ACC/AHA/HRS Guideline

2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary

A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Richard L. Page, José A. Joglar, Mary A. Caldwell, Hugh Calkins, Jamie B. Conti, Barbara J. Deal, N.A. Mark Estes, Michael E. Field, Zachary D. Goldberger, Stephen C. Hammill, Julia H. Indik, Bruce D. Lindsay, Brian Olshansky, Andrea M. Russo, Win-Kuang Shen, Cynthia M. Tracy, Sana M. Al-Khatib
and Evidence Review Committee Chair‡
https://doi.org/10.1161/CIR.0000000000000310
Circulation. 2016;133:e471-e505
Originally published September 23, 2015

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Table of Contents

Preamble e472

  1. Introduction e473

    • 1.1. Methodology and Evidence Review e473

    • 1.2. Organization of the GWC e473

    • 1.3. Document Review and Approval e474

    • 1.4. Scope of the Guideline e474

  2. General Principles e475

    • 2.1. Mechanisms and Definitions e475

    • 2.2. Epidemiology, Demographics, and Public Health Impact e475

    • 2.3. Evaluation of the Patient With Suspected or Documented SVT e476

      • 2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms e476

      • 2.3.2. Evaluation of the ECG e477

    • 2.4. Principles of Medical Therapy e478

      • 2.4.1. Acute Treatment: Recommendations e478

      • 2.4.2. Ongoing Management: Recommendations e479

    • 2.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation e479

  3. Sinus Tachyarrhythmias e480

    • 3.1. Physiological Sinus Tachycardia e480

    • 3.2. Inappropriate Sinus Tachycardia e480

      • 3.2.1. Acute Treatment e480

      • 3.2.2. Ongoing Management: Recommendations e480

  4. Nonsinus Focal Atrial Tachycardia and MAT e481

    • 4.1. Focal Atrial Tachycardia e481

      • 4.1.1. Acute Treatment: Recommendations e481

      • 4.1.2. Ongoing Management: Recommendations e482

    • 4.2. Multifocal Atrial Tachycardia e482

      • 4.2.1. Acute Treatment: Recommendation e482

      • 4.2.2. Ongoing Management: Recommendations e482

  5. Atrioventricular Nodal Reentrant Tachycardia e482

    • 5.1. Acute Treatment: Recommendations e482

    • 5.2. Ongoing Management: Recommendations e483

  6. Manifest and Concealed Accessory Pathways e483

    • 6.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways e484

      • 6.1.1. Acute Treatment: Recommendations e484

      • 6.1.2. Ongoing Management: Recommendations e484

    • 6.2. Management of Asymptomatic Pre-Excitation e484

      • 6.2.1. PICOTS Critical Questions e484

      • 6.2.2. Asymptomatic Patients With Pre-Excitation: Recommendations e485

    • 6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations e485

  7. Atrial Flutter e485

    • 7.1. Cavotricuspid Isthmus-Dependent Atrial Flutter e485

    • 7.2. Non–Isthmus-Dependent Atrial Flutters e486

    • 7.3. Acute Treatment: Recommendations e486

    • 7.4. Ongoing Management: Recommendations e487

  8. Junctional Tachycardia e487

    • 8.1. Acute Treatment: Recommendations e487

    • 8.2. Ongoing Management: Recommendations e487

  9. Special Populations e487

    • 9.1. Pediatrics e487

    • 9.2. Patients With Adult Congenital Heart Disease e489

      • 9.2.1. Clinical Features e489

      • 9.2.2. Acute Treatment: Recommendations e490

      • 9.2.3. Ongoing Management: Recommendations e490

    • 9.3. Pregnancy e490

      • 9.3.1. Acute Treatment: Recommendations e490

      • 9.3.2. Ongoing Management: Recommendations e491

    • 9.4. SVT in Older Populations e491

      • 9.4.1. Acute Treatment and Ongoing Management: Recommendation e491

  10. Quality-of-Life Considerations e491

  11. Cost-Effectiveness e491

  12. Shared Decision Making e491

  • References e492

  • Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e501

  • Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) e502

Preamble

Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, based on systematic methods to evaluate and classify evidence, provide a cornerstone of quality cardiovascular care.

In response to reports from the Institute of Medicine1,2 and a mandate to evaluate new knowledge and maintain relevance at the point of care, the ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) modified its methodology.3–5 The relationships between guidelines, data standards, appropriate use criteria, and performance measures are addressed elsewhere.4

Intended Use

Practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations may have a broader target. Although guidelines may inform regulatory or payer decisions, they are intended to improve quality of care in the interest of patients.

Evidence Review

Guideline Writing Committee (GWC) members review the literature; weigh the quality of evidence for or against particular tests, treatments, or procedures; and estimate expected health outcomes. In developing recommendations, the GWC uses evidence-based methodologies that are based on all available data.4–6 Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. Only selected references are cited.

The Task Force recognizes the need for objective, independent Evidence Review Committees (ERCs) that include methodologists, epidemiologists, clinicians, and biostatisticians who systematically survey, abstract, and assess the evidence to address key clinical questions posed in the PICOTS format (P=population, I=intervention, C=comparator, O=outcome, T=timing, S=setting).4,5 Practical considerations, including time and resource constraints, limit the ERCs to evidence that is relevant to key clinical questions and lends itself to systematic review and analysis that could affect the strength of corresponding recommendations. Recommendations developed by the GWC on the basis of the systematic review are marked “SR”.

Guideline-Directed Medical Therapy

The term “guideline-directed medical therapy” refers to care defined mainly by ACC/AHA Class I recommendations. For these and all recommended drug treatment regimens, the reader should confirm dosage with product insert material and carefully evaluate for contraindications and interactions. Recommendations are limited to treatments, drugs, and devices approved for clinical use in the United States.

Class of Recommendation and Level of Evidence

The Class of Recommendation (COR; ie, the strength of the recommendation) encompasses the anticipated magnitude and certainty of benefit in proportion to risk. The Level of Evidence (LOE) rates evidence supporting the effect of the intervention on the basis of the type, quality, quantity, and consistency of data from clinical trials and other reports (Table 1).5,7 Unless otherwise stated, recommendations are sequenced by COR and then by LOE. Where comparative data exist, preferred strategies take precedence. When >1 drug, strategy, or therapy exists within the same COR and LOE and no comparative data are available, options are listed alphabetically. Each recommendation is followed by supplemental text linked to supporting references and evidence tables.

View this table:
Table 1.

Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care*

Relationships With Industry and Other Entities

The ACC and AHA sponsor the guidelines without commercial support, and members volunteer their time. The Task Force zealously avoids actual, potential, or perceived conflicts of interest that might arise through relationships with industry or other entities (RWI). All GWC members and reviewers are required to disclose current industry relationships or personal interests from 12 months before initiation of the writing effort. Management of RWI involves selecting a balanced GWC and assuring that the chair and a majority of committee members have no relevant RWI (Appendix 1). Members are restricted with regard to writing or voting on sections to which their RWI apply. For transparency, members’ comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is also available online. The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds representing different geographic regions, sexes, ethnicities, intellectual perspectives/biases, and scopes of clinical practice, and by inviting organizations and professional societies with related interests and expertise to participate as partners or collaborators.

Individualizing Care in Patients With Associated Conditions and Comorbidities

Managing patients with multiple conditions can be complex, especially when recommendations applicable to coexisting illnesses are discordant or interacting.8 The guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances. The recommendations should not replace clinical judgment.

Clinical Implementation

Management in accordance with guideline recommendations is effective only when followed. Adherence to recommendations can be enhanced by shared decision making between clinicians and patients, with patient engagement in selecting interventions based on individual values, preferences, and associated conditions and comorbidities. Consequently, circumstances may arise in which deviations from these guidelines are appropriate.

Policy

The recommendations in this guideline represent the official policy of the ACC and AHA until superseded by published addenda, statements of clarification, focused updates, or revised full-text guidelines. To ensure that guidelines remain current, new data are reviewed biannually to determine whether recommendations should be modified. In general, full revisions are posted in 5-year cycles.3,5

The reader is encouraged to consult the full-text guideline9 for additional guidance and details with regard to SVT because the executive summary contains limited information.

Jonathan L. Halperin, MD, FACC, FAHA

Chair, ACC/AHA Task Force on Clinical Practice Guidelines

1. Introduction

1.1. Methodology and Evidence Review

The recommendations listed in this guideline are, whenever possible, evidence based. An extensive evidence review was conducted in April 2014 that included literature published through September 2014. Other selected references published through May 2015 were incorporated by the GWC. Literature included was derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. The relevant search terms and data are included in evidence tables in the Online Data Supplement. Additionally, the GWC reviewed documents related to supraventricular tachycardia (SVT) previously published by the ACC, AHA, and Heart Rhythm Society (HRS). References selected and published in this document are representative and not all-inclusive.

An independent ERC was commissioned to perform a systematic review of key clinical questions, the results of which were considered by the GWC for incorporation into this guideline. The systematic review report on the management of asymptomatic patients with Wolff-Parkinson-White (WPW) syndrome is published in conjunction with this guideline.10

1.2. Organization of the GWC

The GWC consisted of clinicians, cardiologists, electrophysiologists (including those specialized in pediatrics), and a nurse (in the role of patient representative) and included representatives from the ACC, AHA, and HRS.

1.3. Document Review and Approval

This document was reviewed by 8 official reviewers nominated by the ACC, AHA, and HRS, and 25 individual content reviewers. Reviewers’ RWI information was distributed to the GWC and is published in this document (Appendix 2).

This document was approved for publication by the governing bodies of the ACC, the AHA, and the HRS.

1.4. Scope of the Guideline

The purpose of this joint ACC/AHA/HRS document is to provide a contemporary guideline for the management of adults with all types of SVT other than atrial fibrillation (AF). Although AF is, strictly speaking, an SVT, the term SVT generally does not refer to AF. AF is addressed in the 2014 ACC/AHA/HRS Guideline for the Management of Atrial Fibrillation (2014 AF guideline).11 The present guideline addresses other SVTs, including regular narrow–QRS complex tachycardias, as well as other, irregular SVTs (eg, atrial flutter with irregular ventricular response and multifocal atrial tachycardia [MAT]). This guideline supersedes the “2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias.”12 Although this document is aimed at the adult population (≥18 years of age) and offers no specific recommendations for pediatric patients, as per the reference list, we examined literature that included pediatric patients. In some cases, the data from noninfant pediatric patients helped inform this guideline.

2. General Principles

2.1. Mechanisms and Definitions

For the purposes of this guideline, SVT is defined as per Table 2, which provides definitions and the mechanism(s) of each type of SVT. The term SVT does not generally include AF, and this document does not discuss the management of AF.

View this table:
Table 2.

Relevant Terms and Definitions

2.2. Epidemiology, Demographics, and Public Health Impact

The best available evidence indicates that the prevalence of SVT in the general population is 2.29 per 1000 persons.13 When adjusted by age and sex in the US population, the incidence of paroxysmal supraventricular tachycardia (PSVT) is estimated to be 36 per 100 000 persons per year.13 There are approximately 89 000 new cases per year and 570 000 persons with PSVT.13 Compared with patients with cardiovascular disease, those with PSVT without any cardiovascular disease are younger (37 versus 69 years; P=0.0002) and have faster PSVT (186 versus 155 bpm; P=0.0006). Women have twice the risk of men of developing PSVT.13 Individuals >65 years of age have >5 times the risk of younger persons of developing PSVT.13

Atrioventricular nodal reentrant tachycardia (AVNRT) is more common in persons who are middle-aged or older, whereas in adolescents the prevalence may be more balanced between atrioventricular reentrant tachycardia (AVRT) and AVNRT, or AVRT may be more prevalent.13 The relative frequency of tachycardia mediated by an accessory pathway decreases with age. The incidence of manifest pre-excitation or WPW pattern on electrocardiogram/electrocardiographic (ECG) tracings in the general population is 0.1% to 0.3%. However, not all patients with manifest ventricular pre-excitation develop PSVT.14–16

2.3. Evaluation of the Patient With Suspected or Documented SVT

2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms

The diagnosis of SVT is often made in the emergency department, but it is common to elicit symptoms suggestive of SVT before initial electrocardiographic documentation. SVT symptom onset often begins in adulthood; in one study in adults, the mean age of symptom onset was 32±18 years of age for AVNRT, versus 23±14 years of age for AVRT.17 In contrast, in a study conducted in pediatric populations, the mean ages of symptom onset of AVRT and AVNRT were 8 and 11 years, respectively.18 In comparison with AVRT, patients with AVNRT are more likely to be female, with an age of onset >30 years.16,19–21

SVT has an impact on quality of life, which varies according to the frequency of episodes, the duration of SVT, and whether symptoms occur not only with exercise but also at rest.18,22 In 1 retrospective study in which the records of patients <21 years of age with WPW pattern on the ECG were reviewed, 64% of patients had symptoms at presentation, and an additional 20% developed symptoms during follow-up.23 Modes of presentation included documented SVT in 38%, palpitations in 22%, chest pain in 5%, syncope in 4%, AF in 0.4%, and sudden cardiac death (SCD) in 0.2%.23 A confounding factor in diagnosing SVT is the need to differentiate symptoms of SVT from symptoms of panic and anxiety disorders or any condition of heightened awareness of sinus tachycardia (such as postural orthostatic tachycardia syndrome). When AVNRT and AVRT are compared, symptoms appear to differ substantially. Patients with AVNRT more frequently describe symptoms of “shirt flapping” or “neck pounding”19,24 that may be related to pulsatile reversed flow when the right atrium contracts against a closed tricuspid valve (cannon a-waves).

