A change in QT interval and ST-segment after radiofrequency catheter ablation in pediatric patients with Wolff–Parkinson–White syndrome

doi:10.21203/rs.3.rs-3250877/v1

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A change in QT interval and ST-segment after radiofrequency catheter ablation in pediatric patients with Wolff–Parkinson–White syndrome

https://doi.org/10.21203/rs.3.rs-3250877/v1

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Background

Few studies have examined QT, JT interval, and ST-segment changes due to radiofrequency catheter ablation (RFA) in manifest Wolff–Parkinson–White (WPW) syndrome in pediatric patients.

Methods

The study involved 27 patients (male-to-female, 13:14; age, 12 (5–16) years) who were diagnosed with WPW syndrome and underwent RFA in our hospital between 2009 and 2022. Electrocardiographic (ECG) changes were compared between the group with ventricular preexcitation due to an accessory pathway (manifest group, n = 16) and those without it (concealed group, n = 11).

Results

The QT interval before RFA was significantly longer in the manifest group than in the concealed group (402 [362–482] vs. 344 [323–427]; p = 0.001). The QT interval was significantly shortened in the manifest group before and after RFA (402 [362–482] vs. 360 [298–422] msec; p = 0.01). At 1 month, the QT interval difference between the manifest and concealed groups disappeared (366 [305–437] vs. 335 [301–436] msec; p = 0.001). ST-segment changes were found after RFA in 63% (10/16) of the patients in the manifest group but not in the concealed group. ECG changes presenting the Brugada-pattern were found in two patients. One month later, ECG abnormalities persisted in only one patient.

Conclusions

In cases of prolonged QT interval or ST-segment abnormalities lasting > 1 month after RFA, the coexistence of manifest WPW syndrome with long QT syndrome or Brugada syndrome may be considered.

JT interval

QT interval

ST-segment change

radiofrequency catheter ablation

Wolff–Parkinson–White syndrome

Wolff–Parkinson–White (WPW) syndrome is a relatively common arrhythmic disorder in children and can cause sudden cardiac death (SCD), paroxysmal supraventricular tachycardia (SVT), and atrial fibrillation (AF) [1, 2]. On the contrary, long QT syndrome (LQTS) and Brugada syndrome (BrS) are hereditary lethal arrhythmias that can cause syncope and SCD even in children [3, 4]. Electrocardiographic (ECG) findings, such as prolonged QT interval and coved type ST-segment elevation in the right precordial leads (V1–V3), are important for the diagnosis of LQTS and BrS, respectively. In manifest WPW syndrome, it may be difficult to decipher the ECG waveform because it is altered by ventricular preexcitation. Few studies have examined the QT interval, JT interval, and ST-segment changes due to radiofrequency catheter ablation (RFA) in pediatric patients with WPW syndrome [5–7]. Thus, this study aimed to determine the changes in QT interval and ST-segment before and after RFA in pediatric patients with WPW syndrome.

The study analyzed 30 pediatric patients with WPW syndrome who underwent an electrophysiologic study (EPS) and RFA for atrioventricular reciprocating tachycardia (AVRT) in our hospital between April 2009 and March 2022, and data were analyzed by medical records, 12-lead ECGs, echocardiography, and EPS findings. This study did not include patients with structural heart diseases. ECG recordings were analyzed the day before RFA, day after RFA, next day after RFA, and 2–4 weeks after RFA at the outpatient visits. Three patients were excluded: one patient who had a recurrence of the delta wave within 1 month after RFA, one who was taking group III antiarrhythmic drug (amiodaron) orally, and one whose electrocardiography was not performed after 1 month. Finally, this study enrolled 27 patients (male:female, 13:14; age, 12 (5–16) years). Patients were divided into two groups: those with ventricular preexcitation due to an accessory pathway before RFA (manifest group, n = 16) and those without it (concealed group, n = 11), and the two groups were compared. Each group was compared before and after RFA.

