For risk stratification purposes when a higher risk would alter the approach to therapy. (See 'Risk stratification of asymptomatic patients with WPW pattern' below.) As part of a therapeutic catheter ablation procedure. In certain asymptomatic patients with a WPW pattern when there is a coexistent cardiac comorbidity (eg, cardiomyopathy, coronary artery disease, significant valvular disease, congenital heart defects, etc) and catheter ablation is being considered. The more difficult decision involves otherwise healthy patients with preexcitation on their ECG but no symptoms (ie, the WPW pattern) and no cardiac comorbidities. In such cases, the principle reasons for EPS are: To confirm the diagnosis if doubt exists. To determine if the accessory pathway is capable of supporting reentrant tachycardia. To measure the conduction characteristics of the accessory pathway in an effort to estimate the patient's risk for rapid conduction if an episode of AF were to develop in the future. DIFFERENTIAL DIAGNOSIS https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 12/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Differential diagnosis of ECG findings The ECG findings in persons with the WPW pattern can be similar to ECG findings seen in other cardiac conditions [48]: Myocardial infarction (MI) A negative delta wave (presenting as a Q wave) may mimic an MI pattern. Conversely, a positive delta wave may mask the presence of a previous MI. (See "ECG tutorial: Myocardial ischemia and infarction".) Ventricular premature beats (VPBs) or idioventricular rhythm Intermittent WPW may be mistaken for frequent VPBs. The WPW pattern is occasionally seen on alternate beats and may suggest ventricular bigeminy. If the WPW pattern persists for several beats, the rhythm may be misdiagnosed as an accelerated idioventricular rhythm. (See "Premature ventricular complexes: Clinical presentation and diagnostic evaluation" and "ECG tutorial: Ventricular arrhythmias", section on 'Accelerated idioventricular rhythm'.) Bundle branch block The QRS duration is equal to or greater than 0.12 seconds because of preexcitation (ie, the delta wave). Preexcited beats are sometimes confused with left or right bundle branch block as a result. However, the terminal portion of the QRS is usually normal, due to normal conduction through the AV node and ventricular activation via the Purkinje system. This is in contrast to intraventricular conduction defects such as right or left bundle branch block in which the conduction delay occurs in either the terminal portion of or throughout the QRS complex. (See "Right bundle branch block", section on 'ECG findings and diagnosis' and "Left bundle branch block", section on 'ECG findings and diagnosis'.) Some patients with cardiomyopathy and certain congenital heart defects (eg, single ventricle) may have atrial enlargement combined with abnormal ventricular activation that can result in a pattern of "pseudo-preexcitation." Some cases of HCM may mimic a WPW pattern as the PR is often short and the QRS widened because of hypertrophy [49]. Differential diagnosis of supraventricular tachycardia The differential diagnosis for SVT is fairly extensive and is discussed in detail separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Types of narrow QRS complex tachycardia'.) RISK STRATIFICATION OF ASYMPTOMATIC PATIENTS WITH WPW PATTERN Patients who initially present with the WPW pattern on a surface ECG but without a symptomatic arrhythmia represent a significant clinical challenge with regard to risk stratification and management. While the majority of such asymptomatic WPW patients (who are often young and https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 13/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate otherwise healthy) will remain asymptomatic [50], reported rates of symptomatic arrhythmia development have been as high as 20 percent over three years [30]. One approach to asymptomatic patients with WPW pattern is risk stratification using noninvasive tests and/or an electrophysiologic study (EPS) to identify those patients at greatest risk [11,46]. Mechanism of and risk factors for SCD in WPW The mechanism of SCD in patients with WPW syndrome is ventricular fibrillation (VF), which generally occurs during an episode of atrial fibrillation (AF) in which there is rapid conduction to the ventricle, leading to an excessively rapid ventricular response that degenerates into VF. Identifying asymptomatic patients at the greatest risk for VF would provide a rationale for more aggressive therapy (eg, catheter ablation). There is conflicting evidence as to which findings predict the development of symptoms and/or SCD. Some of the findings that have been suggested to predict a higher likelihood of symptoms include [11,46,50-52]: Short refractory period of the accessory pathway Short preexcited