True syncope is infrequent with SVT, but complaints of light-headedness are common. In patients with WPW syndrome, syncope should be taken seriously but is not necessarily associated with increased risk of SCD.25 The rate of AVRT is faster when AVRT is induced during exercise,26 yet the rate alone does not explain symptoms of near-syncope. Elderly patients with AVNRT are more prone to syncope or near-syncope than are younger patients, but the tachycardia rate is generally slower in the elderly.27,28

In a study on the relationship of SVT with driving, 57% of patients with SVT experienced an episode while driving, and 24% of these considered it to be an obstacle to driving.29 This sentiment was most common in patients who had experienced syncope or near-syncope. Among patients who experienced SVT while driving, 77% felt fatigue, 50% had symptoms of near-syncope, and 14% experienced syncope. Women had more symptoms in each category.

2.3.2. Evaluation of the ECG

A 12-lead ECG obtained during tachycardia and during sinus rhythm may reveal the etiology of tachycardia. For the patient who describes prior, but not current, symptoms of palpitations, the resting ECG can identify pre-excitation that should prompt a referral to a cardiac electrophysiologist.

For a patient presenting in SVT, the 12-lead ECG can potentially identify the arrhythmia mechanism (Figure 1). If the SVT is regular, this may represent AT with 1:1 conduction or an SVT that involves the atrioventricular (AV) node. Junctional tachycardias, which originate in the AV junction (including the His bundle), can be regular or irregular, with variable conduction to the atria. SVTs that involve the AV node as a required component of the tachycardia reentrant circuit include AVNRT (Section 6) and AVRT (Section 7). In these reentrant tachycardias, the retrogradely conducted P wave may be difficult to discern, especially if bundle-branch block is present. In typical AVNRT, atrial activation is nearly simultaneous with the QRS, so the terminal portion of the P wave is usually located at the end of the QRS complex, appearing as a narrow and negative deflection in the inferior leads (a pseudo S wave) and a slightly positive deflection at the end of the QRS complex in lead V1 (pseudo R′). In orthodromic AVRT (with anterograde conduction down the AV node), the P wave can usually be seen in the early part of the ST-T segment. In typical forms of AVNRT and AVRT, because the P wave is located closer to the prior QRS complex than the subsequent QRS complex, the tachycardias are referred to as having a “short RP.” In unusual cases of AVNRT (such as “fast-slow”), the P wave is closer to the subsequent QRS complex, providing a long RP. The RP is also long during an uncommon form of AVRT, referred to as the permanent form of junctional reciprocating tachycardia (PJRT), in which an unusual accessory bypass tract with “decremental” (slowly conducting) retrograde conduction during orthodromic AVRT produces delayed atrial activation and a long RP interval.

Figure 1.
Figure 1.

Differential diagnosis for adult narrow QRS tachycardia. Patients with junctional tachycardia may mimic the pattern of slow-fast AVNRT and may show AV dissociation and/or marked irregularity in the junctional rate. *RP refers to the interval from the onset of surface QRS to the onset of visible P wave (note that the 90-ms interval is defined from the surface ECG,30 as opposed to the 70-ms ventriculoatrial interval that is used for intracardiac diagnosis).31 AV indicates atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; ECG, electrocardiogram; MAT, multifocal atrial tachycardia; and PJRT, permanent form of junctional reentrant tachycardia. Modified with permission from Blomström-Lundqvist et al.12

A long RP interval is typical of AT because the rhythm is driven by the atrium and conducts normally to the ventricles. In AT, the ECG will typically show a P wave with a morphology that differs from the P wave in sinus rhythm. In sinus node re-entry tachycardia, a form of focal AT, the P-wave morphology is identical to the P wave in sinus rhythm.

2.4. Principles of Medical Therapy

See Figure 2 for the algorithm for acute treatment of tachycardia of unknown mechanism and Figure 3 for the algorithm for ongoing management of tachycardia of unknown mechanism. See Appendix 1 in the Online Data Supplement for a table of acute drug therapy for SVT (intravenous administration), Appendix 2 for a table of ongoing drug therapy for SVT (oral administration), and Online Data Supplements 1 to 3 for data supporting Section 2.

Figure 2.
Figure 2.

Acute treatment of regular svt of unknown mechanism. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. IV indicates intravenous; and SVT, supraventricular tachycardia.

Figure 3.
Figure 3.

Ongoing management of svt of unknown mechanism. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *Clinical follow-up without treatment is also an option. EP indicates electrophysiological; pt, patient; SHD, structural heart disease (including ischemic heart disease); and SVT, supraventricular tachycardia.

2.4.1. Acute Treatment: Recommendations

Because patients with SVT account for approximately 50 000 emergency department visits each year,32 emergency physicians may be the first to evaluate patients whose tachycardia mechanism is unknown and to have the opportunity to diagnose the mechanism of arrhythmia. It is important to record a 12-lead ECG to differentiate tachycardia mechanisms according to whether the AV node is an obligate component (Section 2.3.2), because treatment that targets the AV node will not reliably terminate tachycardias that are not AV node dependent.

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Recommendations for Acute Treatment of SVT of Unknown Mechanism

2.4.2. Ongoing Management: Recommendations

The recommendations and algorithm (Figure 3) for ongoing management, along with other recommendations and algorithms for specific SVTs that follow, are meant to include consideration of patient preferences and clinical judgment; this may include consideration of consultation with a cardiologist or clinical cardiac electrophyisiologist, as well as patient comfort with possible invasive diagnostic and therapeutic intervention. Recommendations for treatment options (including drug therapy, ablation, or observation) must be considered in the context of frequency and duration of the SVT, along with clinical manifestations, such as symptoms or adverse consequences (eg, development of cardiomyopathy).

View this table:

Recommendations for Ongoing Management of SVT of Unknown Mechanism

2.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation

An invasive EP study permits the precise diagnosis of the underlying arrhythmia mechanism and localization of the site of origin and provides definitive treatment if coupled with catheter ablation. There are standards that define the equipment and training of personnel for optimal performance of EP study.68 EP studies involve placement of multielectrode catheters in the heart at ≥1 sites in the atria, ventricles, or coronary sinus. Pacing and programmed electrical stimulation may be performed with or without pharmacological provocation. By using diagnostic maneuvers during the EP study, the mechanism of SVT can be defined in most cases.31,69 Complications of diagnostic EP studies are rare but can be life threatening.70

A table of success and complication rates for ablation of SVT is included in the full-text guideline and in the Online Data Supplement–Appendix 3. Cardiac mapping is performed during EP studies to identify the site of origin of an arrhythmia or areas of critical conduction to allow targeting of ablation. Multiple techniques have been developed to characterize the temporal and spatial distribution of electrical activation.71

Several tools have been developed to facilitate arrhythmia mapping and ablation, including electroanatomic 3-dimensional mapping and magnetic navigation. Potential benefits of these technologies include more precise definition or localization of arrhythmia mechanism, spatial display of catheters and arrhythmia activation, reduction in fluoroscopy exposure for the patient and staff, and shortened procedure times, particularly for complex arrhythmias or anatomy.72

Fluoroscopy has historically been the primary imaging modality used for EP studies. Attention to optimal fluoroscopic technique and adoption of radiation-reducing strategies can minimize radiation dose to the patient and operator. The current standard is to use the “as low as reasonably achievable” (ALARA) principle on the assumption that there is no threshold below which ionizing radiation is free from harmful biological effect. Alternative imaging systems, such as electroanatomic mapping and intracardiac echocardiography, have led to the ability to perform SVT ablation with no or minimal fluoroscopy, with success and complication rates similar to standard techniques.73–77 A reduced-fluoroscopy approach is particularly important in pediatric patients and during pregnancy.78,79

Radiofrequency current is the most commonly used energy source for SVT ablation.80 Cryoablation is used as an alternative to radiofrequency ablation to minimize injury to the AV node during ablation of specific arrhythmias, such as AVNRT, para-Hisian AT, and para-Hisian accessory pathways, particularly in specific patient populations, such as children and young adults. Selection of the energy source depends on operator experience, arrhythmia target location, and patient preference.

3. Sinus Tachyarrhythmias

In normal individuals, the sinus rate at rest is generally between 50 bpm and 90 bpm, reflecting vagal tone.81–84 Sinus tachycardia refers to the circumstance in which the sinus rate exceeds 100 bpm. On the ECG, the P wave is upright in leads I, II, and aVF and is biphasic in lead V1.

3.1. Physiological Sinus Tachycardia

Physiological sinus tachycardia may result from pathological causes, including infection with fever, dehydration, anemia, heart failure, and hyperthyroidism, in addition to exogenous substances, including caffeine, drugs with a beta-agonist effect (eg, albuterol, salmeterol), and illicit stimulant drugs (eg, amphetamines, cocaine). In these cases, tachycardia is expected to resolve with correction of the underlying cause.

3.2. Inappropriate Sinus Tachycardia

Inappropriate sinus tachycardia (IST) is defined as sinus tachycardia that is unexplained by physiological demands. Crucial to this definition is the presence of associated, sometimes debilitating, symptoms that include weakness, fatigue, lightheadedness, and uncomfortable sensations, such as heart racing. Patients with IST commonly show resting heart rates >100 bpm and average rates that are >90 bpm in a 24-hour period.81 The cause of IST is unclear, and mechanisms related to dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity have been proposed.

It is important to distinguish IST from secondary causes of tachycardia, including hyperthyroidism, anemia, dehydration, pain, and use of exogenous substances. Anxiety is also an important trigger, and patients with IST may have associated anxiety disorders.81 IST must also be distinguished from other forms of tachycardia, including AT arising from the superior aspect of the crista terminalis and sinus node reentrant tachycardia (Section 4). It is also important to distinguish IST from postural orthostatic tachycardia syndrome, although overlap may be present within an individual. Patients with postural orthostatic tachycardia syndrome have predominant symptoms related to a change in posture, and treatment to suppress the sinus rate may lead to severe orthostatic hypotension. Thus, IST is a diagnosis of exclusion.

3.2.1. Acute Treatment

There are no specific recommendations for acute treatment of IST.

3.2.2. Ongoing Management: Recommendations

Because the prognosis of IST is generally benign, treatment is for symptom reduction and may not be necessary. Treatment of IST is difficult, and it should be recognized that lowering the heart rate may not alleviate symptoms. Therapy with beta blockers or calcium channel blockers is often ineffective or not well tolerated because of cardiovascular side effects, such as hypotension. Exercise training may be of benefit, but the benefit is unproven.

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Recommendations for Ongoing Management of IST

Ivabradine is an inhibitor of the “I-funny” or “If ” channel, which is responsible for normal automaticity of the sinus node; therefore, ivabradine reduces the sinus node pacemaker activity, which results in slowing of the heart rate. On the basis of the results of 2 large, randomized, placebo-controlled trials, this drug was recently approved by the FDA for use in patients with systolic heart failure. The drug has no other hemodynamic effects aside from lowering the heart rate. As such, it has been investigated for use to reduce the sinus rate and improve symptoms related to IST.85–93

Radiofrequency ablation to modify the sinus node can reduce the sinus rate, with acute procedural success rates reported in the range of 76% to 100% in nonrandomized cohorts.94–100 Nonetheless, symptoms commonly recur after several months, with IST recurrence in up to 27% and overall symptomatic recurrence (IST or non-IST AT) in 45% of patients.94,96,97,99 Complications can be significant. In view of the modest benefit of this procedure and its potential for significant harm, sinus node modification should be considered only for patients who are highly symptomatic and cannot be adequately treated by medication, and then only after informing the patient that the risks may outweigh the benefits of ablation.

See Online Data Supplements 4 and 5 for data supporting Section 3.

4. Nonsinus Focal Atrial Tachycardia and MAT

See Figure 4 for the algorithm for acute treatment of suspected focal atrial tachycardia (AT), Figure 5 for the algorithm for ongoing management of focal AT, and Online Data Supplements 6, 7, and 8 for additional data supporting Section 4.

Figure 4.
Figure 4.

Acute treatment of suspected focal atrial tachycardia. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. IV indicates intravenous.

Figure 5.
Figure 5.

Ongoing management of focal atrial tachycardia. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. Pt indicates patient; and SHD, structural heart disease (including ischemic heart disease).

4.1. Focal Atrial Tachycardia

Focal AT is defined in Table 2. Focal AT can be sustained or nonsustained. The atrial rate during focal AT is usually between 100 bpm and 250 bpm.102 Presence and severity of symptoms during focal ATs are variable among patients. Focal AT in the adult population is usually associated with a benign prognosis, although AT-mediated cardiomyopathy has been reported in up to 10% of patients referred for ablation of incessant SVT.103,104 Nonsustained focal AT is common and often does not require treatment.

The diagnosis of focal AT is suspected when the ECG criteria are met (Section 2). Algorithms have been developed to estimate the origin of the focal AT from the P-wave morphology recorded on a standard 12-lead ECG.105,106 The precise location of the focal AT is ultimately confirmed by mapping during EP studies when successful ablation is achieved.107–116 Focal AT originates more frequently from the right atrium than from the left atrium.117,118

Sinus node reentrant tachycardia is an uncommon type of focal AT that involves a microreentrant circuit in the region of the sinoatrial node, causing a P-wave morphology that is identical to that of sinus tachycardia (although this is not sinus tachycardia). Characteristics that distinguish sinus node reentry from sinus tachycardia are an abrupt onset and termination and often a longer RP interval than that observed during normal sinus rhythm.

4.1.1. Acute Treatment: Recommendations

RCTs of drug therapy for comparative effectiveness in patients with focal AT in the acute setting are not available. Many of the clinical outcomes are reported from small observational studies that included infants or pediatric patients.119,120 In the clinical setting, if the diagnosis is uncertain, vagal maneuvers may be attempted to better identify the mechanism of SVT.

