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Episodic symptoms, often reported during exertion, complicate the assessment of suspected supraventricular tachycardia (SVT).
To examine the diagnostic sensitivity of graded exercise testing in young patients with documented SVT or ventricular pre-excitation.
A single-centre retrospective review identified 53 patients (5.1 to 17.5 years of age) with structurally normal hearts who had undergone 65 graded treadmill exercise tests in the setting of either documented SVT with normal resting electrocardiograms (n=30) or ventricular pre-excitation (n=23). Twenty-five patients (13 pre-excited and 12 nonpre-excited) had exercise-related symptoms. SVT induction during exercise testing was assessed in relation to pre-excitation and the patient’s history of exercise-induced symptoms.
SVT was induced during six of the 65 exercise tests performed in three of 53 patients (overall sensitivity 5.7%). All three patients had a history of exercise-induced symptoms, and two had ventricular pre-excitation. SVT was induced in 12% of patients with exercise-related symptoms. No other rhythm disturbances occurred during exercise testing.
The diagnostic yield of graded exercise testing in patients with suspected SVT is limited, even among those with exercise-related symptoms.
Des symptômes épisodiques, souvent déclarés pendant l’effort, compliquent l’évaluation d’une tachycardie supraventriculaire présumée (TSP).
Examiner la sensibilité diagnostique des épreuves d’exercices gradués chez de jeunes patients présentant une TSP ou une pré-excitation ventriculaire documentée.
Une analyse rétrospective unicentrique a permis de repérer 53 patients (de 5,1 à 17,5 ans) ayant un cœur structurellement normal qui avaient subi 65 épreuves d’exercices gradués en raison d’une TSP (n=30) ou d’une pré-excitation ventriculaire (n=23) documentées aux tests d’électrocardiogramme normal. Vingt-cinq patients (13 avec pré-excitation et 12 sans pré-excitation) présentaient des symptômes liés à l’exercice. On a évalué l’induction de la TSP pendant l’épreuve d’exercices selon la pré-excitation et les antécédents de symptômes induits par l’exercice chez le patient.
La TSP a été induite dans six des 65 épreuves effectuées chez trois des 53 patients (sensibilité globale de 5,7 %). Ces trois patients avaient des antécédents de symptômes induits par l’exercice, et deux, une pré-excitation ventriculaire. La TSP était induite chez 12 % des patients ayant des symptômes liés à l’exercice. Aucune autre perturbation du rythme ne s’est produite pendant l’épreuve d’exercice.
Le rendement diagnostique des épreuves d’exercices gradués chez les patients atteints d’une TSP présumée est limité, même chez ceux qui présentent des symptômes liés à l’exercice.
Supraventricular tachycardia (SVT) is the most common symptomatic dysrhythmia in the pediatric population. However, the assessment of a patient with a suspected history of SVT can be difficult. While electrocardiographic (ECG) rhythm documentation during symptoms is clearly ideal, the episodic nature of events often precludes this possibility. Electrophysiological testing using either intracardiac or transesophageal electrodes can be quite informative, but is not available to all general pediatric cardiologists and may be considered overly invasive as an initial diagnostic tool (1).
Frequently, patients report the onset of SVT symptoms during exertion or athletic participation, and graded exercise testing could therefore serve as an ideal noninvasive provocative test for SVT induction in suspected cases. While other studies have examined the significance of exercise-induced ventricular tachycardia in the pediatric age group, the efficacy of graded exercise stress testing as either a precipitating stimulus or a predictive tool in recurrent pediatric SVT has been minimally explored. No data related to the efficacy of graded exercise stress testing in eliciting SVT have been published (2–6). The purpose of the present study was to assess the efficacy of graded exercise stress testing in eliciting SVT among patients with an established or presumed SVT predisposition.
A single-centre, retrospective review was performed of patients with documented atrioventricular re-entrant tachycardia or ventricular pre-excitation who had undergone graded exercise stress testing at the Winnipeg Children’s Hospital (Winnipeg, Manitoba) during a 10-year period (1988 to 1998). Patients were identified through a computerized search of the clinical database using both the broad diagnostic term ‘arrhythmia’ and specific terms including ‘supraventricular tachycardia’, ‘ventricular pre-excitation’, and ‘Wolff-Parkinson-White’. Records identified in this manner were then crosschecked against the exercise testing logbook. Patients with significant structural heart disease were excluded.
A total of 65 exercise test records were available for 53 patients who met the inclusion criteria. The patients ranged in age from 5.1 years to 17.5 years (mean [± SEM] age 11.6±0.5 years).