RR interval during AF Younger age Male gender Inducible AV reentrant (or reciprocating) tachycardia (AVRT) or AF during EPS Multiple accessory pathways Short preexcited RR interval during rapid atrial pacing Ebstein malformation The refractory period refers to the amount of time required after one conducted impulse for the accessory pathway (or any cardiac tissue) to "reset" and be able to conduct a subsequent impulse. This characteristic often defines how frequently an accessory pathway can conduct to the ventricle. The refractory period is usually similar to the shortest preexcited RR interval during AF, though the correlation is far from perfect. Approach to risk stratification In general, patients with asymptomatic ventricular preexcitation are at low risk of a cardiac arrest. Those patients who have had a cardiac arrest almost always experience symptoms of tachycardia first. Therefore, most patients who truly have no symptoms can simply be reassured and advised to notify their clinician immediately if they experience any rapid palpitation or syncope. At times however, patients seek further reassurance and can be evaluated further with additional risk stratification. Risk stratification of asymptomatic patients with the WPW pattern ( algorithm 1) can be performed noninvasively or via invasive EPS, though it must be emphasized that all risk-stratification schemes are imperfect and can be associated with false https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 14/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate positives as well as false negatives, especially in young patients [50]. Our approach to risk stratification is as follows: Begin with noninvasive evaluation Although the refractory period of an accessory pathway is usually measured during an EPS, patients with an accessory pathway that has a long refractory period can often be identified noninvasively. Intermittent loss of preexcitation (as detected by loss of delta wave on an ECG) suggests that the accessory pathway has a long refractory period and will not be able to conduct frequently enough during AF to produce VF. Intermittent preexcitation or loss of preexcitation may be seen in the following settings: Resting ECG At increased heart rates during exercise Ambulatory ECG monitoring for 24 to 48 hours Following intravenous administration of a sodium channel blocker, such as procainamide We proceed with risk stratification as follows ( algorithm 1): We perform a resting 12-lead ECG in everyone. Unless there is intermittent preexcitation at rest, an exercise ECG test should be performed in all patients who are able to exercise on a treadmill. We perform ambulatory ECG monitoring only in patients who are unable to perform treadmill exercise (eg, young children). Only rarely do we perform sodium channel blocker challenge. The observation of an abrupt and unambiguous loss of preexcitation at faster sinus rates on an ECG, exercise testing, ambulatory ECG monitoring, or sodium channel blocker challenge is generally considered a sufficient sign that the accessory pathway has limited antegrade conduction potential and is unlikely to result in life-threatening ventricular rates during AF. Expert consensus is that these "low-risk" patients can usually be followed without invasive testing as long as they remain asymptomatic. If preexcitation persists at maximum heart rates during exercise testing, or is persistent during the entire period of ambulatory monitoring or sodium channel blocker challenge, it does not necessarily mean that the patient is "high-risk," but rather that the risk cannot be determined by noninvasive means. A decision to proceed to EPS in these indeterminate https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 15/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate cases for better resolution of accessory pathway profile must be made on a case-by-case basis with careful discussion between clinician and patient. Follow-up if needed with invasive EPS In patients whose noninvasive testing reveals persistent preexcitation, or for patients in whom noninvasive testing is not feasible or nondiagnostic, we proceed with invasive EPS. An alternative approach to risk stratification is to proceed directly to EPS as an initial means of risk stratification in all patients with an asymptomatic WPW ECG pattern [46]. Options for invasive EPS include the standard transvenous intracardiac EPS or, less commonly, a transesophageal atrial EPS. Among a cohort of 224 asymptomatic patients with ventricular preexcitation, 76 patients aged 35 years or less were found to have inducible AVRT or AF during EPS and were randomly assigned to catheter ablation (37 patients, median follow-up 27 months) of the accessory pathway or no therapy (35 patients, median follow-up 21 months) [53]. In the ablation group, only two patients (5 percent) had