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Recommendations for Acute Treatment of Suspected Focal Atrial Tachycardia

4.1.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of Suspected Focal Atrial Tachycardia

4.2. Multifocal Atrial Tachycardia

MAT is defined in Table 2. The mechanism of MAT is not well established. MAT is commonly associated with underlying conditions, including pulmonary disease, pulmonary hypertension, coronary disease, and valvular heart disease,137 as well as hypomagnesemia and theophylline therapy.138 The first-line treatment is management of the underlying condition. Intravenous magnesium may also be helpful in patients with normal magnesium levels.139 Antiarrhythmic medications in general are not helpful in suppression of MAT.140 Cardioversion is not useful in MAT.137

4.2.1. Acute Treatment: Recommendation

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Recommendations for Acute Treatment of Multifocal Atrial Tachycardia

4.2.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of Multifocal Atrial Tachycardia

5. Atrioventricular Nodal Reentrant Tachycardia

See Figure 6 for the algorithm for acute treatment of AVNRT, Figure 7 for the algorithm for ongoing management of AVNRT, and Online Data Supplements 9 and 10 for additional data supporting Section 5.

Figure 6.
Figure 6.

Acute treatment of avnrt. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. AVNRT indicates atrioventricular nodal reentrant tachycardia; and IV, intravenous.

Figure 7.
Figure 7.

Ongoing management of avnrt. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. AVNRT indicates atrioventricular nodal reentrant tachycardia; pt, patient; and SHD, structural heart disease (including ischemic heart disease).

AVNRT is the most common SVT and is defined in Table 2. It is usually seen in young adults without structural heart disease or ischemic heart disease, and >60% of cases are observed in women.16 The ventricular rate is often 180 bpm to 200 bpm but ranges from 110 bpm to >250 bpm (and in rare cases, the rate can be <100 bpm).19 The anatomic substrate of AVNRT is dual AV nodal physiology (Table 2).

5.1. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of AVNRT

5.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of AVNRT

6. Manifest and Concealed Accessory Pathways

Accessory pathways (defined in Table 2) can conduct in the anterograde direction, retrograde direction, or both; and can be associated with several different supraventricular arrhythmias. Some anterograde pathways may place patients at risk of SCD.

The most common tachycardia associated with an accessory pathway is orthodromic AVRT, with a circuit that uses the AV node and His Purkinje system in the anterograde direction, followed by conduction through the ventricle, retrograde conduction over the accessory pathway, and completion of the circuit by conduction through the atrium back into the AV node. Orthodromic AVRT accounts for approximately 90% to 95% of AVRT episodes in patients with a manifest accessory pathway. Pre-excited AVRT, including antidromic AVRT, accounts for 5% of the AVRT episodes in patients with a manifest pathway and involves conduction from the atrium to the ventricle via the accessory pathway, causing a preexcited QRS complex. This is called antidromic AVRT tachycardia when the return reentrant conduction occurs retrogradely via the AV node. In rare cases of pre-excited AVRT, the return conduction occurs via a second accessory AV pathway. AF can occur in patients with accessory pathways, which may result in extremely rapid conduction to the ventricle over a manifest pathway, which increases the risk of inducing ventricular fibrillation and SCD.

Rapid anterograde accessory pathway conduction during AF can result in SCD in patients with a manifest accessory pathway, with a 10-year risk ranging from 0.15% to 0.24%.164,165 Unfortunately, SCD may be the first presentation of patients with undiagnosed WPW. Increased risk of SCD is associated with a history of symptomatic tachycardia, multiple accessory pathways, and a shortest pre-excited R-R interval of <250 ms during AF. The risk of SCD associated with WPW appears highest in the first 2 decades of life.165–169

6.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways

See Figure 8 for the algorithm for acute treatment of orthodromic AVRT, Figure 9 for the algorithm for ongoing management of orthodromic AVRT, and Online Data Supplements 11 to 15 for additional data supporting Section 6.

Figure 8.
Figure 8.

Acute treatment of orthodromic avrt. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. AVRT indicates atrioventricular reentrant tachycardia; ECG, electrocardiogram; and IV, intravenous.

Figure 9.
Figure 9.

Ongoing management of orthodromic avrt. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. AVRT indicates atrioventricular reentrant tachycardia; ECG, electrocardiogram; pt, patient; and SHD, structural heart disease (including ischemic heart disease).

6.1.1. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of Orthodromic AVRT

6.1.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of Orthodromic AVRT

6.2. Management of Asymptomatic Pre-Excitation

6.2.1. PICOTS Critical Questions

See the ERC systematic review report, “Risk Stratification for Arrhythmic Events in Patients With Asymptomatic Pre-Excitation” for the complete evidence review on the management of asymptomatic pre-excitation,10 and see Online Data Supplements 13, 14, and 15 for additional data on asymptomatic pre-excitation, which were reproduced directly from the ERC’s systematic review. These recommendations have been designated with the notation SR to emphasize the rigor of support from the ERC’s systematic review. PICOTS Question 1 did not provide adequate data for a recommendation; the other 3 PICOTS questions are addressed in the recommendations in Section 6.2.2.

The following 4 questions were considered by the ERC:

  1. What is the comparative predictive accuracy of invasive EP study (without catheter ablation of the accessory pathway) versus noninvasive testing for predicting arrhythmic events (including SCD) in patients with asymptomatic pre-excitation?

  2. What is the usefulness of invasive EP study (without catheter ablation of the accessory pathway) versus no testing for predicting arrhythmic events (including SCD) in patients with asymptomatic pre-excitation?

  3. What is the usefulness of invasive EP study (without catheter ablation of the accessory pathway) or noninvasive EP study for predicting arrhythmic events (including SCD) in patients with asymptomatic pre-excitation?

  4. What are the efficacy and effectiveness of invasive EP study with catheter ablation of the accessory pathway as appropriate versus noninvasive tests with treatment (including observation) or no testing/ablation as appropriate for preventing arrhythmic events (including SCD) and improving outcomes in patients with asymptomatic pre-excitation?

6.2.2. Asymptomatic Patients With Pre-Excitation: Recommendations

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Recommendations for Management of Asymptomatic Patients With Pre-Excitation

6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations

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Recommendations for Management of Symptomatic Patients With Manifest Accessory Pathways

7. Atrial Flutter

See Figure 10 for the algorithm for acute treatment of atrial flutter, Figure 11 for the algorithm for ongoing management of atrial flutter, and Online Data Supplements 16 and 17 for data supporting Section 7.

Figure 10.
Figure 10.

Acute treatment of atrial flutter. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *Anticoagulation as per guideline is mandatory. †For rhythms that break or recur spontaneously, synchronized cardioversion or rapid atrial pacing is not appropriate. IV indicates intravenous.

Figure 11.
Figure 11.

Ongoing management of atrial flutter. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *After assuring adequate anticoagulation or excluding left atrial thrombus by transesophageal echocardiography before conversion. †Should be combined with AV nodal–blocking agents to reduce risk of 1:1 conduction during atrial flutter. AV indicates atrioventricular; SHD, structural heart disease (including ischemic heart disease).

7.1. Cavotricuspid Isthmus-Dependent Atrial Flutter

Cavotricuspid isthmus (CTI)–dependent atrial flutter is defined in Table 2. Although the atrial rates for flutter typically range from 250 bpm to 330 bpm, the rates may be slower in patients with severe atrial disease or in patients taking antiarrhythmic agents or after unsuccessful catheter ablation.214

Atrial flutter can occur in clinical settings similar to those associated with AF, and atrial flutter can be triggered by AT or AF.215,216 It is common for AF and atrial flutter to coexist in the same patient. After CTI ablation, 22% to 50% of patients have been reported to develop AF after a mean follow-up of 14 to 30 months, although 1 study reported a much higher rate of AF development, with 82% of patients treated by catheter ablation for atrial flutter manifesting AF within 5 years.217 Risk factors for the manifesting AF after atrial flutter ablation include prior AF, depressed left ventricular function, structural heart disease or ischemic heart disease, inducible AF, and increased LA size.216–221

7.2. Non–Isthmus-Dependent Atrial Flutters

Non–isthmus-dependent atrial flutter or atypical flutter describes macroreentrant ATs that are not dependent on conduction through the CTI, as defined in Table 2.

Catheter ablation of non–CTI-dependent flutter requires more extensive mapping than does ablation of CTI-dependent flutter, and success rates are lower (Online Data Supplement–Appendix 3). The location of the circuit determines ablation approach and risks.

The development of a microreentrant or macroreentrant left AT after AF ablation occurs in approximately 5% of patients.222–224 This is less frequent if ablation is limited to pulmonary vein isolation. On the other hand, these arrhythmias are more common in patients with longer-duration persistent AF or more dilated left atria or when linear ablation lesions are used.223–228 Detailed activation and entrainment mapping of the tachycardia during a second procedure result in effective ablation in approximately 90% of patients.225

7.3. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of Atrial Flutter

7.4. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of Atrial Flutter

8. Junctional Tachycardia

See Figure 12 for the algorithm for ongoing management of junctional tachycardia and Online Data Supplements 18 and 19 for data supporting Section 8.

Figure 12.
Figure 12.

Ongoing management of junctional tachycardia. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. SHD indicates structural heart disease (including ischemic heart disease).

Junctional tachycardia (defined in Table 2) is a rapid, occasionally irregular, narrow-complex tachycardia (with rates typically of 120 bpm to 220 bpm) that arises from the AV junction (including the His bundle). AV dissociation (often isorhythmic) may be seen, and when present, excludes the misdiagnosis of AVRT and makes AVNRT highly unlikely. If it is irregular, junctional tachycardia may be misdiagnosed as AF or MAT. The mechanism for junctional tachycardia is enhanced (abnormal) automaticity from an ectopic focus in the AV junction (including the His bundle).275

Junctional tachycardia is uncommon in adults275; it is typically seen in infants postoperatively, after cardiac surgery for congenital heart disease; this is also known as junctional ectopic tachycardia. As such, there is limited evidence with regard to diagnosis and management of junctional tachycardia in adult patients.

A related rhythm, nonparoxysmal junctional tachycardia (more commonly known as accelerated AV junctional rhythm), is far more common in adults than paroxysmal junctional tachycardia. The mechanism of nonparoxysmal junctional tachycardia is associated with automaticity or triggered activity. It occurs at a slower rate (70 bpm to 130 bpm) and is often due to digoxin toxicity276 or myocardial infarction.277,278 Treatment of this rhythm centers on addressing the underlying condition.

8.1. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of Junctional Tachycardia

8.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of Junctional Tachycardia

9. Special Populations

9.1. Pediatrics

As discussed in the Scope (Section 1.4), the present document is aimed at the adult population (≥18 years of age) and offers no specific recommendations for pediatric patients. Nevertheless, a brief discussion of SVT in pediatric patients is included below, highlighting major considerations with regard to SVT in younger patients, including adolescent patients.

SVT in young patients varies significantly from SVT in adult patients in terms of mechanism, risk of developing heart failure or cardiac arrest, risks associated with interventional therapy, natural history, and psychosocial impact. Approximately half of pediatric SVT presents in the first 4 months of life, with age-related peaks in occurrence subsequently at 5 to 8 years and after 13 years. Accessory pathway–mediated tachycardia accounts for >70% of SVT in infants, decreasing to approximately 55% in adolescents.21,289–291 AVNRT increases with age, from 9% to 13% of SVT in infants, to 30% to 50% of SVT in teenagers. Atrial flutter is seen in some neonates and in older children is predominantly observed after congenital heart disease. AF is uncommon in childhood, accounting for <3% of supraventricular arrhythmias, and may be a consequence of AVRT or AVNRT in adolescents or may be associated with repaired congenital heart disease. Congestive heart failure is present in up to 20% of infants and in older children with incessant tachycardia and in rare cases may necessitate mechanical cardiopulmonary support during initial therapy.292

The risk of ventricular fibrillation or SCD related to WPW in childhood is 1.3% to 1.6% and is highest in the first 2 decades of life.23,165–168 The risk of cardiac arrest is higher in patients with AVRT precipitating AF, short accessory connection refractory periods, and posteroseptal accessory pathways.23,165–168 Pharmacological therapy of SVT in childhood is largely based on practice patterns because RCTs of antiarrhythmic medications in children are lacking. AV nodal–blocking drugs are widely used for the most common arrhythmias, AVRT, and AVNRT. Higher initial doses of adenosine are needed in children than in adults, with children receiving from 150 mcg/kg to 250 mcg/kg.293–295 Digoxin is avoided in the presence of pre-excitation because its use in infancy has been associated with SCD or ventricular fibrillation.296,297 Amiodarone, sotalol, propafenone, or flecainide can be used for refractory SVT in infants. In older children presenting with SVT, beta-blocker therapy is most often the initial therapy used. Because of the rare occurrence of adverse events with flecainide, including in patients without structural heart disease, flecainide is not used as a first-line medication in children.298

Catheter ablation can be successfully performed in children of all ages, with acute success rates comparable to those reported in adults.192,193,299,300 Complications were reported in 4% to 8% of the initial large series, with major complications in 0.9% to 3.2%, and complication rates were higher in patients weighing <15 kg.192,299–301 The implications of complications, including AV block requiring pacing, perforation, and coronary artery or mitral valve injury, are profound in young patients.302–304 In early series, death was reported in 0.12% of children with normal hearts and was associated with lower weight and increased number of ablation lesions.305 Although most centers perform elective ablation for children weighing >12 kg to 15 kg, ablation in younger or smaller children is generally reserved for those with medically refractory SVT or tachycardia-induced cardiomyopathy or before surgery that may limit access for subsequent catheter-based procedures.