Among 30 patients without ventricular pre-excitation, SVT was documented before graded exercise testing with a surface ECG (n=22), continuous ambulatory monitoring (n=4) and transesophageal (n=1) or intracardiac electrophysiological study (n=4). SVT symptoms in these patients included palpitations (77%), chest discomfort or pain (13%), and syncope or presyncope (10%). In this group, the proven or suspected mechanism of SVT was long ventricular-atrial interval (more than 80 ms) orthodromic reciprocating tachycardia (n=15), short ventricular-atrial interval orthodromic reciprocating tachycardia (n=8) or ectopic atrial tachycardia (n=4). The SVT mechanism was unknown in three patients.
There were 23 patients with ventricular pre-excitation, 19 (83%) of whom reported symptoms consistent with SVT (16 with palpitations, two with syncope or presyncope, and one with chest pain). Four (17%) patients were asymptomatic.
At the time of their exercise studies, 28% of all patients were on medications including digoxin (n=11), beta-blockers (n=3), calcium channel blockers (n=2) and sotalol (n=1).
Exercise studies were performed with a motor-driven treadmill (Quinton model Q55; Quinton, USA). A progressive and uninterrupted format was used based on the standard multistage Bruce protocol (7,8). Exercise was continued until a cardiac dysrhythmia was elicited or a patient-determined maximal effort end point was reached. This was used to define the peak level of voluntary effort. Vital signs and ECGs were monitored continuously. A sample ECG strip was recorded on a multichannel ECG at the end of each 3 min stage of exercise, at times of significant symptoms, at the end of maximal exercise and at serial points in the recovery period. Subjects were encouraged to continue the exertion until a self-determined end point of fatigue or other limiting symptom intervened. All studies were performed by trained technologists and supervised directly by the medical staff. No significant complications occurred during the exercise studies.
Statistical data analysis was performed using the unpaired Student’s t test. P<0.05 was considered to be significant.
Exercise times ranged between 6.6 min and 16.3 min (mean 10.4 min). The peak heart rate ranged between 158 beats/min and 222 beats/min (mean 197 beats/min). Graded exercise testing provoked SVT on six occasions in three different patients. None of these patients was on medication at the time of the exercise study, and all had previously reported exercise-related symptoms. In all cases of exercise test-induced SVT, the dysrhythmia was heralded by the complaint of palpitations or precordial hyperactivity. There were no complaints of chest pain, nor were there any episodes of presyncope or syncope. Two of the three patients had ventricular pre-excitation on the resting surface ECG and, with exercise, developed narrow-complex tachycardia preceded by disappearance of the delta wave (Figure 1), consistent with orthodromic atrioventricular reciprocating tachycardia. The mechanism of SVT in the third patient, who did not have ventricular pre-excitation, could not be determined.
The sensitivity of exercise testing was one in 30 (3.3%) among patients without pre-excitation and two in 23 (8.7%) among patients with ventricular pre-excitation. The sensitivity was highest (two in 13 [15.4%]) among pre-excited patients with exercise-related symptoms. All exercise test-induced SVT episodes occurred near peak exercise. The induction of SVT was not related to total exercise time (11.2±0.8 min with SVT induction versus 10.2±0.3 min without SVT induction; P nonsignificant), nor was it related to the peak sinus heart rate achieved (189±3 beats/min with SVT induction versus 196±2 beats/min without SVT induction; P nonsignificant). All SVT episodes that were induced during exercise testing were brief and self-limited.
Dysrhythmias occur in approximately 2% of otherwise healthy children and in approximately 4% of children with cardiac structural lesions (9). The incidence of SVT has historically been quoted as approximately one in 25,000 healthy young individuals but, as methods of detection improve and awareness increases, it is now recognized that SVT is much more common and likely occurs in one in 250 children to one in 1000 children (10). As with all events that occur sporadically, clear documentation of such dysrhythmias in symptomatic patients can be challenging. Determining the exact mechanism of the tachycardia is helpful in the selection of appropriate drug therapy and in the planning of a formal electrophysiological study, including possible radiofrequency ablation. The mechanism of tachycardia can also have prognostic significance (11). While a careful history and an examination of the standard surface ECG can occasionally yield helpful information, the most important noninvasive tool is ECG rhythm documentation during symptoms. Unfortunately, in many cases, this diagnostic information is not available. The effectiveness of ambulatory monitoring is limited by the typically sporadic and unpredictable nature of SVT episodes (12,13).