arrhythmic events, both due to a mechanism that was unrelated to the ablated accessory pathway (AV nodal reentrant tachycardia), while in the control group, 21 patients (60 percent) had arrhythmic events (VF in one patient, SVT in 15 patients, and AF in five patients). The five-year estimated incidence of arrhythmic events was significantly lower for patients treated with ablation than for controls (7 versus 77 percent). A 2015 systematic review of asymptomatic patients with the WPW pattern, which included patients from six studies (one randomized trial of ablation versus no ablation in 76 patients, and five prospective cohorts that included 883 patients who did not undergo ablation), reported the likelihood of arrhythmic events over a range of follow-up as long as eight years [54]. Among the 76 patients randomized to ablation or no ablation, the five-year Kaplan-Meier estimate of arrhythmic events was 7 percent in the ablation group compared with 77 percent in the group who did not undergo ablation. Among the 883 patients in the cohort studies who did not undergo ablation, most patients had an uneventful course, but up to 9 percent developed malignant AF (RR interval 250 milliseconds), and up to 2 percent experienced VF. In summary, initial risk-stratification with EPS successfully identified those with a higher likelihood of developing symptoms, and treatment of these high-risk patients with ablation reduced arrhythmic events [11]. However, life-threatening arrhythmias were rare in the absence of ablation and serious complications developed in 2 percent of patients undergoing risk stratification. Thus, it remains unknown whether initial risk stratification with EPS produces a net reduction in morbidity or mortality. A full discussion of the approach to accessory pathway ablation in asymptomatic patients is presented separately. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Catheter ablation'.) https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 16/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Supraventricular arrhythmias".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topic (see "Patient education: Wolff-Parkinson-White syndrome (The Basics)") Beyond the Basics topic (see "Patient education: Wolff-Parkinson-White syndrome (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS Definition Wolff-Parkinson-White (WPW) syndrome is a condition resulting from conduction via one or more accessory pathways that directly connects the atria and ventricles and bypasses the atrioventricular (AV) node. Individuals with this condition have a short PR interval and a widened QRS complex on their ECG and paroxysmal tachycardia. (See 'Introduction' above.) Manifest versus concealed pathways Most accessory pathways are capable of antegrade conduction (exhibiting either antegrade conduction alone or bidirectional conduction) from atrium to ventricle and thus manifest as WPW pattern. However, some https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 17/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate accessory pathways conduct only in a retrograde fashion from ventricle to atrium. When there is no antegrade conduction through the accessory pathway (ie, no preexcitation), the characteristic WPW ECG pattern is absent, and the pathway is described as "concealed." (See 'Normal AV conduction versus accessory AV pathway conduction' above.) Anatomy The accessory pathway may be located anywhere along the AV ring (groove) or in the septum. The most frequent locations are left lateral (50 percent), posteroseptal (30 percent), right anteroseptal (10 percent), and right lateral (10 percent). Up to 13 percent of individuals with preexcitation have more than one accessory pathway. (See 'Anatomy' above.) Prevalence The prevalence of a WPW pattern on the surface ECG is estimated at 0.13 to 0.25 percent in the general population. The WPW pattern on the ECG may be intermittent and may even disappear permanently over time, depending on the conduction properties of the accessory pathway. The prevalence of WPW syndrome (the WPW pattern plus tachyarrhythmia) is substantially lower than that of the WPW pattern alone, perhaps as low as 2 percent of patients with the WPW pattern on the surface ECG. (See 'Prevalence of WPW pattern' above and 'Prevalence of WPW syndrome' above.) ECG features The classic ECG pattern of preexcitation in sinus rhythm is characterized by a fusion between conduction via the accessory pathway and the normal AV node/His- Purkinje system, resulting in the following ECG characteristics (see 'Electrocardiographic findings' above): The PR interval is short (less than 0.12 seconds) due to rapid AV conduction through the accessory pathway and bypass of the AV node. The initial part of ventricular activation is slowed, and the upstroke of the QRS complex is slurred because of slow