Junctional ectopic tachycardia occurs predominantly in very young patients either as a congenital form or, more commonly, after intracardiac repair of congenital heart disease. Nonpostoperative junctional tachycardia has been reported to respond to amiodarone or combination therapy including beta blockers, flecainide, procainamide, or propafenone.306 Ablation for patients with refractory tachycardia or ventricular dysfunction has shown efficacy of 82% to 85%, but inadvertent AV block occurred in 18% and recurrence was seen in 14% of patients.306 Postoperative junctional tachycardia occurs in 2% to 10% of young patients undergoing intracardiac surgery.307,308 Treatment includes sedation with muscle relaxation, limitation of inotropic medications, reduction of core temperature to 34 to 35°C, atrial overdrive pacing, and procainamide or amiodarone infusions.309–313 In general, postoperative junctional tachycardia resolves and does not require ongoing therapy.

Although this guideline focuses on adults, it should be noted that SVT may occur in the fetus and, if sustained, may put the fetus at risk of cardiovascular collapse manifested by hydrops. Mothers require safety monitoring by adult cardiologists during treatment. The most common mechanisms for fetal SVT are AVRT and atrial flutter.314 Persistent SVT with hydrops carries a high mortality rate, and therefore, prompt and aggressive treatment is warranted. Maternal administration of antiarrhythmic agents has been shown to be effective through transplacental delivery.

9.2. Patients With Adult Congenital Heart Disease

See Figure 13 for the algorithm for acute treatment of non–pre-excited SVT in adult congenital heart disease (ACHD) patients; Figure 14 for the algorithm for ongoing management of non–pre-excited SVT in ACHD patients; and Online Data Supplements 20 and 21 for data supporting Section 9.

Figure 13.
Figure 13.

Acute treatment of svt in achd patients. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. *For rhythms that break or recur spontaneously, synchronized cardioversion is not appropriate. ACHD indicates adult congenital heart disease; IV, intravenous; and SVT, supraventricular tachycardia.

Figure 14.
Figure 14.

Ongoing management of svt in achd patients. Colors correspond to Class of Recommendation in Table 1; drugs listed alphabetically. ACHD indicates adult congenital heart disease; intra-op, intraoperative; pre-op, preoperative; and SVT, supraventricular tachycardia.

9.2.1. Clinical Features

SVT is observed in 10% to 20% of ACHD patients, and is associated with a significantly increased risk of heart failure, stroke, and SCD.315–319 The most common mechanism of SVT in ACHD patients is macroreentrant AT (also called flutter), which accounts for at least 75% of SVT and frequently involves the CTI. Focal AT, AVNRT, and accessory pathway–mediated tachycardia each account for less than about 8% of SVT, whereas the incidence of AF is about 10% and increases with age.320–325

The management of SVT in ACHD patients is influenced by the underlying cardiac anatomy and surgical repair, the current hemodynamic sequelae of the anatomy and repairs, and mechanism of SVT. Management of ACHD patients should be undertaken only in collaboration with a cardiologist who has specialized training or experience in managing such patients.

Overall acute success rates of catheter ablation procedures for SVT in ACHD patients range from 70% to 85%, with recurrences in 20% to 60% of patients within 2 years.326–331 Catheter ablation is challenged by limitations of venous access to the heart, hypertrophied atrial tissue, multiple atrial reentrant circuits, and atrial baffles partitioning the coronary sinus and CTI to the pulmonary venous atrium. The development of atrial arrhythmias in ACHD patients is often an indicator of progressive hemodynamic changes, which require in-depth functional and hemodynamic assessment. Intervention for residual hemodynamic/structural defects may need to be planned as part of chronic arrhythmia management.

9.2.2. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of SVT in ACHD Patients

9.2.3. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of SVT in ACHD Patients

9.3. Pregnancy

Pregnancy may confer an increased susceptibility to a variety of arrhythmias, even in the absence of underlying heart disease.378 Pregnancy is also associated with an increased risk of arrhythmia exacerbation, such as more frequent and refractory tachycardia episodes, in patients with a pre-existing arrhythmic substrate.379 Although there is potential toxicity to the fetus with certain pharmacological and nonpharmacological therapies, safe options exist to allow for treating most cases of maternal SVT effectively.

The literature on therapeutic options for the management of arrhythmias in pregnancy is generally limited to single case reports or small series and favors the use of older antiarrhythmic agents because of more abundant reports on the safe use of these drugs. Although all medications have potential side effects to both the mother and the fetus at any stage of pregnancy, if possible, drugs should be avoided in the first trimester, when risk of congenital malformations is greatest. The lowest recommended dose should be used initially, accompanied by regular monitoring of clinical response.

9.3.1. Acute Treatment: Recommendations

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Recommendations for Acute Treatment of SVT in Pregnant Patients

9.3.2. Ongoing Management: Recommendations

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Recommendations for Ongoing Management of SVT in Pregnant Patients

9.4. SVT in Older Populations

9.4.1. Acute Treatment and Ongoing Management: Recommendation

The natural history of SVT is steadily changing because most patients with SVT undergo ablation at a younger age, but in general, the relative proportion of AT is higher in older populations, and AVNRT is more prevalent than AVRT among patients undergoing ablation.16 Atypical atrial flutter and macroreentrant AT are on the rise as consequences of increasing AF ablation in this patient population, yet there are limited outcome data from RCTs for this segment of the population. Therapeutic decisions should be balanced between the overall risks and benefits of the invasive nature of ablation versus long-term commitment to pharmacological therapy.

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Recommendations for Acute Treatment and Ongoing Management of SVT in Older Populations

10. Quality-of-Life Considerations

Patients with SVT may experience recurring symptoms that negatively impact their quality of life. Episodes of tachycardia can cause lightheadedness and syncope, which can become an obstacle to the performance of usual activities of daily living (eg, driving).29 However, there are minimal data on the effect of treatment on the quality of life for patients with SVT.

See Online Data Supplement 22 for data supporting Section 10.

11. Cost-Effectiveness

The small body of literature evaluating cost-effectiveness strategies in PSVT has traditionally centered on an evaluation of medical therapy versus catheter ablation. A rigorous cost-effectiveness Markov model was conducted in 2000 to compare radiofrequency ablation to medical management with generic metoprolol from the societal perspective.57 The estimated population consisted of patients with AVNRT (approximately 65%) and AVRT. On the basis of this simulation, the authors concluded that, for symptomatic patients with monthly episodes of PSVT, radiofrequency ablation was the more effective and less expensive strategy when compared with medical therapy. An observational cohort study of patients with atrial flutter supported early ablation to significantly reduce hospital-based healthcare utilization and the risk of AF.397

These studies, along with other older literature, favor catheter ablation over medical therapy as the more cost-effective approach to treating PSVT and atrial flutter. However, the results of these studies were based on cost data and practice patterns that do not apply to the current environment and practice. Therefore, no recommendations are provided.

See Online Data Supplement 23 for data supporting Section 11.

12. Shared Decision Making

It is important that the patient be included in clinical decision-making processes, with consideration of his/her preferences and goals for therapy, as well as his/her unique physical, psychological, and social situation. In selected cases, personalized, self-directed interventions can be developed in partnership with the patient, such as vagal maneuvers and “pill-in-the-pocket” drug therapy.

Shared decision making is especially important for patients with SVT. As seen in this guideline, SVT treatment can be nuanced and requires expert knowledge of EP processes and treatment options. Treatment options are highly specific to the exact type of arrhythmia and can depend on certain characteristics of a particular arrhythmia. The various choices for therapy, including drugs, cardioversion, invasive treatment, or a combination thereof, can be confusing to the patient, so a detailed explanation of the benefits and risks must be included in the conversation.

Patients are encouraged to ask questions with time allotted for caregivers to respond. Providing a relaxed atmosphere, anticipating patient concerns, and encouraging patients to keep a notebook with questions could facilitate productive conversations.

It is also important that clinicians use lay terminology to explain treatment options to their patients. It is the responsibility of the physician and healthcare team to provide the patient with the best possible understanding of all management options in terms of risks, benefits, and potential effects on quality of life.

Presidents and Staff

American College of Cardiology

Kim A. Williams, Sr, MD, FACC, FAHA, President

Shalom Jacobovitz, Chief Executive Officer

William J. Oetgen, MD, MBA, FACC, Executive Vice President, Science, Education, and Quality

Amelia Scholtz, PhD, Publications Manager, Science, Education, and Quality

American College of Cardiology/American Heart Association

Lisa Bradfield, CAE, Director, Guidelines and Clinical Policy

Abdul R. Abdullah, MD, Associate Science and Medicine Advisor

Alexa Papaila, Project Manager, Science and Clinical Policy

American Heart Association

Mark A. Creager, MD, FACC, FAHA, President

Nancy Brown, Chief Executive Officer

Rose Marie Robertson, MD, FAHA, Chief Science Officer

Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science Operations

Marco Di Buono, PhD, Vice President, Science, Research, and Professional Education

Jody Hundley, Production Manager, Scientific Publications, Office of Science Operations

Acknowledgments

We thank Dr. Daniel B. Mark for his invaluable assistance in reviewing studies relating to quality of life and cost-effectiveness. His research and insight informed much of the discussion on these topics. We also thank Dr. Sarah A. Spinler for her contributions with regard to antiarrhythmic drug therapy.

Appendix

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Appendix 1.

Author Relationships With Industry and Other Entities (Relevant)—2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia (April 2014)

Appendix

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Appendix 2.

Reviewer Relationships With Industry and Other Entities (Relevant)—2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia (March 2015)

Footnotes

  • This document was approved by the American College of Cardiology Board of Trustees and Executive Committee, the American Heart Association Science Advisory and Coordinating Committee, and the Heart Rhythm Society Board of Trustees in August 2015 and the American Heart Association Executive Committee in September 2015.

  • The Author Comprehensive Relationships Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000310/-/DC1.

  • The Data Supplement files are available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000310/-/DC2.

  • The American Heart Association requests that this document be cited as follows: Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NAM 3rd, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen W-K, Tracy CM, Al-Khatib SM. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: executive summary: 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:e471–e505. DOI: 10.1161/CIR.0000000000000310.

  • This article has been copublished in the Journal of the American College of Cardiology and HeartRhythm Journal.

  • Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (professional.heart.org), and the Heart Rhythm Society (www.hrsonline.org). A copy of the document is available at http://professional.heart.org/statements by using either “Search for Guidelines & Statements” or the “Browse By Topic” area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay{at}wolterskluwer.com.

  • Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements. Select the “Guidelines & Statements” drop-down menu, then click “Publication Development.”

  • Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.