Exercise is not only the most common physiological stress, but also poses the greatest physiological load on the cardiovascular system and can provoke cardiac abnormalities that are not present at rest (14–16). A variety of cardiac rhythm disorders, especially ventricular ectopic rhythms, can be induced or unmasked by exercise testing (17–23). Graded exercise testing has been considered as an integral part of the diagnostic evaluation of many children and young adults with cardiac disorders (24,25). In addition to the investigation of chest pain, there is an increasing number of applications for graded exercise testing in the pediatric population, including the evaluation of syncope and the hemodynamic assessment of left ventricular outflow tract obstruction (26–29). Alterations in cardiac rhythm occur frequently with exercise and are of considerable importance in understanding a patient’s functional and cardiovascular status, as well as prognosis, in various types of pediatric heart disease (16,30).
During physical activity, there is a complex neurohumoral interaction that occurs between the heart and the central nervous, endocrine and peripheral vascular systems. Sinus tachycardia is accompanied by elevated circulating catecholamines and alterations in afterload. The autonomic nervous system plays a significant role as a modifier of cardiac function during exercise and, with activity, there is an increase in sympathetic neural input to the heart which, in turn, may change the underlying electrophysiological properties of the heart (for example, by shortening the refractory period of both the myocardium and the His-Purkinje system, and increasing the velocity of impulse conduction through these tissues). The parasympathetic tone that plays an important protective role against dysrhythmias is abruptly withdrawn and much of the vagal input declines. These autonomic nervous system changes have a direct effect on the action potential of pacemaker cells by accelerating the rate of phase 4 depolarization toward the threshold, with subsequent increased normal and ectopic cardiac activity. The increase in circulating catecholamines resulting from exertion enhances the excitability of the myocardial cells by triggering afterpotentials and shortening both myocardial conduction time and refractory periods (31). Heightened sympathetic activity and catecholamines may also contribute to delayed afterdepolarizations (triggered automaticity), which are thought to be responsible for some cases of exercise-induced ventricular tachycardia.
Previously, many investigators believed that exercise testing was a useful adjunct in the management of patients with dysrhythmias, particularly in the assessment of ventricular tachydysrhythmias. However, more recently, others have questioned the prognostic significance of exercise-induced dysrhythmias (32,33). Graded exercise testing has been used in children to help differentiate benign premature ventricular contractions from more malignant forms of ventricular ectopy (33,34).
Several studies have evaluated dysrhythmias induced by exercise in patients with Wolff-Parkinson-White syndrome (35–38). However, little information is available on the utility of exercise testing in the pediatric population to unmask suspected SVT. In our study population, the overall sensitivity of exercise testing was quite low (5.7%). In the subgroup of 25 patients with a history of exercise-related symptoms, the sensitivity was slightly higher (12%), rising further to 15.4% among those with pre-excitation. Possible reasons for this low diagnostic yield might include failure of the exercise study to reproduce the critically timed premature beats that are often requisite for SVT induction; ineffectiveness of the exercise study to replicate the autonomic conditions that arise during spontaneous exercise or play; failure to achieve a sinus rate associated with antegrade accessory pathway block in Wolff-Parkinson-White patients; and inclusion of patients taking antidysrhythmic medication at the time of exercise testing, none of whom had induced SVT; or a combination of these factors.
The potential usefulness of repeat exercise testing to assess the efficacy of antiarrhythmic drugs among patients with exercise test-inducible SVT was not evaluated in the present study. Finally, patients with substantial structural heart disease may conceivably exhibit greater reproducibility of exercise-induced dysrhythmia than the patients included in the present study, who had structurally normal hearts.
The results reported in the present study should be interpreted with caution because of the retrospective nature of the study. Although most patients in the exercise-capable pediatric age group with known or suspected SVT are thought to have undergone graded exercise testing during the 10-year period encompassed by the present study, selection bias could still arise in relation to the unknown number of patients who did not undergo graded exercise testing, and with respect to the variable number of exercise test episodes among those who did. The statistical power of the results would have been enhanced by the inclusion of more patients, but multicentre participation is often the only practical solution to this commonly encountered challenge in pediatric clinical investigations.
Graded exercise testing was an insensitive tool for SVT detection in the present group of pediatric patients with documented SVT or ventricular pre-excitation, even among patients with known exercise-induced symptoms. Nevertheless, exercise testing can still be useful in defining accessory pathway conduction characteristics among patients with ventricular pre-excitation, and possibly to determine the existence of multiple accessory pathways (39). Clinicians aiming to document heart rhythm disturbances noninvasively among pediatric patients with suspected SVT should consider transtelephonic event monitoring, which has a substantially higher yield than graded exercise testing in this setting (40).