Evaluation of the clinical course and therapeutic approaches in neonatal supraventricular tachycardia: a retrospective study

Authors

Abstract

Aim The purpose of this study was to evaluate the clinical course of and therapeutic approaches toward neonatal supraventricular tachycardia (SVT) in the neonatal intensive care unit (NICU).
Materials and Methods Data for demographic characteristics, clinical course, echocardiographic findings, treatments applied, and responses to treatment in neonates diagnosed with SVT in the NICU between January 2007 and January 2023 were evaluated retrospectively.
Results Thirty-five neonates with SVT were included in the study. The prevalence of SVT was 0.48% in our unit during the study period. Six neonates (17.1%) had antenatal diagnoses of SVT. Hydrops fetalis was present in two neonates (5.7%) and congenital heart malformation in 14 (40%). Congestive heart failure developed in 11 patients (31.4%), while recurrence of SVT was documented in 17 (48.6%). SVT resolved spontaneously in four cases and with vagal maneuvers in three. The other 28 neonates required antiarrhythmic therapy. The patients were divided into groups according to the presence or absence of congestive heart failure and SVT recurrence. A statistically significant relationship was observed between the development of congestive heart failure and antenatal diagnosis of SVT (p = 0.041). Statistically significant differences were also determined between the recurrence of SVT and mean heart rate (p = 0.025), mean length of hospitalization (p = 0.09), and prophylactic medication requirements (p = 0.005).
Discussion If a neonate with SVT has a history of antenatal SVT, hydrops fetalis, recurrence, congestive heart failure, or congenital heart malformation, these conditions cause more serious morbidity and mortality.

Keywords

Introduction

Supraventricular tachycardia (SVT) is the most common arrhythmia, with an estimated incidence of 0.1%-0.4 % in infants and children [1, 2, 3]. The first SVT attack typically occurs during the first months of life in newborns and infants [4]. It may also begin in the antenatal period and cause severe complications, such as hemodynamic instability, congestive heart failure, hydrops, and even death, due to its rapid or prolonged course [5]. Since the clinical course of SVT is non- specific and easily confused with other acute illnesses, such as sepsis, it may be difficult to identify early in the neonatal period. Early recognition before complications occur, in addition to emergent treatment and management of SVT, is therefore of critical importance.
While SVT attacks may terminate spontaneously, they may also require therapeutic options ranging from simple vagal maneuvers to complex treatments such as multiple drug therapies, cardioversion, or electrophysiological studies [5, 6].
Numerous studies of SVT have investigated pediatric patients from different age groups together, including neonates. The present study was intended to examine SVT in a study population consisting only of neonates. The aim was to evaluate the clinical course, therapeutic approaches, and outcomes in neonates diagnosed with SVT and to contribute to the existing literature on the subject.

Materials and Methods

All cases of SVT diagnosed within the first 28 days of life and followed up and treated in the Neonatal Intensive Care Unit (NICU) of Karadeniz Technical University, Faculty of Medicine, Turkey, between January 2007 and January 2023 were included in the study.
Data for demographic characteristics, clinical course, echocardiographic (ECHO) findings, treatments applied, responses to treatment, prenatal histories, and maternal features of neonates diagnosed with SVT during the study period were analyzed retrospectively.
The patients were divided into groups according to the presence or absence of congestive heart failure and SVT recurrence.
The diagnosis of SVT was based on ECG findings, and that of congestive heart failure on ECHO and clinical findings such as hepatomegaly, tachypnea, tachycardia, poor feeding, and impaired peripheral perfusion. SVT was defined as a narrow- complex QRS tachycardia with abrupt onset and termination, a rapid increase in heart rate, and the absence of normal P-wave morphology on ECG [7]. Recurrence of SVT was defined as the development of SVT after treatment of the first SVT attack during hospitalization.
Statistical Analysis
All statistical analyses were performed in IBM SPSS 22.0 enviroment (licensed by Karadeniz Technical University, Trabzon, Türkiye). Continuous variables were expressed as means ± SD, and categorical variables were expressed as percentages and numbers. A Student t-test was used to compare the means of the variables between two groups, and the Mann-Whitney U test was used for nonparametric variables. The categorical variables were analyzed with the Chi-Square test. Results were evaluated at a 95% confidence interval, and p-values less than 0.05 were considered statistically significant.
Ethical Approval
The study was approved by the Ethics Committee of Karadeniz Technical University, Faculty of Medicine (Date: 2023-09-25, No: 172).