References

  1. 1.↵
    Committee on Standards for Developing Trustworthy Clinical Practice Guidelines, Institute of Medicine (US). Clinical Practice Guidelines We Can Trust. Washington, DC: National Academies Press, 2011.
  2. 2.↵
    Committee on Standards for Systematic Reviews of Comparative Effectiveness Research, Institute of Medicine (US). Finding What Works in Health Care: Standards for Systematic Reviews. Washington, DC: National Academies Press, 2011.
  3. 3.↵
    ACCF/AHA Task Force on Practice Guidelines. Methodology Manual and Policies From the ACCF/AHA Task Force on Practice Guidelines. American College of Cardiology and American Heart Association. 2010. Available at: http://assets.cardiosource.com/Methodology_Manual_for_ACC_AHA_Writing_Committees.pdf and http://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/documents/downloadable/ucm_319826.pdf. Accessed January 23, 2015.
  4. 4.↵
    1. Jacobs AK,
    2. Kushner FG,
    3. Ettinger SM,
    4. et al
    . ACCF/AHA clinical practice guideline methodology summit report: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127:268–310.
    OpenUrlFREE Full Text
  5. 5.↵
    1. Jacobs AK,
    2. Anderson JL,
    3. Halperin JL
    . The evolution and future of ACC/AHA clinical practice guidelines: a 30-year journey: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130:1208–17.
    OpenUrlFREE Full Text
  6. 6.↵
    1. Anderson JL,
    2. Heidenreich PA,
    3. Barnett PG,
    4. et al
    . ACC/AHA statement on cost/value methodology in clinical practice guidelines and performance measures: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures and Task Force on Practice Guidelines. Circulation. 2014;129:2329–45.
    OpenUrlFREE Full Text
  7. 7.↵
    1. Halperin JL,
    2. Levine GN,
    3. Al-Khatib SM
    . Further evolution of the ACC/AHA clinical practice guideline recommendation classification system: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2016;133:1426–28.
    OpenUrlFREE Full Text
  8. 8.↵
    1. Arnett DK,
    2. Goodman RA,
    3. Halperin JL,
    4. et al
    . AHA/ACC/HHS strategies to enhance application of clinical practice guidelines in patients with cardiovascular disease and comorbid conditions: from the American Heart Association, American College of Cardiology, and US Department of Health and Human Services. Circulation. 2014;130:1662–7.
    OpenUrlFREE Full Text
  9. 9.↵
    1. Page RL,
    2. Joglar JA,
    3. Al-Khatib SM,
    4. et al
    . 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:e506–74.
    OpenUrlFREE Full Text
  10. 10.↵
    1. Al-Khatib SM,
    2. Arshad A,
    3. Balk EM,
    4. et al
    . 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 [published ahead of print September 23, 2015]. Circulation. 2015; IN PRESS. doi: 10.1161/CIR.0000000000000309.
  11. 11.↵
    1. January CT,
    2. Wann LS,
    3. Alpert JS,
    4. et al
    . 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2014;130:e199–267.
    OpenUrlFREE Full Text
  12. 12.↵
    1. Blomström-Lundqvist C,
    2. Scheinman MM,
    3. Aliot EM,
    4. et al
    . ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Developed in collaboration with NASPE-Heart Rhythm Society. Circulation. 2003;108:1871–909.
    OpenUrlFREE Full Text
  13. 13.↵
    1. Orejarena LA,
    2. Vidaillet H,
    3. DeStefano F,
    4. et al
    . Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31:150–7.
    OpenUrlCrossRefPubMed
  14. 14.↵
    1. Lu C-W,
    2. Wu M-H,
    3. Chen H-C,
    4. et al
    . Epidemiological profile of Wolff-Parkinson-White syndrome in a general population younger than 50 years of age in an era of radiofrequency catheter ablation. Int J Cardiol. 2014;174:530–4.
    OpenUrlCrossRefPubMed
  15. 15.↵
    1. Whinnett ZI,
    2. Sohaib SMA,
    3. Davies DW
    . Diagnosis and management of supraventricular tachycardia. BMJ. 2012;345:e7769.
    OpenUrlFREE Full Text
  16. 16.↵
    1. Porter MJ,
    2. Morton JB,
    3. Denman R,
    4. et al
    . Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm. 2004;1:393–6.
    OpenUrlCrossRefPubMed
  17. 17.↵
    1. Goyal R,
    2. Zivin A,
    3. Souza J,
    4. et al
    . Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia. Am Heart J. 1996;132:765–7.
    OpenUrlCrossRefPubMed
  18. 18.↵
    1. Maryniak A,
    2. Bielawska A,
    3. Bieganowska K,
    4. et al
    . Does atrioventricular reentry tachycardia (AVRT) or atrioventricular nodal reentry tachycardia (AVNRT) in children affect their cognitive and emotional development? Pediatr Cardiol. 2013;34:893–7.
    OpenUrlCrossRefPubMed
  19. 19.↵
    1. González-Torrecilla E,
    2. Almendral J,
    3. Arenal A,
    4. et al
    . Combined evaluation of bedside clinical variables and the electrocardiogram for the differential diagnosis of paroxysmal atrioventricular reciprocating tachycardias in patients without pre-excitation. J Am Coll Cardiol. 2009;53:2353–8.
    OpenUrlCrossRefPubMed
  20. 20.↵
    1. Liu S,
    2. Yuan S,
    3. Hertervig E,
    4. et al
    . Gender and atrioventricular conduction properties of patients with symptomatic atrioventricular nodal reentrant tachycardia and Wolff-Parkinson-White syndrome. J Electrocardiol. 2001;34:295–301.
    OpenUrlCrossRefPubMed
  21. 21.↵
    1. Anand RG,
    2. Rosenthal GL,
    3. Van Hare GF,
    4. et al
    . Is the mechanism of supraventricular tachycardia in pediatrics influenced by age, gender or ethnicity? Congenit Heart Dis. 2009;4:464–8.
    OpenUrlCrossRefPubMed
  22. 22.↵
    1. Walfridsson U,
    2. Strömberg A,
    3. Janzon M,
    4. et al
    . Wolff-Parkinson-White syndrome and atrioventricular nodal re-entry tachycardia in a Swedish population: consequences on health-related quality of life. Pacing Clin Electrophysiol. 2009;32:1299–306.
    OpenUrlCrossRefPubMed
  23. 23.↵
    1. Cain N,
    2. Irving C,
    3. Webber S,
    4. et al
    . Natural history of Wolff-Parkinson-White syndrome diagnosed in childhood. Am J Cardiol. 2013;112:961–5.
    OpenUrlCrossRefPubMed
  24. 24.↵
    1. Laurent G,
    2. Leong-Poi H,
    3. Mangat I,
    4. et al
    . Influence of ventriculoatrial timing on hemodynamics and symptoms during supraventricular tachycardia. J Cardiovasc Electrophysiol. 2009;20:176–81.
    OpenUrlCrossRefPubMed
  25. 25.↵
    1. Auricchio A,
    2. Klein H,
    3. Trappe HJ,
    4. et al
    . Lack of prognostic value of syncope in patients with Wolff-Parkinson-White syndrome. J Am Coll Cardiol. 1991;17:152–8.
    OpenUrlCrossRefPubMed
  26. 26.↵
    1. Drago F,
    2. Turchetta A,
    3. Calzolari A,
    4. et al
    . Reciprocating supraventricular tachycardia in children: low rate at rest as a major factor related to propensity to syncope during exercise. Am Heart J. 1996;132:280–5.
    OpenUrlCrossRefPubMed
  27. 27.↵
    1. Kalusche D,
    2. Ott P,
    3. Arentz T,
    4. et al
    . AV nodal re-entry tachycardia in elderly patients: clinical presentation and results of radiofrequency catheter ablation therapy. Coron Artery Dis. 1998;9:359–63.
    OpenUrlCrossRefPubMed
  28. 28.↵
    1. Haghjoo M,
    2. Arya A,
    3. Heidari A,
    4. et al
    . Electrophysiologic characteristics and results of radiofrequency catheter ablation in elderly patients with atrioventricular nodal reentrant tachycardia. J Electrocardiol. 2007;40:208–13.
    OpenUrlCrossRefPubMed
  29. 29.↵
    1. Walfridsson U,
    2. Walfridsson H
    . The impact of supraventricular tachycardias on driving ability in patients referred for radiofrequency catheter ablation. Pacing Clin Electrophysiol. 2005;28:191–5.
    OpenUrlCrossRefPubMed
  30. 30.
    1. Letsas KP,
    2. Weber R,
    3. Siklody CH,
    4. et al
    . Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway. Acta Cardiol. 2010;65:171–6.
    OpenUrlCrossRefPubMed
  31. 31.↵
    1. Knight BP,
    2. Ebinger M,
    3. Oral H,
    4. et al
    . Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol. 2000;36:574–82.
    OpenUrlCrossRefPubMed
  32. 32.↵
    1. Murman DH,
    2. McDonald AJ,
    3. Pelletier AJ,
    4. et al
    . US emergency department visits for supraventricular tachycardia, 1993–2003. Acad Emerg Med. 2007;14:578–81.
    OpenUrlCrossRefPubMed
  33. 33.
    1. Lim SH,
    2. Anantharaman V,
    3. Teo WS,
    4. et al
    . Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med. 1998;31:30–5.
    OpenUrlCrossRefPubMed
  34. 34.
    1. Luber S,
    2. Brady WJ,
    3. Joyce T,
    4. et al
    . Paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2001;19:40–2.
    OpenUrlCrossRefPubMed
  35. 35.
    1. Waxman MB,
    2. Wald RW,
    3. Sharma AD,
    4. et al
    . Vagal techniques for termination of paroxysmal supraventricular tachycardia. Am J Cardiol. 1980;46:655–64.
    OpenUrlCrossRefPubMed
  36. 36.
    1. Brady WJ,
    2. DeBehnke DJ,
    3. Wickman LL,
    4. et al
    . Treatment of out-of-hospital supraventricular tachycardia: adenosine vs verapamil. Acad Emerg Med. 1996;3:574–85.
    OpenUrlCrossRefPubMed
  37. 37.
    1. Cairns CB,
    2. Niemann JT
    . Intravenous adenosine in the emergency department management of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1991;20:717–21.
    OpenUrlCrossRefPubMed
  38. 38.
    1. Gausche M,
    2. Persse DE,
    3. Sugarman T,
    4. et al
    . Adenosine for the prehospital treatment of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1994;24:183–9.
    OpenUrlCrossRefPubMed
  39. 39.
    1. Madsen CD,
    2. Pointer JE,
    3. Lynch TG
    . A comparison of adenosine and verapamil for the treatment of supraventricular tachycardia in the prehospital setting. Ann Emerg Med. 1995;25:649–55.
    OpenUrlCrossRefPubMed
  40. 40.
    1. McCabe JL,
    2. Adhar GC,
    3. Menegazzi JJ,
    4. et al
    . Intravenous adenosine in the prehospital treatment of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1992;21:358–61.
    OpenUrlCrossRefPubMed
  41. 41.
    1. Rankin AC,
    2. Oldroyd KG,
    3. Chong E,
    4. et al
    . Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. Br Heart J. 1989;62:195–203.
    OpenUrlAbstract/FREE Full Text
  42. 42.
    1. Lim SH,
    2. Anantharaman V,
    3. Teo WS,
    4. et al
    . Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80:523–8.
    OpenUrlCrossRefPubMed
  43. 43.
    1. DiMarco JP,
    2. Miles W,
    3. Akhtar M,
    4. et al
    . Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. Ann Intern Med. 1990;113:104–10.
    OpenUrlCrossRefPubMed
  44. 44.
    1. Roth A,
    2. Elkayam I,
    3. Shapira I,
    4. et al
    . Effectiveness of prehospital synchronous direct-current cardioversion for supraventricular tachyarrhythmias causing unstable hemodynamic states. Am J Cardiol. 2003;91:489–91.
    OpenUrlCrossRefPubMed
  45. 45.
    1. Stec S,
    2. Kryñski T,
    3. Kułakowski P
    ,. Efficacy of low energy rectilinear biphasic cardioversion for regular atrial tachyarrhythmias. Cardiol J. 2011;18:33–8.
    OpenUrlPubMed
  46. 46.
    1. Lim SH,
    2. Anantharaman V,
    3. Teo WS
    . Slow-infusion of calcium channel blockers in the emergency management of supraventricular tachycardia. Resuscitation. 2002;52:167–74.
    OpenUrlCrossRefPubMed
  47. 47.
    1. Gupta A,
    2. Naik A,
    3. Vora A,
    4. et al
    . Comparison of efficacy of intravenous diltiazem and esmolol in terminating supraventricular tachycardia. J Assoc Physicians India. 1999;47:969–72.
    OpenUrlPubMed
  48. 48.
    1. Dorian P,
    2. Naccarelli GV,
    3. Coumel P,
    4. et al
    . A randomized comparison of flecainide versus verapamil in paroxysmal supraventricular tachycardia. The Flecainide Multicenter Investigators Group. Am J Cardiol. 1996;77:89A–95A.
    OpenUrlCrossRefPubMed
  49. 49.
    1. Mauritson DR,
    2. Winniford MD,
    3. Walker WS,
    4. et al
    . Oral verapamil for paroxysmal supraventricular tachycardia: a long-term, double-blind randomized trial. Ann Intern Med. 1982;96:409–12.
    OpenUrlCrossRefPubMed
  50. 50.
    1. Winniford MD,
    2. Fulton KL,
    3. Hillis LD
    . Long-term therapy of paroxysmal supraventricular tachycardia: a randomized, double-blind comparison of digoxin, propranolol and verapamil. Am J Cardiol. 1984;54:1138–9.
    OpenUrlCrossRefPubMed
  51. 51.
    1. Jackman WM,
    2. Beckman KJ,
    3. McClelland JH,
    4. et al