EPS and RFA were performed in patients who had ECG findings of SVT or ECG evidence of delta waves and awareness of palpitations. During an EPS and RFA, sedation and analgesia were performed using intravenous anesthesia with midazolam, pentazocine, and dexmedetomidine continuous infusion. None of the patients received general anesthesia through inhalation anesthesia, muscle relaxants, or tracheal intubation. An EPS was performed by inserting 2-Fr 4-electrode catheters in the high right atrium, His bundle, and right ventricular apex, and 2-Fr 8- or 5-Fr 10-electrode catheters in the coronary sinus. The induction of tachycardia consisted of premature and continuous stimulations from the ventricles and atria. If induction of tachycardia was not possible, continuous infusion of isoproterenol was administered. RFA was performed using a 7-Fr, 4-mm tip ablation catheter. After RFA in all patients, we confirmed the absence of conduction recurrence in the accessory pathway for > 20 min. Acute success of RFA was defined as loss of antegrade and retrograde accessory pathway conductions in the manifest group and loss of accessory pathway retrograde conduction in the concealed group.

The PQ, QRS, QT, and JT intervals were measured in lead V5 or II. The tangential method was used to measure the QT and JT interval, and Bazett’s and Fridericia’s formulas were also used [8, 9].

Echocardiography was performed the day before and after RFA. Echocardiography was performed using an iE 33 Echocardiographic System (Philips Medical System, Andover, MA, USA) or Vivid E9 Echocardiographic System (GE Healthcare, Horten, Norway). In all patients, no medications that affected cardiac function were taken during electrocardiography and echocardiography examinations, and antiarrhythmic drugs had a washout period of more than five times their half-life.

In statistical studies, data are usually presented as median with range. Comparisons of numbers between two unmatched groups were made using the Mann–Whitney U test, and Wilcoxon’s coded rank test was used for comparisons between two matched groups. Values among the three groups were compared using the Steel-Dwass test. A p < 0.05 was considered statistically significant.

This study was approved by our institutional ethics committee (No.63 − 27), and written informed consent was obtained from the parents of our patients.

Patient characteristics and 12-lead ECG, echocardiogram, and EPS findings are presented in Table 1. The manifest group was older and correspondingly larger. None of the patients had AF, wide QRS tachycardia with rapid conduction of antegrade AP conduction due to AF, or torsade de pointes on ECG during the study period. None of the patients had cardiac events such as convulsions, syncope, and cardiac arrest. Regarding SVT, palpitations of several minutes occurred less than five times before RFA in all patients. In both groups, various antiarrhythmic drugs were administered to prevent SVT recurrence. Although sodium channel blockers were administered in the manifest group, no patients lost manifest accessory pathways before RFA. Although the left ventricular ejection fraction (manifest vs. concealed 64.9% [42.7–79.4%] vs. 76.5% [60.0–80.4%]; p = 0.02) was within normal limits in both groups, it was significantly lower in the manifest group than in the concealed group. The heart rate in AVRT induced during EPS was approximately 170 beats per minute, with no significant difference between the two groups. The effective refractory period of the antegrade accessory pathway was 245 (190–480) msec. Regarding SVT induction in EPS, the SVT was not induced in two patients. Antidromic AVRT was induced in one patient in the manifest group. In other patients, orthodromic AVRT was induced (N = 24).

ECG findings showed that the QRS duration (128 [104–153] msec vs. 74 [57–93] msec; p < 0.001) and QT interval (402 [362–484] vs. 347 [322–427] msec; p < 0.001) were significantly longer in the manifest group than in the concealed group. The QT interval was significantly longer in the manifest group than in the concealed group with both Bazett’s formula (419 [389–458] vs. 381 [353–407] msec; p < 0.001) and Fridericia’s formula (418 [383–447] vs. 371 [352–399] msec; p < 0.001). The PQ interval was significantly shorter in the manifest group than in the concealed group (83 [59–98] vs. 132 [113–166] msec; p < 0.001). The JT interval (283 [233–347] vs. 274 [257–349] msec; p = 0.45), Bazett’s formula (304 [244–334] vs. 290 [273–324] msec; p = 0.88), or Fridericia’s formula (302 [240–331] vs. 290 [273–324] msec; p = 0.63) did not differ significantly between the manifest group and the concealed group (Table 2). None of the patients had marked QT prolongation before RFA or fulfilled the diagnostic criteria for LQTS.

