Supraventricular tachycardia (SVT) stands as the most common sustained arrhythmia in the neonatal age group, with an estimated incidence of infants as 0.25 per 1000 in infants and 0.06 per 1000 patients younger than one month [16]. AHF occurrs more commonly in 35% of patients under 4 months of age [17], a rate similar to the 39.5% incidence observed in our study. Due to the high tolerance and mild symptoms of neonates with supraventricular tachycardia (SVT) in the first 12–24 h, SVT often goes unnoticed for an extended period [18], resulting in frequent episodes of acute heart failure. Identifying risk factors contributing to the occurrence of AHF would assist in early detection and preventing decompensation.

In this study, we found that a longer duration of SVT— time to initial control of tachycardia > 24 h — could increase the risk of AHF. This finding is consistent with the study by Nadas et al., which reported a 19% incidence of AHF if tachycardia continued for 30 h, and a 50% incidence of AHF if tachycardia lasted for 48 h [19]. Comorbid conditions such as an inflammatory state, hypoxia, acidosis and electrolyte imbalance may trigger SVT and result in hemodynamic instability [20, 21]. In our study, hyperkalemia and anemia were identified as risk factors for AHF in SVT. B-type natriuretic peptide (BNP), a cardiac peptide released by the heart ventricles in response to changes in the ventricular pressure and/or volume, has been reported to be associated with AHF in children from other causes such as CHD [22]. Salas et al. have found that an increase in BNP levels, measured in critically ill neonates requiring assisted mechanical ventilation, may predict hemodynamic changes and a poor prognosis [23]. BNP in our study was identified to be a risk factor for AHF in neonates secondary to SVT.

Structural heart disease contributes to cardiovascular collapse during a tachycardia episode [24], but our study did not identify it as a risk factor. This may be because the majority of subjects had simple congenital heart diseases with small shunt volumes, while other studies involved large shunt volumes or complex congenital heart disease. As cardiac pump reserve function is limited, especially in immature infants, a fast heart rate can lead to a declined cardiac output. Prenatal history, prematurity, intrauterine tachycardia and urgent caesarean section are considered indicators of decreased fetal circulation and may be associated with unfavorable clinical outcome in neonates with SVT [25, 26]. However, we didn’t find these results. Perhaps the condition of the newborns in our study is not as serious. Lower body weight and younger age were reported to be associated with a fatal or near-fatal outcome in infant with SVT [8]. However, in our study, this association does not appear to be linked to AHF, potentially due to the inclusion of subjects with similar age and weight in each group.

Indeed, BNP is rarely used as a biomarker in newborns, because it can be affected by extra-cardiac conditions such as anemia, severe infections. It can also be influenced by certain prenatal and postnatal factors, such as mothers with type 1 diabetes, prematurity, cesarean Sect. [27]. Reeves et al. observed an extremely high level of approximately 20,000 pg/mL of N-terminal pro-brain natriuretic peptide (NT-proBNP), which originates from the breakdown of BNP, in 3 neonates with decompensated SVT [28]. This finding indicates the potential of plasma BNP in predicting AHF secondary to SVT in neonates. In our study, the value of BNP for predicting AHF was found to be 2460.5pg/ml. That is significantly higher than 758.7 pg/mL ~ 741.4 pg/mL at the 97.5th percentile in normal infants aged from 0-30d, as reported by Cantinotti et al. [27]. Furthermore, among the associated risk factors, BNP > 2460.5pg/ml was identified as an independent predictor. This indicates that the incidence of AHF secondary to SVT is not only influenced by the tachycardia itself, but also by various other factors related to the overall cardiovascular status. Specifically, BNP may accurately reflect the overall situation.

In addition to early intervention based on the type of tachycardia, it is crucial to have an effective treatment option to promptly terminate SVT and prevent decompensation. Digitalis was the most commonly used first-line drug in our study. However, it does not appear to be superior to other first-line drugs in preventing HF. Although the combination of positive inotropic activity with negative chronotropic effects has been shown to reduce hospital admissions in heart failure [29], esmolol appears to be more effective in preventing AHF. Our findings indicate that esmolol successfully terminated SVT without developing HF in 4 neonates, including those who did not respond to digitalis. This suggests that the positive inotropic effect may not be fully advantageous when dealing with tachycardia with preserved ejection fraction. In this case, esmolol alone or in combination with digitalis may be more effective in controlling elevated haemodynamic parameters in patients with SVT, as reported [30].

Till now, cardiologists still face a dilemma in balancing efficiency and safety when terminating acute recurrent and persistent SVT in neonates. Compared to first-line treatment, second-line therapy has attractive efficacy in case of refractory SVT. However, it is considered a reserved option due to the reported relatively high incidence of systemic adverse effects. These effects include propafenone-induced cardiac arrest, amiodarone-induced hypothyroidism and pulmonary fibrosis, cardiac depression caused by DC cardioversion, and the potential for pro-arrhythmia [2, 15]. However, some authors advocate that amiodarone and propafenone are equally safe and effective when used with monitoring as the first-choice drugs, especially in infancy [31,32,33]. In this study, 8 newborns who developed AHF were successfully treated with second-line therapy to terminated the prolonged SVT without any adverse effects. We also observed that neonates with a BNP > 2460.5pg/ml had a higher likelihood of requiring second-line therapy to control SVT. The equal value of BNP in predicting AHF and anti-arrhythmic treatment may not be coincidental. That’s exactly what Bjeloševič et al. reported: heart failure is a possible predictor of arrhythmia persistence. The need for ablation and mortality rate are reduced by the common use of amiodarone and propafenone in terminating arrhythmia [34]. Though the diagnostic accuracy is not significant, further study is warranted to explore the value of BNP in monitoring and predicting treatment response.

This study has some limitations. First, the sample size of this study is small, and we cannot further subdivide the research subjects, such as by age. Second, the diagnosis of heart failure is made using ROSS score, which is partly subjective. Third, the selection of anti-arrhythmic drugs and doses was based on the preference of attending physician. This circumstance made it impossible to study and characterize a clearly defined therapy protocol. Fourth, the retrospective study design hindered the assessment of adverse effects of anti-arrhythmic treatment. None of these neonates exhibited significant adverse reactions. Therefore, the definition of relatively higher risk anti-arrhythmic treatment is based on previous literature reports. Finally, there are many factors that influence BNP levels, which should be considered in conjunction with the clinical condition of children when applying it. Despite these limitations, we believe that our data about neonatal SVT can be valuable for neonatologists. Further multicenter prospective studies are needed to confirm our findings.