Sinoatrial node reentrant tachycardia in infants with congenital heart disease.

T exact nature of sinoatrial node reentrant tachycardia (SANRT) is debated, but has been reported to occur as a clinical entity in 1.8% to 16.9% of adults undergoing electrophysiologic evaluation for supraventricular tachycardia (SVT). Although SANRT has been occasionally mentioned in reports of pediatric SVT, the reports are few in number and sparse in data. –11 SANRT has electrocardiographic features that are similar to sinus tachycardia, and it may be easily misdiagnosed, particularly when there is a high likelihood of sympathetic and/or catecholaminergic stimulation. Because SANRT has a high association with structural heart disease and has been noted to cause hemodynamic embarrassment, situations may arise when the diagnosis of SANRT rather than sinus tachycardia may be critical for patient management (e.g., after surgery for congenital heart disease). The purpose of this study was to assess the relative incidence and clinical characteristics of SANRT in a pediatric population. • • • The pediatric electrophysiologic study database at the Medical University of South Carolina was reviewed for cases of SANRT in children 0 to 18 years of age diagnosed by intracardiac, transesophageal, or epicardial pacing wire electrophysiologic study performed to investigate a previously documented clinical SVT between January 1999 and November 2000. Studies were performed before initiation of any antiarrhythmic therapy or after therapy had begun. Studies were generally performed on an elective basis unless they were performed for postoperative arrhythmia evaluation, in which case they were performed as close to presentation as possible. Transesophageal electrophysiologic studies were performed with administration of midazolam and/or fentanyl. Intracardiac studies were usually performed with the patient under deep sedation or general anesthesia, and epicardial pacing wire studies were typically performed without sedation. All studies were performed in the fasting state. Study protocols consisted of single and double atrial extrastimuli after either sensed atrial rhythm and/or a fixed atrial drive train (500 and 400 ms, if underlying rhythm permitting, or 30 ms below baseline rhythm cycle length), followed by rapid atrial pacing. Ventricular stimulation was used when possible to investigate retrograde conduction. Because all of the studies were not intracardiac, all previously described criteria of SANRT could not be demonstrated (Table 1). 3–6,9 Thus, for the purposes of this study, SANRT was defined as a paroxysmal or reproducibly inducible and terminable tachycardia, with a P-wave axis and morphology in all 12 surface leads nearly identical to sinus rhythm. The reentrant mechanism of the tachycardia was confirmed by the ability to initiate the tachycardia with programmed atrial stimulation. Tachycardia response to adenosine, when available, was used to support the diagnosis of an atrial arrhythmia. Demographic and electrophysiologic variables as well as short-term management and follow-up are noted in the review. Because of the small number of subjects, variables are described as median and range unless otherwise noted. Group comparisons are made with Yates’ coefficient. Of the 106 patients, aged 1 day to 18 years, who underwent electrophysiologic study for documented SVT during the study period, 7 male patients (6.6%) met this study’s criteria for SANRT (Figures 1A and 1B). All identified patients were infants with structural heart disease (Table 2). Of the 6 patients with congenital heart disease, 5 had undergone surgical repair or palliation within the past 0 to 11 days (median 5) before presentation, 4 of those for palliation of hypoplastic left heart syndrome. One patient had a dilated cardiomyopathy. The incidence of structural heart disease and congenital heart disease was much greater in those with SANRT than in the remaining 99 patients with other SVT mechanisms (100% vs 26%, p 0.0003; 86% vs 24%, p 0.002, respectively). However, if only infants are considered, differences between the SANRT and non-SANRT groups in the incidence of structural heart disease and congenital heart disease do not reach statistical significance (100% vs 60%, p 0.14; 86% vs 53%, p 0.3, respectively). This may be a reflection of the fact that the proportion of infants in the SANRT group was From the Children’s Heart Program of South Carolina–Medical University of South Carolina, Charleston, South Carolina. Dr. Blaufox is supported by National Institutes of Health Training Grant T32 HL07710-06, Bethesda, Maryland. Dr. Blaufox’s address is: Children’s Heart Program of South Carolina–MUSC, 165 Ashley Avenue, PO Box 250915, Charleston, South Carolina 29425. E-mail: Blaufoad@musc.edu. Manuscript received April 25, 2001; revised manuscript received and accepted June 21, 2001. TABLE 1 Previously Described Criteria for SANRT