The acute success rate of RFA for the accessory pathway was 100%. The QT interval before and after RFA was significantly shortened after RFA in the manifest group (prior RFA vs. post-RFA vs. 1-month post-RFA, 407 [362–482] vs. 358 [298–422] vs. 362 [305–437] msec; p = 0.01). Both Bazett’s formula (prior RFA vs. post-RFA vs. 1-month post-RFA, 419 [389–458] vs. 400 [346–423] vs. 379 [335–409] msec; p = 0.01) and Fridericia’s formula (prior RFA vs. post-RFA vs. 1-month post-RFA, 418 [383–447] vs. 381 [337–413] vs. 375 [330–418] msec; p = 0.01) showed significant shortening of the QT interval, and Fridericia’s formula shortened the QT interval in all patients. In the concealed group, no statistically significant change in the QT interval was found before or post-RFA (Fig. 1a–1f). In addition, no statistically significant changes in the JT interval were found in either group before or post-RFA. Regarding ECG findings 2–4 weeks after RFA, the QRS duration was significantly longer in the manifest group, but no statistically significant differences in the PQ, QT, and JT intervals were noted between the two groups (Table 3).

ST-segment change and T-wave abnormalities were observed in 10 of 16 patients (63%) in the manifest group from the day of RFA to the next day. No patients in the concealed group had ST-segment changes or T-wave abnormalities. The most common abnormalities were negative T waves in the inferior leads in 4 (40%) patients, J-point elevation in 3 (30%), Brugada-pattern ECG changes in 2 (20%), and T-wave elevation in 1 (10%). The sites of the accessory pathway in the two patients with Brugada-pattern ECG change were right posteroseptal and left lateral, and the ECG on the day after RFA showed a saddleback type in lead V2 and a coved type in lead V1 relatively (Fig. 2a, 2b). The Brugada-pattern ECG normalized after 1 month. After 2–4 weeks, the ECG was normalized in 15 of 16 patients (94%) (Table 4). One patient with elevated T waves showed continuous ECG changes 1 month later; however, a normal ECG was obtained at the time of the outpatient visit 1 year later.

In this study, the QT interval shortened in all patients in the manifest group after RFA. ST-segment changes are common; however, ECG findings were found to normalize in approximately 1 month. The JT interval did not change before and after RFA. No changes in the PQ, QRS, QT, or JT interval were noted before and after RFA, and no ST-segment changes were found in the concealed group. Therefore, the ST-segment changes in the manifest group may not be due to the effect of RFA on the cardiomyocytes but to the absence of ventricular preexcitation.

In adult patients, the coexistence of LQTS and WPW syndrome has been reported [10–13]. SCD in WPW syndrome is thought to be caused by AF with a rapid ventricular response via an AP. In some patients with WPW syndrome, SCD may be included with LQTS. In previous reports, most patients diagnosed with LQTS after RFA of WPW syndrome have significant QT prolongation before RFA [11–13]. In the present study, none of the patients had an extremely prolonged QT interval before RFA and fulfilled the diagnostic criteria for LQTS. Even in patients with manifest WPW syndrome, if the ECG shows significant QT prolongation, syncope, or an episode of cardiac arrest that requires resuscitation, careful interpretation of the ECG may be necessary to check for the coexistence of LQTS.

Studies have reported that the JT interval does not change before and after RFA in pediatric patients with WPW syndrome, and prolonged QT interval in WPW syndrome is not a repolarization abnormality [5–7]. The JT interval is as predictive of cardiac events as the QT interval in LQTS [14, 15]. In this study, the QT interval in the manifest group was significantly longer than that in the concealed group and shortened after RFA. However, the JT interval was not significantly different between the manifest and concealed groups before RFA and was not significantly different between the manifest and concealed groups before and after RFA. The QT interval was prolonged by approximately 40–50 msec in the manifest group compared with that in the concealed group; no change in the JT interval was noted. Prolonged QT interval may have a low potential risk of sudden death, and prolonging the JT interval in pediatric patients with manifest WPW syndrome may be important.