Results

A total of 7,326 neonates were hospitalized in the NICU during the study period, 35 of whom were diagnosed with SVT. The prevalence of SVT in our unit was 0.48%. The neonates’ mean gestational week was 37.2±2.6, the mean birth weight was 3085 ± 611.6 g, the mean age at the time of first SVT was 7.3±9.3 days, and the mean length of hospitalization was 17.5±12.4 days (Supplementary Table S1).
Six neonates (17.1%) had antenatal diagnoses of SVT. Two of the 35 neonates (5.7%) had hydrops fetalis, one of whom also had an antenatal diagnosis of SVT. The incidence of hydrops associated with antenatal SVT was 50%. Congenital heart malformation was present in 14 of the 35 neonates (40%), atrial septal defect in 11, ventricular septal defect in one, hypoplastic left heart syndrome in one, and total anomalous pulmonary venous return in one.
Congestive heart failure developed in 11 of the 35 patients (31.4%), and in four of the six patients diagnosed with antenatal SVT. Three of the four neonates were discharged, and the remaining one was referred for electrophysiological examination. Recurrence of SVT was observed in six of the 11 patients who developed congestive heart failure. Recurrence of SVT during hospitalization in the NICU was documented in 17 of the 35 patients (48.6%) (Supplementary Table S1).
SVT resolved spontaneously in four neonates and with vagal maneuvers in three. The other 28 neonates required antiarrhythmic therapy for SVT termination. Adenosine was the most commonly used first-line medication for SVT termination, followed by amiodarone and digoxin (65.7%, 11.4%, and 5.7%, respectively) (Supplementary Table S1). SVT remained resistant to the first medications in 19 of the 35 neonates (54.3%), and these required a second drug for termination. Prophylactic pharmacological therapy was used in 21 of the 35 neonates (60%) (Supplementary Tables S2 and S3) and consisted of digoxin in seven (20%), amiodarone in six (17.1%), propranolol in five (14.3%), and combined amiodarone and propranolol in three (8.6%).
Twenty-nine neonates (82.9%) were discharged, and three (8.6%) were referred to another center for electrophysiological examination. The ECHO findings of the three referred neonates were reported as atrial septal defect in one, total abnormal pulmonary venous return in another, and normal in the third. Mortality occurred in three (8.6%) of the 35 neonates. One of the exitus patients was a mature neonate with normal ECHO findings who died after SVT on the third day of life. The other was a premature infant with normal ECHO findings who died three days after SVT on the 50th day of life. The final exitus patient, with hypoplastic left heart syndrome, died four days after SVT on the 12th day of life.
A statistically significant relationship was observed between the development of congestive heart failure and a history of antenatal SVT (p = 0.041) (Supplementary Table S2). In addition, statistically significant associations were found between the recurrence of SVT and mean heart rate (p = 0.025), first medication for SVT termination (p = 0.018), and medication for prophylaxis (p < 0.05). No statistically significant relationship was found between SVT recurrence and mean length of hospitalization (p = 0.09) (Supplementary Table S3).