    . Treatment of supraventricular tachycardia due to atrioventricular nodal reentry, by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992;327:313–8.
    OpenUrlCrossRefPubMed
  52. 52.
    1. Hindricks G
    . The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart J. 1993;14:1644–53.
    OpenUrlAbstract/FREE Full Text
  53. 53.
    1. Hindricks G
    . Incidence of complete atrioventricular block following attempted radiofrequency catheter modification of the atrioventricular node in 880 patients. Results of the Multicenter European Radiofrequency Survey (MERFS) The Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart J. 1996;17:82–8.
    OpenUrlAbstract/FREE Full Text
  54. 54.
    1. Spector P,
    2. Reynolds MR,
    3. Calkins H,
    4. et al
    . Meta-analysis of ablation of atrial flutter and supraventricular tachycardia. Am J Cardiol. 2009;104:671–7.
    OpenUrlCrossRefPubMed
  55. 55.
    1. Calkins H,
    2. Yong P,
    3. Miller JM,
    4. et al
    . Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. The Atakr Multicenter Investigators Group. Circulation. 1999;99:262–70.
    OpenUrlAbstract/FREE Full Text
  56. 56.
    1. Scheinman MM,
    2. Huang S
    . The 1998 NASPE prospective catheter ablation registry. Pacing Clin Electrophysiol. 2000;23:1020–8.
    OpenUrlCrossRefPubMed
  57. 57.↵
    1. Cheng CH,
    2. Sanders GD,
    3. Hlatky MA,
    4. et al
    . Cost-effectiveness of radiofrequency ablation for supraventricular tachycardia. Ann Intern Med. 2000;133:864–76.
    OpenUrlCrossRefPubMed
  58. 58.
    1. Bohnen M,
    2. Stevenson WG,
    3. Tedrow UB,
    4. et al
    . Incidence and predictors of major complications from contemporary catheter ablation to treat cardiac arrhythmias. Heart Rhythm. 2011;8:1661–6.
    OpenUrlCrossRefPubMed
  59. 59.
    1. Tendera M,
    2. Wnuk-Wojnar AM,
    3. Kulakowski P,
    4. et al
    . Efficacy and safety of dofetilide in the prevention of symptomatic episodes of paroxysmal supraventricular tachycardia: a 6-month double-blind comparison with propafenone and placebo. Am Heart J. 2001;142:93–8.
    OpenUrlCrossRefPubMed
  60. 60.
    A randomized, placebo-controlled trial of propafenone in the prophylaxis of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation. UK Propafenone PSVT Study Group. Circulation. 1995;92:2550–7.
    OpenUrlPubMed
  61. 61.
    1. Chimienti M,
    2. Cullen MT,
    3. Casadei G
    . Safety of flecainide versus propafenone for the long-term management of symptomatic paroxysmal supraventricular tachyarrhythmias. Report from the Flecainide and Propafenone Italian Study (FAPIS) Group. Eur Heart J. 1995;16:1943–51.
    OpenUrlAbstract/FREE Full Text
  62. 62.
    1. Anderson JL,
    2. Platt ML,
    3. Guarnieri T,
    4. et al
    . Flecainide acetate for paroxysmal supraventricular tachyarrhythmias. The Flecainide Supraventricular Tachycardia Study Group. Am J Cardiol. 1994;74:578–84.
    OpenUrlCrossRefPubMed
  63. 63.
    1. Pritchett EL,
    2. DaTorre SD,
    3. Platt ML,
    4. et al
    . Flecainide acetate treatment of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation: dose-response studies. The Flecainide Supraventricular Tachycardia Study Group. J Am Coll Cardiol. 1991;17:297–303.
    OpenUrlCrossRefPubMed
  64. 64.
    1. Pritchett EL,
    2. McCarthy EA,
    3. Wilkinson WE
    . Propafenone treatment of symptomatic paroxysmal supraventricular arrhythmias. A randomized, placebo-controlled, crossover trial in patients tolerating oral therapy. Ann Intern Med. 1991;114:539–44.
    OpenUrlCrossRefPubMed
  65. 65.
    1. Henthorn RW,
    2. Waldo AL,
    3. Anderson JL,
    4. et al
    . Flecainide acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group. Circulation. 1991;83:119–25.
    OpenUrlAbstract/FREE Full Text
  66. 66.
    1. Wanless RS,
    2. Anderson K,
    3. Joy M,
    4. et al
    . Multicenter comparative study of the efficacy and safety of sotalol in the prophylactic treatment of patients with paroxysmal supraventricular tachyarrhythmias. Am Heart J. 1997;133:441–6.
    OpenUrlCrossRefPubMed
  67. 67.
    1. Gambhir DS,
    2. Bhargava M,
    3. Nair M,
    4. et al
    . Comparison of electrophysiologic effects and efficacy of single-dose intravenous and long-term oral amiodarone therapy in patients with AV nodal reentrant tachycardia. Indian Heart J. 1996;48:133–7.
    OpenUrlPubMed
  68. 68.↵
    1. Haines DE,
    2. Beheiry S,
    3. Akar JG,
    4. et al
    . Heart Rythm Society expert consensus statement on electrophysiology laboratory standards: process, protocols, equipment, personnel, and safety. Heart Rhythm. 2014;11:e9–51.
    OpenUrlCrossRefPubMed
  69. 69.↵
    1. Knight BP,
    2. Zivin A,
    3. Souza J,
    4. et al
    . A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol. 1999;33:775–81.
    OpenUrlCrossRefPubMed
  70. 70.↵
    1. Horowitz LN,
    2. Kay HR,
    3. Kutalek SP,
    4. et al
    . Risks and complications of clinical cardiac electrophysiologic studies: a prospective analysis of 1,000 consecutive patients. J Am Coll Cardiol. 1987;9:1261–8.
    OpenUrlCrossRefPubMed
  71. 71.↵
    1. Huang SW,
    2. Wood M
    1. Asirvatham S,
    2. Narayan O
    . Advanced catheter mapping and navigation system. In: Huang SW, Wood M, editors. Catheter Ablation of Cardiac Arrhythmias. Philadelphia, PA: Saunders/Elsevier, 2006:135–61.
  72. 72.↵
    1. Sporton SC,
    2. Earley MJ,
    3. Nathan AW,
    4. et al
    . Electroanatomic versus fluoroscopic mapping for catheter ablation procedures: a prospective randomized study. J Cardiovasc Electrophysiol. 2004;15:310–5.
    OpenUrlCrossRefPubMed
  73. 73.↵
    1. Alvarez M,
    2. Tercedor L,
    3. Almansa I,
    4. et al
    . Safety and feasibility of catheter ablation for atrioventricular nodal re-entrant tachycardia without fluoroscopic guidance. Heart Rhythm. 2009;6:1714–20.
    OpenUrlCrossRefPubMed
  74. 74.↵
    1. Casella M,
    2. Pelargonio G,
    3. Dello RA,
    4. et al
    . “Near-zero” fluoroscopic exposure in supraventricular arrhythmia ablation using the EnSite NavX mapping system: personal experience and review of the literature. J Interv Card Electrophysiol. 2011;31:109–18.
    OpenUrlCrossRefPubMed
  75. 75.↵
    1. Razminia M,
    2. Manankil MF,
    3. Eryazici PLS,
    4. et al
    . Nonfluoroscopic catheter ablation of cardiac arrhythmias in adults: feasibility, safety, and efficacy. J Cardiovasc Electrophysiol. 2012;23:1078–86.
    OpenUrlCrossRefPubMed
  76. 76.↵
    1. Earley MJ,
    2. Showkathali R,
    3. Alzetani M,
    4. et al
    . Radiofrequency ablation of arrhythmias guided by non-fluoroscopic catheter location: a prospective randomized trial. Eur Heart J. 2006;27:1223–9.
    OpenUrlAbstract/FREE Full Text
  77. 77.↵
    1. Hindricks G,
    2. Willems S,
    3. Kautzner J,
    4. et al
    . Effect of electroanatomically guided versus conventional catheter ablation of typical atrial flutter on the fluoroscopy time and resource use: a prospective randomized multicenter study. J Cardiovasc Electrophysiol. 2009;20:734–40.
    OpenUrlCrossRefPubMed
  78. 78.↵
    1. Xu D,
    2. Yang B,
    3. Shan Q,
    4. et al
    . Initial clinical experience of remote magnetic navigation system for catheter mapping and ablation of supraventricular tachycardias. J Interv Card Electrophysiol. 2009;25:171–4.
    OpenUrlCrossRefPubMed
  79. 79.↵
    1. Sommer P,
    2. Wojdyla-Hordynska A,
    3. Rolf S,
    4. et al
    . Initial experience in ablation of typical atrial flutter using a novel three-dimensional catheter tracking system. Europace. 2013;15:578–81.
    OpenUrlAbstract/FREE Full Text
  80. 80.↵
    1. Cummings JE,
    2. Pacifico A,
    3. Drago JL,
    4. et al
    . Alternative energy sources for the ablation of arrhythmias. Pacing Clin Electrophysiol. 2005;28:434–43.
    OpenUrlCrossRefPubMed
  81. 81.↵
    1. Olshansky B,
    2. Sullivan RM
    . Inappropriate sinus tachycardia. J Am Coll Cardiol. 2013;61:793–801.
    OpenUrlCrossRefPubMed
  82. 82.↵
    1. Marcus B,
    2. Gillette PC,
    3. Garson A
    . Intrinsic heart rate in children and young adults: an index of sinus node function isolated from autonomic control. Am Heart J. 1990;119:911–6.
    OpenUrlCrossRefPubMed
  83. 83.↵
    1. Jose AD,
    2. Collison D
    . The normal range and determinants of the intrinsic heart rate in man. Cardiovasc Res. 1970;4:160–7.
    OpenUrlAbstract/FREE Full Text
  84. 84.↵
    1. Alboni P,
    2. Malcarne C,
    3. Pedroni P,
    4. et al
    . Electrophysiology of normal sinus node with and without autonomic blockade. Circulation. 1982;65:1236–42.
    OpenUrlFREE Full Text
  85. 85.↵
    1. Cappato R,
    2. Castelvecchio S,
    3. Ricci C,
    4. et al
    . Clinical efficacy of ivabradine in patients with inappropriate sinus tachycardia: a prospective, randomized, placebo-controlled, double-blind, crossover evaluation. J Am Coll Cardiol. 2012;60:1323–9.
    OpenUrlCrossRefPubMed
  86. 86.↵
    1. Benezet-Mazuecos J,
    2. Rubio JM,
    3. Farré J,
    4. et al
    . Long-term outcomes of ivabradine in inappropriate sinus tachycardia patients: appropriate efficacy or inappropriate patients. Pacing Clin Electrophysiol. 2013;36:830–6.
    OpenUrlCrossRefPubMed
  87. 87.↵
    1. Ptaszynski P,
    2. Kaczmarek K,
    3. Ruta J,
    4. et al
    . Metoprolol succinate vs. ivabradine in the treatment of inappropriate sinus tachycardia in patients unresponsive to previous pharmacological therapy. Europace. 2013;15:116–21.
    OpenUrlAbstract/FREE Full Text
  88. 88.↵
    1. Ptaszynski P,
    2. Kaczmarek K,
    3. Ruta J,
    4. et al
    . Ivabradine in the treatment of inappropriate sinus tachycardia in patients after successful radiofrequency catheter ablation of atrioventricular node slow pathway. Pacing Clin Electrophysiol. 2013;36:42–9.
    OpenUrlCrossRefPubMed
  89. 89.↵
    1. Ptaszynski P,
    2. Kaczmarek K,
    3. Ruta J,
    4. et al
    . Ivabradine in combination with metoprolol succinate in the treatment of inappropriate sinus tachycardia. J Cardiovasc Pharmacol Ther. 2013;18:338–44.
    OpenUrlAbstract/FREE Full Text
  90. 90.↵
    1. Calò L,
    2. Rebecchi M,
    3. Sette A,
    4. et al
    . Efficacy of ivabradine administration in patients affected by inappropriate sinus tachycardia. Heart Rhythm. 2010;7:1318–23.
    OpenUrlCrossRefPubMed
  91. 91.↵
    1. Kaplinsky E,
    2. Comes FP,
    3. Urondo LSV,
    4. et al
    . Efficacy of ivabradine in four patients with inappropriate sinus tachycardia: a three month-long experience based on electrocardiographic, Holter monitoring, exercise tolerance and quality of life assessments. Cardiol J. 2010;17:166–71.
    OpenUrlPubMed
  92. 92.↵
    1. Rakovec P
    . Treatment of inappropriate sinus tachycardia with ivabradine. Wien Klin Wochenschr. 2009;121:715–8.
    OpenUrlCrossRefPubMed
  93. 93.↵
    1. Zellerhoff S,
    2. Hinterseer M,
    3. Felix Krull B,
    4. et al
    . Ivabradine in patients with inappropriate sinus tachycardia. Naunyn Schmiedebergs Arch Pharmacol. 2010;382:483–6.
    OpenUrlCrossRefPubMed
  94. 94.↵
    1. Man KC,
    2. Knight B,
    3. Tse HF,
    4. et al
    . Radiofrequency catheter ablation of inappropriate sinus tachycardia guided by activation mapping. J Am Coll Cardiol. 2000;35:451–7.
    OpenUrlCrossRefPubMed
  95. 95.↵
    1. Lin D,
    2. Garcia F,
    3. Jacobson J,
    4. et al
    . Use of noncontact mapping and saline-cooled ablation catheter for sinus node modification in medically refractory inappropriate sinus tachycardia. Pacing Clin Electrophysiol. 2007;30:236–42.
    OpenUrlCrossRefPubMed
  96. 96.↵
    1. Lee RJ,
    2. Kalman JM,
    3. Fitzpatrick AP,
    4. et al
    . Radiofrequency catheter modification of the sinus node for “inappropriate” sinus tachycardia. Circulation. 1995;92:2919–28.
    OpenUrlAbstract/FREE Full Text
  97. 97.↵
    1. Marrouche NF,
    2. Beheiry S,
    3. Tomassoni G,
    4. et al
    . Three-dimensional nonfluoroscopic mapping and ablation of inappropriate sinus tachycardia. Procedural strategies and long-term outcome. J Am Coll Cardiol. 2002;39:1046–54.
    OpenUrlCrossRefPubMed
  98. 98.↵
    1. Callans DJ,
    2. Ren JF,
    3. Schwartzman D,
    4. et al
    . Narrowing of the superior vena cava-right atrium junction during radiofrequency catheter ablation for inappropriate sinus tachycardia: analysis with intracardiac echocardiography. J Am Coll Cardiol. 1999;33:1667–70.