In this study, ST-segment change and T-wave abnormalities were not found in the concealed group after RFA but in 10 of 16 patients (63%) in the manifest group. Negative T waves were the most common abnormalities. In addition, Brugada-pattern ECG, early repolarization in inferior leads, and T-wave elevation were observed. ECG abnormalities nearly normalized 2–4 weeks after RFA. ST-segment change and T-wave abnormalities are considered abnormalities in the repolarization process. Cardiac memory is thought to be involved in the mechanism of ST-segment change and T-wave abnormalities after the disappearance of delta waves, such as after the cessation of pacing in patients with right ventricular apical pacing or after the disappearance of delta waves in patients with WPW syndrome [16–19]. Based on the present results, ST-segment change and T-wave abnormalities after RFA in pediatric patients with manifest WPW syndrome were normalized 2–4 weeks after RFA in most patients. If abnormalities in ST-segment changes and T waves continue for a longer period, careful follow-up may be necessary.

In this study, the Brugada-pattern ECG was found in two patients after RFA. One patient had a right posteroseptal AP, and the other had a left lateral AP. Many young adult patients with the coexistence of WPW syndrome and BrS have been reported with a right posteroseptal AP [20–25]. In both patients, the ECG was normalized 2–4 weeks after RFA due to transient changes. Brugada phenocopy was first proposed by Baranchuk et al., which was different from Brugada syndrome [26]. Brugada phenocopy is induced by certain condition (e.g., some drugs such as IA and IC antiarrhythmic drugs, myocardial ischemia, fever, and other illness), whereas Brugada syndrome is induced by a genetic mutation, which are considered different [26–28]. In these two patients who were not administered any drugs that might cause Brugada phenocopy, we consider that Brugada-pattern ECG changes were induced by the disappearance of the delta wave. To our knowledge, this is the first case to be induced by Brugada-pattern ECG after RFA for manifest WPW syndrome in pediatric patients. Brugada phenocopy is not considered to have the same risk of SCD as BrS. On the contrary, the risk of ventricular tachycardia and SCD in pediatric patients with manifest WPW syndrome who are given oral antiarrhythmic drugs, psychotropic drugs, and anti-attention-deficit/hyperactivity disorder drugs that cause QT prolongation and Brugada phenocopy has not been fully investigated [29–31]. When medications are administered for manifest WPW syndrome in pediatric patients, ECG changes must be closely monitored.

Limitations

This is a retrospective study of a small number of patients; thus, more detailed studies on a large number of patients are needed. Although changes in both QT interval and Brugada-pattern ECG are affected by oral prophylactic medications, the ECGs studied were taken long enough after the cessation of oral intake of prophylactic medications, and we believe that the drugs did not affect the findings. Although the adverse effects of coronary artery injury on RFA have not been excluded by coronary angiography or enhanced computed tomography, these unlike affect patient’s symptoms and other examinations after RFA.

In pediatric patients, the QT interval was prolonged in manifest compared with concealed WPW syndrome but shortened after RFA. In the manifest group, transient ST-segment change and T-wave abnormalities were often observed after RFA; however, the ECG normalized in approximately 1 month. Although WPW syndrome with LQTS or BrS is a rare condition, in manifest WPW syndrome, close attention to the QT interval and Brugada-pattern ECG before and after RFA is necessary.

Acknowledgements: The authors would like to thank Enago (www.enago.jp) for the English language review.

Disclosures: Authors declare that there is no conflict of interest.

Ethics: This study was approved by our institutional ethics committee (No.63-27), and written informed consent was obtained from the parents of our patients.

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Tables 1 to 4 are available in the Supplementary Files section.

No competing interests reported.

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A change in QT interval and ST-segment after radiofrequency catheter ablation in pediatric patients with Wolff–Parkinson–White syndrome

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