Discussion

Thirty-five neonates diagnosed with SVT in this study were retrospectively evaluated in terms of demographic characteristics, clinical course, ECHO findings, therapeutic approaches, and outcomes. According to the study findings, i) the prevalence of SVT was 0.48%, ii) antenatal diagnosis of SVT was an important indicator for the development of congestive heart failure, iii) prophylactic medication requirements, and mean heart rate were statistically higher in neonates with SVT recurrence, and iv) the association between SVT recurrence and the mean length of hospitalization did not reach statistical significance.
The prevalence of SVT (0.48%) in this research was similar to that in previous studies, and the rate of antenatal SVT among these neonates was 17.1% [1, 2, 3]. Although antenatal tachyarrhythmias are very rare during pregnancy (< 0.1%), the most common type is SVT [8]. Antenatal SVT can lead to congestive heart failure, hydrops fetalis, and even mortality in case of an increased heart rate or prolonged course [5]. Sreeram and Wren investigated 29 SVT patients younger than three months and reported that congestive heart failure occurred in 22 (76%) cases [9]. The rate of development of congestive heart failure in the present study was 31.4%. Similar to our study, Ludomirsky and Garson reported that heart failure developed in 35% of patients with SVT under four months of age [10]. Research has also described younger age, faster heart rate, and the presence of congenital heart disease as essential factors in the development of congestive heart failure. In the present study, congenital heart disease was determined in six (54.5%) of the 11 neonates with congestive heart failure. The presence of antenatal SVT emerged as a significant risk factor for the development of congestive heart failure.
The incidence of hydrops fetalis associated with antenatal SVT has been reported to be as high as 40% in previous studies [13]. Since hydrops fetalis developed in one of the two cases with antenatal SVT, the findings of the present study are very similar to those of other studies investigating the relationship between antenatal SVT and hydrops fetalis.
Several studies have cited a wide range of rates of SVT recurrence in pediatric patients [1, 14, 15, 16, 17, 18]. Vari et al. investigated 90 patients under six months of age with documented SVT, and they found that 19 (21%) experienced a recurrence of SVT within 31 days of discharge [18]. Another study reported a recurrence rate of SVT during follow-up of 83% in 217 children whose first attack occurred at a median age of 24 months [1]. The SVT recurrence rate during hospitalization in the present study was 48.6%.
Therapeutic approaches in SVT include, first, acute treatment of the attack, and second, prophylactic pharmacological therapy for the prevention of recurrences. The first-line pharmacological agent in SVT is adenosine, as in the present study [8]. Adenosine, due to its very short half-life and ability to transiently block atrioventricular nodal conduction, remains the first-line pharmacologic agent for the acute termination of supraventricular tachycardia (SVT) in neonates [8]. In terms of prophylactic therapy, there are various approaches regarding the type and duration of antiarrhythmic agents, and applications may vary among clinicians in terms of optimal strategy [4, 14, 15, 19]. The most commonly used prophylactic agents, in descending order of frequency, were digoxin, amiodarone, propranolol, and a combination of amiodarone and propranolol as dual therapy. Another important finding of this study was that prophylactic medication requirements were significantly higher in neonates with recurrent SVT.
The data from this study also indicate that the presence of SVT recurrence was associated with a longer duration of hospitalization; however, this finding was not statistically significant. Seslar et al. reviewed 171 patients with SVT under one year of age in their multicenter study and reported a mean length of hospital stay of 6.8 ± 7 days in 65 neonates, the duration increasing in line with the need for intensive care [20]. However, the length of stay in our patients was higher than that in Seslar et al., and was even longer in neonates with SVT recurrence [20].
A faster heart rate in a fetus or neonate with SVT can cause problems ranging from hemodynamic compromise to mortality [5]. The mean heart rate in the present study was significantly higher in neonates with SVT recurrence and lower in those with congestive heart failure, although this was not statistically significant.
Another important aspect of neonatal SVT is that it can be life- threatening. Környei et al. reviewed 157 patients under one year of age with symptomatic tachyarrhythmia and observed a mortality rate of 3% [21]. In another study, involving a multicenter data analysis of 2,848 infants diagnosed with SVT, the mortality rate was 2% in the entire patient group, but 6% in the congenital heart disease group [22]. The mortality rate of 8.6% in the present study population was quite high compared to previous studies. This may be attributable to the presence of fatal heart disease in one and to another being a premature newborn.

Limitations

The principal limitations of this study lie in its retrospective nature and small patient numbers. We think that a longer follow-up period and investigation of the type and duration of use of antiarrhythmic agents would have yielded more definite information about SVT in our patients. Further prospective studies with larger sample sizes are now needed for a more effective evaluation of outcomes, clinical course, and appropriate treatments (optimal duration with the most effective drug) in cases of neonatal SVT.

Conclusion

In conclusion, the presence of an underlying congenital heart malformation or antenatal SVT, and recurrence of SVT during follow-up in a neonate with SVT may affect the course of the disease. It is therefore necessary to specifically inquire into these parameters in the follow-up of neonatal SVT and to proceed accordingly.