    OpenUrlCrossRefPubMed
  99. 99.↵
    1. Frankel DS,
    2. Lin D,
    3. Anastasio N,
    4. et al
    . Frequent additional tachyarrhythmias in patients with inappropriate sinus tachycardia undergoing sinus node modification: an important cause of symptom recurrence. J Cardiovasc Electrophysiol. 2012;23:835–9.
    OpenUrlCrossRefPubMed
  100. 100.↵
    1. Takemoto M,
    2. Mukai Y,
    3. Inoue S,
    4. et al
    . Usefulness of non-contact mapping for radiofrequency catheter ablation of inappropriate sinus tachycardia: new procedural strategy and long-term clinical outcome. Intern Med. 2012;51:357–62.
    OpenUrlCrossRefPubMed
  101. 101.
    1. Klein I,
    2. Ojamaa K
    . Thyroid hormone and the cardiovascular system. N Engl J Med. 2001;344:501–9.
    OpenUrlCrossRefPubMed
  102. 102.↵
    1. Steinbeck G,
    2. Hoffmann E
    . ‘True’ atrial tachycardia. Eur Heart J. 1998; 19 Suppl E:E48–9.
    OpenUrl
  103. 103.↵
    1. Wren C
    . Incessant tachycardias. Eur Heart J. 1998;19 Suppl E:E54–9.
    OpenUrl
  104. 104.↵
    1. Medi C,
    2. Kalman JM,
    3. Haqqani H,
    4. et al
    . Tachycardia-mediated cardiomyopathy secondary to focal atrial tachycardia: long-term outcome after catheter ablation. J Am Coll Cardiol. 2009;53:1791–7.
    OpenUrlCrossRefPubMed
  105. 105.↵
    1. Tang CW,
    2. Scheinman MM,
    3. Van Hare GF,
    4. et al
    . Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol. 1995;26:1315–24.
    OpenUrlCrossRefPubMed
  106. 106.↵
    1. Kistler PM,
    2. Roberts-Thomson KC,
    3. Haqqani HM,
    4. et al
    . P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. 2006;48:1010–7.
    OpenUrlCrossRefPubMed
  107. 107.↵
    1. Chen SA,
    2. Chiang CE,
    3. Yang CJ,
    4. et al
    . Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90:1262–78.
    OpenUrlAbstract/FREE Full Text
  108. 108.↵
    1. Kalman JM,
    2. Olgin JE,
    3. Karch MR,
    4. et al
    . “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol. 1998;31:451–9.
    OpenUrlCrossRefPubMed
  109. 109.↵
    1. Morton JB,
    2. Sanders P,
    3. Das A,
    4. et al
    . Focal atrial tachycardia arising from the tricuspid annulus: electrophysiologic and electrocardiographic characteristics. J Cardiovasc Electrophysiol. 2001;12:653–9.
    OpenUrlCrossRefPubMed
  110. 110.↵
    1. Kistler PM,
    2. Sanders P,
    3. Fynn SP,
    4. et al
    . Electrophysiological and electrocardiographic characteristics of focal atrial tachycardia originating from the pulmonary veins: acute and long-term outcomes of radiofrequency ablation. Circulation. 2003;108:1968–75.
    OpenUrlAbstract/FREE Full Text
  111. 111.↵
    1. Kistler PM,
    2. Sanders P,
    3. Hussin A,
    4. et al
    . Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol. 2003;41:2212–9.
    OpenUrlCrossRefPubMed
  112. 112.↵
    1. Gonzalez MD,
    2. Contreras LJ,
    3. Jongbloed MRM,
    4. et al
    . Left atrial tachycardia originating from the mitral annulus-aorta junction. Circulation. 2004;110:3187–92.
    OpenUrlAbstract/FREE Full Text
  113. 113.↵
    1. Kistler PM,
    2. Fynn SP,
    3. Haqqani H,
    4. et al
    . Focal atrial tachycardia from the ostium of the coronary sinus: electrocardiographic and electrophysiological characterization and radiofrequency ablation. J Am Coll Cardiol. 2005;45:1488–93.
    OpenUrlCrossRefPubMed
  114. 114.↵
    1. Ouyang F,
    2. Ma J,
    3. Ho SY,
    4. et al
    . Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol. 2006;48:122–31.
    OpenUrlCrossRefPubMed
  115. 115.↵
    1. Roberts-Thomson KC,
    2. Kistler PM,
    3. Haqqani HM,
    4. et al
    . Focal atrial tachycardias arising from the right atrial appendage: electrocardiographic and electrophysiologic characteristics and radiofrequency ablation. J Cardiovasc Electrophysiol. 2007;18:367–72.
    OpenUrlCrossRefPubMed
  116. 116.↵
    1. Biviano AB,
    2. Bain W,
    3. Whang W,
    4. et al
    . Focal left atrial tachycardias not associated with prior catheter ablation for atrial fibrillation: clinical and electrophysiological characteristics. Pacing Clin Electrophysiol. 2012;35:17–27.
    OpenUrlCrossRefPubMed
  117. 117.↵
    1. Walters TE,
    2. Kistler PM,
    3. Kalman JM
    . Radiofrequency ablation for atrial tachycardia and atrial flutter. Heart Lung Circ. 2012;21:386–94.
    OpenUrlCrossRefPubMed
  118. 118.↵
    1. Lee G,
    2. Sanders P,
    3. Kalman JM
    . Catheter ablation of atrial arrhythmias: state of the art. Lancet. 2012;380:1509–19.
    OpenUrlCrossRefPubMed
  119. 119.↵
    1. Gillette PC,
    2. Garson A Jr.
    . Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia. Circulation. 1977;56:571–5.
    OpenUrlFREE Full Text
  120. 120.↵
    1. Mehta AV,
    2. Sanchez GR,
    3. Sacks EJ,
    4. et al
    . Ectopic automatic atrial tachycardia in children: clinical characteristics, management and follow-up. J Am Coll Cardiol. 1988;11:379–85.
    OpenUrlCrossRefPubMed
  121. 121.
    1. Markowitz SM,
    2. Stein KM,
    3. Mittal S,
    4. et al
    . Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol. 1999;10:489–502.
    OpenUrlCrossRefPubMed
  122. 122.
    1. Reisinger J,
    2. Gstrein C,
    3. Winter T,
    4. et al
    . Optimization of initial energy for cardioversion of atrial tachyarrhythmias with biphasic shocks. Am J Emerg Med. 2010;28:159–65.
    OpenUrlCrossRefPubMed
  123. 123.
    1. Engelstein ED,
    2. Lippman N,
    3. Stein KM,
    4. et al
    . Mechanism-specific effects of adenosine on atrial tachycardia. Circulation. 1994;89:2645–54.
    OpenUrlAbstract/FREE Full Text
  124. 124.
    1. Eidher U,
    2. Freihoff F,
    3. Kaltenbrunner W,
    4. et al
    . Efficacy and safety of ibutilide for the conversion of monomorphic atrial tachycardia. Pacing Clin Electrophysiol. 2006;29:358–62.
    OpenUrlCrossRefPubMed
  125. 125.
    1. de Loma-Osorio F,
    2. Diaz-Infante E,
    3. et al
    . Spanish Catheter Ablation Registry. 12th Official Report of the Spanish Society of Cardiology Working Group on Electrophysiology and Arrhythmias (2012). Rev Esp Cardiol (Engl Ed). 2013;66:983–92.
    OpenUrlCrossRefPubMed
  126. 126.
    1. Liu X,
    2. Dong J,
    3. Ho SY,
    4. et al
    . Atrial tachycardia arising adjacent to noncoronary aortic sinus: distinctive atrial activation patterns and anatomic insights. J Am Coll Cardiol. 2010;56:796–804.
    OpenUrlCrossRefPubMed
  127. 127.
    1. Creamer JE,
    2. Nathan AW,
    3. Camm AJ
    . Successful treatment of atrial tachycardias with flecainide acetate. Br Heart J. 1985;53:164–6.
    OpenUrlAbstract/FREE Full Text
  128. 128.
    1. Kunze KP,
    2. Kuck KH,
    3. Schlüter M,
    4. et al
    . Effect of encainide and flecainide on chronic ectopic atrial tachycardia. J Am Coll Cardiol. 1986;7:1121–6.
    OpenUrlCrossRefPubMed
  129. 129.
    1. von Bernuth G,
    2. Engelhardt W,
    3. Kramer HH,
    4. et al
    . Atrial automatic tachycardia in infancy and childhood. Eur Heart J. 1992;13:1410–5.
    OpenUrlAbstract/FREE Full Text
  130. 130.
    1. Lucet V,
    2. Do Ngoc D,
    3. Fidelle J,
    4. et al
    . [Anti-arrhythmia efficacy of propafenone in children. Apropos of 30 cases]. Arch Mal Coeur Vaiss. 1987;80:1385–93.
    OpenUrlPubMed
  131. 131.
    1. Heusch A,
    2. Kramer HH,
    3. Krogmann ON,
    4. et al
    . Clinical experience with propafenone for cardiac arrhythmias in the young. Eur Heart J. 1994;15:1050–6.
    OpenUrlAbstract/FREE Full Text
  132. 132.
    1. Colloridi V,
    2. Perri C,
    3. Ventriglia F,
    4. et al
    . Oral sotalol in pediatric atrial ectopic tachycardia. Am Heart J. 1992;123:254–6.
    OpenUrlCrossRefPubMed
  133. 133.
    1. Guccione P,
    2. Paul T,
    3. Garson A Jr.
    . Long-term follow-up of amiodarone therapy in the young: continued efficacy, unimpaired growth, moderate side effects. J Am Coll Cardiol. 1990;15:1118–24.
    OpenUrlCrossRefPubMed
  134. 134.
    1. Coumel P,
    2. Fidelle J
    . Amiodarone in the treatment of cardiac arrhythmias in children: one hundred thirty-five cases. Am Heart J. 1980;100:1063–9.
    OpenUrlCrossRefPubMed
  135. 135.
    1. Miyazaki A,
    2. Ohuchi H,
    3. Kurosaki K,
    4. et al
    . Efficacy and safety of sotalol for refractory tachyarrhythmias in congenital heart disease. Circ J. 2008;72:1998–2003.
    OpenUrlCrossRefPubMed
  136. 136.
    1. Kang KT,
    2. Etheridge SP,
    3. Kantoch MJ,
    4. et al
    . Current management of focal atrial tachycardia in children: a multicenter experience. Circ Arrhythm Electrophysiol. 2014;7:664–70.
    OpenUrlAbstract/FREE Full Text
  137. 137.↵
    1. Wang K,
    2. Goldfarb BL,
    3. Gobel FL,
    4. et al
    . Multifocal atrial tachycardia. Arch Intern Med. 1977;137:161–4.
    OpenUrlCrossRefPubMed
  138. 138.↵
    1. Bittar G,
    2. Friedman HS
    . The arrhythmogenicity of theophylline. A multivariate analysis of clinical determinants. Chest. 1991;99:1415–20.
    OpenUrlCrossRefPubMed
  139. 139.↵
    1. Iseri LT,
    2. Fairshter RD,
    3. Hardemann JL,
    4. et al
    . Magnesium and potassium therapy in multifocal atrial tachycardia. Am Heart J. 1985;110:789–94.
    OpenUrlCrossRefPubMed
  140. 140.↵
    1. Kastor JA
    . Multifocal atrial tachycardia. N Engl J Med. 1990;322:1713–7.
    OpenUrlCrossRefPubMed
  141. 141.
    1. Arsura EL,
    2. Solar M,
    3. Lefkin AS,
    4. et al
    . Metoprolol in the treatment of multifocal atrial tachycardia. Crit Care Med. 1987;15:591–4.
    OpenUrlCrossRefPubMed
  142. 142.
    1. Levine JH,
    2. Michael JR,
    3. Guarnieri T
    . Treatment of multifocal atrial tachycardia with verapamil. N Engl J Med. 1985;312:21–5.
    OpenUrlCrossRefPubMed
  143. 143.
    1. Salerno DM,
    2. Anderson B,
    3. Sharkey PJ,
    4. et al
    . Intravenous verapamil for treatment of multifocal atrial tachycardia with and without calcium pretreatment. Ann Intern Med. 1987;107:623–8.
    OpenUrlCrossRefPubMed
  144. 144.
    1. Hazard PB,
    2. Burnett CR
    . Verapamil in multifocal atrial tachycardia. Hemodynamic and respiratory changes. Chest. 1987;91:68–70.
    OpenUrlCrossRefPubMed
  145. 145.
    1. Hazard PB,
    2. Burnett CR
    . Treatment of multifocal atrial tachycardia with metoprolol. Crit Care Med. 1987;15:20–5.
    OpenUrlCrossRefPubMed
  146. 146.
    1. Mehta D,
    2. Wafa S,
    3. Ward DE,
    4. et al
    . Relative efficacy of various physical manoeuvres in the termination of junctional tachycardia. Lancet. 1988;1:1181–5.
    OpenUrlCrossRefPubMed
  147. 147.
    1. Wen ZC,
    2. Chen SA,
    3. Tai CT,
    4. et al
    . Electrophysiological mechanisms and determinants of vagal maneuvers for termination of paroxysmal supraventricular tachycardia. Circulation. 1998;98:2716–23.
    OpenUrlAbstract/FREE Full Text
  148. 148.
    1. Glatter KA,
    2. Cheng J,
    3. Dorostkar P,
    4. et al
    . Electrophysiologic effects of adenosine in patients with supraventricular tachycardia. Circulation. 1999;99:1034–40.
    OpenUrlAbstract/FREE Full Text
  149. 149.
    1. Dougherty AH,
    2. Jackman WM,
    3. Naccarelli GV,
    4. et al
    . Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group. Am J Cardiol. 1992;70:587–92.
    OpenUrlCrossRefPubMed
  150. 150.
    1. Waxman HL,
    2. Myerburg RJ,
    3. Appel R,
    4. et al
    . Verapamil for control of ventricular rate in paroxysmal supraventricular tachycardia and atrial fibrillation or flutter: a double-blind randomized cross-over study. Ann Intern Med. 1981;94:1–6.
    OpenUrlCrossRefPubMed
  151. 151.
    1. Amsterdam EA,
    2. Kulcyski J,
    3. Ridgeway MG
    ,. Efficacy of cardioselective beta-adrenergic blockade with intravenously administered metoprolol in the treatment of supraventricular tachyarrhythmias. J Clin Pharmacol. 1991;31:714–8.
    OpenUrlCrossRefPubMed
  152. 152.
    1. Das G,
    2. Tschida V,
    3. Gray R,
    4. et al
    . Efficacy of esmolol in the treatment and transfer of patients with supraventricular tachyarrhythmias to alternate oral antiarrhythmic agents. J Clin Pharmacol. 1988;28:746–50.
    OpenUrlCrossRefPubMed
  153. 153.
    1. Alboni P,
    2. Tomasi C,
    3. Menozzi C,
    4. et al
