writing – original draft, Investigation. Paras Ahuja: Writing – original draft, Investigation. Aaron James Nipper: Writing – original draft, Investigation. Sachi Patel: Writing – original draft, Investigation. Hridhay Sheth: Writing – original draft, Investigation. Induja Gajendran: Writing – review & editing, Supervision, Resources. Reshvinder Dhillon: Writing – review & editing, Writing – original draft, Supervision.
Declaration of Generative AI and AI-assisted technologies in the writing process
AI was not used in preparation of this manuscript.
Funding
Editorial support was provided by the Dean’s Office, University of South Alabama , Frederick P. Whiddon College of Medicine.
Declaration of competing interest
The authors have nothing to declare.
Acknowledgements
We are grateful to Dr. Gul Dadlani for his critical review and John V. Marymont, Emily Wilson, and Elly Trepman for editorial support.
References
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