muscle-fiber-to-muscle-fiber conduction; this is termed a delta wave. The QRS complex is widened and consists of fusion between early ventricular activation caused by preexcitation with the later ventricular activation resulting from transmission through the AV node and the infranodal conduction system to the ventricles. WPW pattern versus syndrome The majority of patients with the WPW pattern on their ECG remain asymptomatic, although a small percentage of patients with the WPW pattern develop arrhythmias as a part of WPW syndrome. Most patients who develop an arrhythmia will present with palpitations, with syncope or SCD occurring much less frequently. (See 'Clinical manifestations' above.) https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 18/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Tachycardias Tachycardias associated with WPW syndrome can be classified into those in which the accessory pathway is necessary for initiation and maintenance of the tachycardia, and those in which the bypass tract acts as a "bystander," providing a route of conduction from the anatomic site of tachycardia origin to other regions of the heart (see 'Arrhythmias associated with WPW' above): AV reentrant (or reciprocating) tachycardia (AVRT) This is a reentrant tachycardia with an anatomically defined circuit that consists of two distinct pathways, the normal AV conduction system, and an AV accessory pathway, linked by common proximal (the atria) and distal (the ventricles) tissues. The two major forms of AVRT are orthodromic and antidromic AVRT, defined by the direction of conduction through the AV node and the accessory pathway. (See 'Tachycardias requiring an accessory pathway for initiation and maintenance' above and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".) Atrial fibrillation (AF) This arrhythmia occurs in 10 to 30 percent of persons with WPW syndrome, somewhat higher than might be expected given the low prevalence of coexisting structural heart disease. When atrial impulses are transmitted along the accessory pathway in AF, ventricular rates may exceed 300 beats per minute and can degenerate into ventricular fibrillation (VF). (See 'Atrial fibrillation' above.) Ventricular fibrillation In most cases, VF occurring in patients with WPW syndrome results from the rapid ventricular response during AF that has persisted and ultimately deteriorated into VF. Although the frequency with which AF with rapid AV conduction via an accessory pathway degenerates into VF is unknown, the incidence of sudden death in patients with WPW syndrome is quite low. (See 'Ventricular fibrillation and sudden death' above.) Diagnosis The diagnosis of the WPW pattern can nearly always be made by reviewing the surface ECG. In addition, in some rare circumstances invasive electrophysiology testing can be helpful in confirming the diagnosis of an accessory pathway. WPW syndrome is diagnosed following the development of an arrhythmia in a patient with a preexisting WPW pattern on an ECG. (See 'Diagnosis' above.) Differential diagnosis The ECG findings in persons with the WPW pattern can be similar to ECG findings seen in other cardiac conditions, including prior myocardial infarction, ventricular premature beats, idioventricular rhythm, and bundle branch block. (See 'Differential diagnosis of ECG findings' above.) https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 19/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Risk stratification for asymptomatic patients Our approach to risk stratification of asymptomatic patients with the WPW pattern is as follows ( algorithm 1) (see 'Approach to risk stratification' above): Initial noninvasive evaluation, including a resting 12-lead ECG in everyone and, unless there is intermittent preexcitation at rest, an exercise ECG test in all patients who are able to exercise on a treadmill. If patients are unable to exercise, ambulatory ECG monitoring and/or sodium channel blocker challenge are additional noninvasive risk stratification options. The observation of an abrupt and unambiguous loss of preexcitation at faster heart rates is generally considered a sufficient sign that the accessory pathway has limited antegrade conduction potential and the patient is considered "low-risk" for life-threatening ventricular rates. If preexcitation persists at maximum heart rates during exercise testing, or is persistent during the entire period of ambulatory monitoring or sodium channel blocker challenge, it does not necessarily mean that the patient is "high-risk," but rather that the risk cannot be determined by noninvasive means. A decision to proceed to electrophysiology study in these indeterminate cases for better resolution of accessory pathway profile must be made on a case-by-case basis with careful discussion between clinician and patient. 