References

1. Garson A, Gillette PC, McNamara DG. Supraventricular tachycardia in children: clinical features, response to treatment, and long-term follow-up in 217 patients. J Pediatr. 1981;98(6):875-82. doi:10.1016/s0022-3476(81)80578-1.
   Article PubMed Google Scholar
2. Weindling SN, Saul JP, Walsh EP. Efficacy and risks of medical therapy for supraventricular tachycardia in neonates and infants. Am Heart J. 1996;131(1):66-72. doi:10.1016/s0002-8703(96)90052-6.
   Article PubMed Google Scholar
3. Spearman AD, Williams P. Supraventricular tachycardia in infancy and childhood. Pediatr Ann. 2014;43(11):456-60. doi:10.3928/00904481-20141022- 13.
   Article PubMed Google Scholar
4. Bruder D, Weber R, Gass M, Balmer C, Cavigelli-Brunner A. Antiarrhythmic medication in neonates and infants with supraventricular tachycardia. Pediatr Cardiol. 2022;43(6):1311-8. doi:10.1007/s00246-022-02853-9.
   Article PubMed Google Scholar
5. Jaeggi E, Öhman A. Fetal and neonatal arrhythmias. Clin Perinatol. 2016;43(1):99-112. doi:10.1016/j.clp.2015.11.007.
   Article PubMed Google Scholar
6. Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol. 2000;11(1):25-38. doi:10.1016/s1058-9813(00)00033-3.
   Article PubMed Google Scholar
7. Cannon B, Snyder CS. In: Martin RJ, Fanaroff AA, Walsh MC, eds. Fanaroff and Martin’s neonatal-perinatal medicine diseases of the fetus and infant. 11th ed. Elsevier, Philadelphia; 2020. p.1375-92.
   PubMed Google Scholar
8. Miyoshi T, Maeno Y, Hamasaki T, et al. Antenatal therapy for fetal supraventricular tachyarrhythmias: multicenter trial. J Am Coll Cardiol. 2019;74(7):874-85. doi:10.1016/j.jacc.2019.06.024.
   Article PubMed Google Scholar
9. Sreeram N, Wren C. Supraventricular tachycardia in infants: response to initial treatment. Arch Dis Child. 1990;65(1):127-9. doi:10.1136/adc.65.1.127.
   Article PubMed Google Scholar
10. Ludimorsky A, Garson Jr. A. Supraventricular syndromes. In: Gillette PC, Garson Jr. A, editors. Pediatric arrhythmias: electrophysiology and pacing. Philadelphia: W.B. Saunders; 1990. p.380-426.
    PubMed Google Scholar
11. Naheed ZJ, Strasburger JF, Deal BJ, Benson DW Jr, Gidding SS. Fetal tachycardia: mechanisms and predictors of hydrops fetalis. J Am Coll Cardiol. 1996;27(7):1736-40. doi:10.1016/0735-1097(96)00054-x.
    Article PubMed Google Scholar
12. Krapp M, Kohl T, Simpson JM, Sharland GK, Katalinic A, Gembruch U. Review of diagnosis, treatment, and outcome of fetal atrial flutter compared with supraventricular tachycardia. Heart. 2003;89(8):913-7. doi:10.1136/ heart.89.8.913.
    Article PubMed Google Scholar
13. Hinkle KA, Peyvandi S, Stiver C, et al. Postnatal outcomes of fetal supraventricular tachycardia: a multicenter study. Pediatr Cardiol. 2017;38(7):1317-23. doi:10.1007/s00246-017-1662-1.
    Article PubMed Google Scholar
14. Bücking C, Michaelis A, Markel F, et al. Evaluation of clinical course and maintenance drug treatment of supraventricular tachycardia in children during the first years of life. A cohort study from Eastern Germany. Pediatr Cardiol. 2022;43(2):332-43. doi:10.1007/s00246-021-02724-9.
    Article PubMed Google Scholar
15. Mecklin M, Linnanmäki A, Hiippala A, et al. Multicenter cohort study on duration of antiarrhythmic medication for supraventricular tachycardia in infants. Eur J Pediatr. 2023;182(3):1089-97. doi:10.1007/s00431-022-04757-5.
    Article PubMed Google Scholar
16. Riggs TW, Byrd JA, Weinhouse E. Recurrence risk of supraventricular tachycardia in pediatric patients. Cardiolog. 1999;91(1):25-30. doi:10.1159/000006873.
    Article PubMed Google Scholar
17. Michel M, Renaud C, Chiu-Man C, Gross G, Jaeggi E. Postnatal recurrence and transesophageal inducibility of prenatally treated fetal supraventricular tachycardia. Heart Rhythm. 2022;19(8):1343-9. doi:10.1016/j.hrthm.2022.04.013.
    Article PubMed Google Scholar
18. Vari D, Kurek N, Zang H, Anderson JB, Spar DS, Czosek RJ. Outcomes in infants with supraventricular tachycardia: risk factors for readmission, recurrence and ablation. Pediatr Cardiol. 2024;45(6):1211-20. doi:10.1007/s00246-022-03035- 3.
    Article PubMed Google Scholar
19. Brugada J, Blom N, Sarquella-Brugada G, et al. Pharmacological and non- pharmacological therapy for arrhythmias in the pediatric population: EHRA and AEPC-Arrhythmia Working Group joint consensus statement. Europace. 2013;15(9):1337-82. doi:10.1093/europace/eut082.
    Article PubMed Google Scholar
20. Seslar SP, Garrison MM, Larison C, Salerno JC. A multi-institutional analysis of inpatient treatment for supraventricular tachycardia in newborns and infants. Pediatr Cardiol. 2013;34(2):408-14. doi:10.1007/s00246-012-0474-6.
    Article PubMed Google Scholar
21. Környei L, Szabó A, Róth G, Ferenci T, Kardos A. Supraventricular tachycardias in neonates and infants: factors associated with fatal or near-fatal outcome. Eur J Pediatr. 2021;180(8):2669-76. doi:10.1007/s00431-021-04159-z.
    Article PubMed Google Scholar
22. Chu PY, Hill KD, Clark RH, Smith PB, Hornik CP. Treatment of supraventricular tachycardia in infants: analysis of a large multicenter database. Early Hum Dev. 2015;91(6):345-50. doi:10.1016/j.earlhumdev.2015.04.001.
    Article PubMed Google Scholar

Declarations

Additional Information

Publisher’s Note
Bayrakol MP remains neutral with regard to jurisdictional and institutional claims.

Rights and Permissions

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0). To view a copy of the license, visit https://creativecommons.org/licenses/by-nc/4.0/

View full license details →

About This Article