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Risk Stratification for Arrhythmic Events in Patients With Asymptomatic Pre-Excitation: A Systematic Review for the 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation 2016; 133:e575. Topic 962 Version 41.0 https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 24/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate GRAPHICS Terminology and anatomic connections of preexcitation pathways Old Proposed or commonly used Anatomic connections terminology terminology Kent bundle* Accessory AV connection or AV bypass Atrium to ventricle tract James fiber Atrionodal bypass tract Atrium to low AV node Atriofascicular bypass tract Atrium to bundle of His Mahaim fiber Atriofascicular bypass tract Atrium to bundle branch Nodofascicular bypass tract AV node to bundle branch Nodoventricular bypass tract AV node to ventricular tissue Fasciculoventricular bypass tract Bundle branch to ventricular tissue AV: atrioventricular. These bypass tracts result in delta waves and the Wolff-Parkinson-White syndrome. These bypass tracts result in the Lown-Ganong-Levine syndrome and enhanced AV nodal conduction. Graphic 53343 Version 6.0 https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 25/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate 12-lead electrocardiogram showing the Wolff-Parkinson- White pattern The 2 main electrocardiographic features of Wolff-Parkinson-White pattern include a short PR interval (<0.12 seconds) and a delta wave (arrows). The QRS complex is wide (>0.12 seconds) and represents a fusion beat; the initial portion (delta wave) results from rapid ventricular activation via the accessory pathway (preexcitation), while the termination of ventricular activation is via the normal conduction system, leading to a fairly normal terminal portion of the QRS. Graphic 75578 Version 10.0 ECG of sinus rhythm to Normal electrocardiogram (ECG) Normal sinus rhythm at a rate of 71 beats/minute, a P wave axis of 45 , and a PR interval of 0.15 seconds. https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 26/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate ECG: electrocardiogram. Courtesy of Morton Arnsdorf, MD. Graphic 58149 Version 5.0 https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 27/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate 12-lead electrocardiogram of a patient in sinus rhythm with Wolff-Parkinson-White pattern Nearly full preexcitation is manifest in normal sinus rhythm on the 12-lead electrocardiogram in this patient with a short accessory pathway refractory period. The ventricular complex in preexcitation is a fusion of the impulse that preexcites the ventricles due to rapid conduction through an accessory pathway and of the impulse that takes the usual route through the atrioventricular node; this fusion creates the delta wave that is characteristic of Wolff-Parkinson-White electrocardiogram pattern. Courtesy of Morton F Arnsdorf, MD. Graphic 76226 Version 9.0 ECG of sinus rhythm to Normal electrocardiogram (ECG) https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 28/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Normal sinus rhythm at a rate of 71 beats/minute, a P wave axis of 45 , and a PR interval of 0.15 seconds. ECG: electrocardiogram. Courtesy of Morton Arnsdorf, MD. Graphic 58149 Version 5.0 https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 29/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Sites of reentry in supraventricular tachyarrhythmias Reentry may occur around a fixed anatomic obstacle or may be functional, developing in the absence of an anatomic obstacle and resulting from the intrinsic heterogeneity of electrophysiologic properties of the myocardial tissue. Reentrant circuits leading to a supraventricular tachyarrhythmia may develop in various parts of the heart: within and around the sinoatrial node (sinus node reentry); within the atrial myocardium (atrial tachycardia, atrial flutter, or atrial fibrillation); within the atrioventricular (AV) node due to the presence of a slow and fast pathway (atrioventricular nodal reentrant tachycardia); or involving the AV node and an accessory pathway (AP) (atrioventricular reentrant tachycardia). LAF: left anterior fascicle; LPF: left posterior fascicle. Graphic 82249 Version 4.0 https://www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical-manifestations-and-diagnosis/print 30/39 7/6/23, 11:15 AM Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis - UpToDate Electrophysiology study (EPS) tracings of surface and intracardiac electrograms showing degeneration of orthodromic atrioventricular reciprocating tachycardia (AVRT) into atrial tachycardia Surface ECG leads I, AVF, and VI and intracardiac electrograms are simultaneously recorded. The first three QRS complexes represent an orthodromic atrioventricular reentrant tachycardia (AVRT). The