    . Efficacy and safety of out-of-hospital self-administered single-dose oral drug treatment in the management of infrequent, well-tolerated paroxysmal supraventricular tachycardia. J Am Coll Cardiol. 2001;37:548–53.
    OpenUrlCrossRefPubMed
  154. 154.
    1. Yeh SJ,
    2. Lin FC,
    3. Chou YY,
    4. et al
    . Termination of paroxysmal supraventricular tachycardia with a single oral dose of diltiazem and propranolol. Circulation. 1985;71:104–9.
    OpenUrlAbstract/FREE Full Text
  155. 155.
    1. Rinkenberger RL,
    2. Prystowsky EN,
    3. Heger JJ,
    4. et al
    . Effects of intravenous and chronic oral verapamil administration in patients with supraventricular tachyarrhythmias. Circulation. 1980;62:996–1010.
    OpenUrlFREE Full Text
  156. 156.
    1. D’Este D,
    2. Zoppo F,
    3. Bertaglia E,
    4. et al
    . Long-term outcome of patients with atrioventricular node reentrant tachycardia. Int J Cardiol. 2007;115:350–3.
    OpenUrlCrossRefPubMed
  157. 157.
    1. Langberg JJ,
    2. Leon A,
    3. Borganelli M,
    4. et al
    . A randomized, prospective comparison of anterior and posterior approaches to radiofrequency catheter ablation of atrioventricular nodal reentry tachycardia. Circulation. 1993;87:1551–6.
    OpenUrlAbstract/FREE Full Text
  158. 158.
    1. Kalbfleisch SJ,
    2. Strickberger SA,
    3. Williamson B,
    4. et al
    . Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1994;23:716–23.
    OpenUrlCrossRefPubMed
  159. 159.
    1. Kay GN,
    2. Epstein AE,
    3. Dailey SM,
    4. et al
    . Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia. Evidence for involvement of perinodal myocardium within the reentrant circuit. Circulation. 1992;85:1675–88.
    OpenUrlAbstract/FREE Full Text
  160. 160.
    1. Bogun F,
    2. Knight B,
    3. Weiss R,
    4. et al
    . Slow pathway ablation in patients with documented but noninducible paroxysmal supraventricular tachycardia. J Am Coll Cardiol. 1996;28:1000–4.
    OpenUrlCrossRefPubMed
  161. 161.
    1. O’Hara GE,
    2. Philippon F,
    3. Champagne J,
    4. et al
    . Catheter ablation for cardiac arrhythmias: a 14-year experience with 5330 consecutive patients at the Quebec Heart Institute, Laval Hospital. Can J Cardiol. 2007; 23 Suppl B:67B–70B.
    OpenUrlCrossRefPubMed
  162. 162.
    1. Gambhir DS,
    2. Bhargava M,
    3. Arora R,
    4. et al
    . Electrophysiologic effects and therapeutic efficacy of intravenous flecainide for termination of paroxysmal supraventricular tachycardia. Indian Heart J. 1995;47:237–43.
    OpenUrlPubMed
  163. 163.
    1. Musto B,
    2. Cavallaro C,
    3. Musto A,
    4. et al
    . Flecainide single oral dose for management of paroxysmal supraventricular tachycardia in children and young adults. Am Heart J. 1992;124:110–5.
    OpenUrlCrossRefPubMed
  164. 164.↵
    1. Munger TM,
    2. Packer DL,
    3. Hammill SC,
    4. et al
    . A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953–1989. Circulation. 1993;87:866–73.
    OpenUrlAbstract/FREE Full Text
  165. 165.↵
    1. Pappone C,
    2. Vicedomini G,
    3. Manguso F,
    4. et al
    . Wolff-Parkinson-white syndrome in the era of catheter ablation: insights from a registry study of 2169 patients. Circulation. 2014;130:811–9.
    OpenUrlAbstract/FREE Full Text
  166. 166.↵
    1. Timmermans C,
    2. Smeets JL,
    3. Rodriguez LM,
    4. et al
    . Aborted sudden death in the Wolff-Parkinson-White syndrome. Am J Cardiol. 1995;76:492–4.
    OpenUrlCrossRefPubMed
  167. 167.↵
    1. Klein GJ,
    2. Bashore TM,
    3. Sellers TD,
    4. et al
    . Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. 1979;301:1080–5.
    OpenUrlCrossRefPubMed
  168. 168.↵
    1. Bromberg BI,
    2. Lindsay BD,
    3. Cain ME,
    4. et al
    . Impact of clinical history and electrophysiologic characterization of accessory pathways on management strategies to reduce sudden death among children with Wolff-Parkinson-White syndrome. J Am Coll Cardiol. 1996;27:690–5.
    OpenUrlCrossRefPubMed
  169. 169.↵
    1. Santinelli V,
    2. Radinovic A,
    3. Manguso F,
    4. et al
    . The natural history of asymptomatic ventricular pre-excitation a long-term prospective follow-up study of 184 asymptomatic children. J Am Coll Cardiol. 2009;53:275–80.
    OpenUrlCrossRefPubMed
  170. 170.
    1. Neumar RW,
    2. Otto CW,
    3. Link MS,
    4. et al
    . Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S729–67.
    OpenUrlFREE Full Text
  171. 171.
    1. Smith GD,
    2. Dyson K,
    3. Taylor D,
    4. et al
    . Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database Syst Rev. 2013;3:CD009502.
    OpenUrlPubMed
  172. 172.
    1. Delaney B,
    2. Loy J,
    3. Kelly A-M
    . The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis. Eur J Emerg Med. 2011;18:148–52.
    OpenUrlCrossRefPubMed
  173. 173.
    1. Furlong R,
    2. Gerhardt RT,
    3. Farber P,
    4. et al
    . Intravenous adenosine as first-line prehospital management of narrow-complex tachycardias by EMS personnel without direct physician control. Am J Emerg Med. 1995;13:383–8.
    OpenUrlCrossRefPubMed
  174. 174.
    1. Schatz I,
    2. Ordog GJ,
    3. Karody R,
    4. et al
    . Wolff-Parkinson-White syndrome presenting in atrial fibrillation. Ann Emerg Med. 1987;16:574–8.
    OpenUrlCrossRefPubMed
  175. 175.
    1. Mittal S,
    2. Ayati S,
    3. Stein KM,
    4. et al
    . Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation. 2000;101:1282–7.
    OpenUrlAbstract/FREE Full Text
  176. 176.
    1. Glatter KA,
    2. Dorostkar PC,
    3. Yang Y,
    4. et al
    . Electrophysiological effects of ibutilide in patients with accessory pathways. Circulation. 2001;104:1933–9.
    OpenUrlAbstract/FREE Full Text
  177. 177.
    1. Sellers TD Jr..,
    2. Campbell RW,
    3. Bashore TM,
    4. et al
    . Effects of procainamide and quinidine sulfate in the Wolff-Parkinson-White syndrome. Circulation. 1977;55:15–22.
    OpenUrlAbstract/FREE Full Text
  178. 178.
    1. Huycke EC,
    2. Sung RJ,
    3. Dias VC,
    4. et al
    . Intravenous diltiazem for termination of reentrant supraventricular tachycardia: a placebo-controlled, randomized, double-blind, multicenter study. J Am Coll Cardiol. 1989;13:538–44.
    OpenUrlCrossRefPubMed
  179. 179.
    1. Hamer A,
    2. Peter T,
    3. Platt M,
    4. et al
    . Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome. Am Heart J. 1981;101:600–12.
    OpenUrlCrossRefPubMed
  180. 180.
    1. Hombach V,
    2. Braun V,
    3. Hopp HW,
    4. et al
    . Antiarrhythmic effects of acute betablockade with atenolol on supraventricular tachycardias at rest and during exercise. Klin Wochenschr. 1981;59:123–33.
    OpenUrlCrossRefPubMed
  181. 181.
    1. Morady F,
    2. DiCarlo LA Jr..,
    3. Baerman JM,
    4. et al
    . Effect of propranolol on ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol. 1987;10:492–6.
    OpenUrlCrossRefPubMed
  182. 182.
    1. Sellers TD Jr..,
    2. Bashore TM,
    3. Gallagher JJ
    . Digitalis in the pre-excitation syndrome. Analysis during atrial fibrillation. Circulation. 1977;56:260–7.
    OpenUrlAbstract/FREE Full Text
  183. 183.
    1. Sheinman BD,
    2. Evans T
    . Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982;285:999–1000.
    OpenUrlAbstract/FREE Full Text
  184. 184.
    1. Boriani G,
    2. Biffi M,
    3. Frabetti L,
    4. et al
    . Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996;131:1214–6.
    OpenUrlCrossRefPubMed
  185. 185.
    1. Shiraishi H,
    2. Ishibashi K,
    3. Urao N,
    4. et al
    . Two cases of polymorphic ventricular tachycardia induced by the administration of verapamil against paroxysmal supraventricular tachycardia. Intern Med. 2002;41:445–8.
    OpenUrlCrossRefPubMed
  186. 186.
    1. Schützenberger W,
    2. Leisch F,
    3. Gmeiner R
    . Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987;16:93–5.
    OpenUrlCrossRefPubMed
  187. 187.
    1. Jackman WM,
    2. Wang XZ,
    3. Friday KJ,
    4. et al
    . Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current. N Engl J Med. 1991;324:1605–11.
    OpenUrlCrossRefPubMed
  188. 188.
    1. Calkins H,
    2. Langberg J,
    3. Sousa J,
    4. et al
    . Radiofrequency catheter ablation of accessory atrioventricular connections in 250 patients. Abbreviated therapeutic approach to Wolff-Parkinson-White syndrome. Circulation. 1992;85:1337–46.
    OpenUrlAbstract/FREE Full Text
  189. 189.
    1. Dagres N,
    2. Clague JR,
    3. Kottkamp H,
    4. et al
    . Radiofrequency catheter ablation of accessory pathways. Outcome and use of antiarrhythmic drugs during follow-up. Eur Heart J. 1999;20:1826–32.
    OpenUrlAbstract/FREE Full Text
  190. 190.
    1. Schläpfer J,
    2. Fromer M
    . Late clinical outcome after successful radiofrequency catheter ablation of accessory pathways. Eur Heart J. 2001;22:605–9.
    OpenUrlAbstract/FREE Full Text
  191. 191.
    1. Belhassen B,
    2. Rogowski O,
    3. Glick A,
    4. et al
    . Radiofrequency ablation of accessory pathways: a 14 year experience at the Tel Aviv Medical Center in 508 patients. Isr Med Assoc J. 2007;9:265–70.
    OpenUrlPubMed
  192. 192.↵
    1. Kugler JD,
    2. Danford DA,
    3. Deal BJ,
    4. et al
    . Radiofrequency catheter ablation for tachyarrhythmias in children and adolescents. The Pediatric Electrophysiology Society. N Engl J Med. 1994;330:1481–7.
    OpenUrlCrossRefPubMed
  193. 193.↵
    1. Kugler JD,
    2. Danford DA,
    3. Houston K,
    4. et al
    . Radiofrequency catheter ablation for paroxysmal supraventricular tachycardia in children and adolescents without structural heart disease. Pediatric EP Society, Radiofrequency Catheter Ablation Registry. Am J Cardiol. 1997;80:1438–43.
    OpenUrlCrossRefPubMed
  194. 194.
    1. Sakurai M,
    2. Yasuda H,
    3. Kato N,
    4. et al
    . Acute and chronic effects of verapamil in patients with paroxysmal supraventricular tachycardia. Am Heart J. 1983;105:619–28.
    OpenUrlCrossRefPubMed
  195. 195.
    1. Hopson JR,
    2. Buxton AE,
    3. Rinkenberger RL,
    4. et al
    . Safety and utility of flecainide acetate in the routine care of patients with supraventricular tachyarrhythmias: results of a multicenter trial. The Flecainide Supraventricular Tachycardia Study Group. Am J Cardiol. 1996;77:72A–82A.
    OpenUrlCrossRefPubMed
  196. 196.
    1. Feld GK,
    2. Nademanee K,
    3. Weiss J,
    4. et al
    . Electrophysiologic basis for the suppression by amiodarone of orthodromic supraventricular tachycardias complicating pre-excitation syndromes. J Am Coll Cardiol. 1984;3:1298–307.
    OpenUrlCrossRefPubMed
  197. 197.
    1. Feld GK,
    2. Nademanee K,
    3. Stevenson W,
    4. et al
    . Clinical and electrophysiologic effects of amiodarone in patients with atrial fibrillation complicating the Wolff-Parkinson-White syndrome. Am Heart J. 1988;115:102–7.
    OpenUrlCrossRefPubMed
  198. 198.
    1. Bauernfeind RA,
    2. Wyndham CR,
    3. Dhingra RC,
    4. et al
    . Serial electrophysiologic testing of multiple drugs in patients with atrioventricular nodal reentrant paroxysmal tachycardia. Circulation. 1980;62:1341–9.
    OpenUrlAbstract/FREE Full Text
  199. 199.
    1. Sharma AD,
    2. Yee R,
    3. Guiraudon G,
    4. et al
    . Sensitivity and specificity of invasive and noninvasive testing for risk of sudden death in Wolff-Parkinson-White syndrome. J Am Coll Cardiol. 1987;10:373–81.
    OpenUrlCrossRefPubMed
  200. 200.
    1. Gaita F,
    2. Giustetto C,
    3. Riccardi R,
    4. et al
    . Stress and pharmacologic tests as methods to identify patients with Wolff-Parkinson-White syndrome at risk of sudden death. Am J Cardiol. 1989;64:487–90.
    OpenUrlCrossRefPubMed
  201. 201.
    1. Spar DS,
    2. Silver ES,
    3. Hordof AJ,
    4. et al
    . Relation of the utility of exercise testing for risk assessment in pediatric patients with ventricular preexcitation to pathway location. Am J Cardiol. 2012;109:1011–4.
    OpenUrlCrossRefPubMed
  202. 202.
    1. Wackel P,
    2. Irving C,
    3. Webber S,
    4. et al
    . Risk stratification in Wolff-Parkinson-White syndrome: the correlation between noninvasive and invasive testing in pediatric patients. Pacing Clin Electrophysiol. 2012;35:1451–7.
    OpenUrlCrossRefPubMed
  203. 203.
    1. Beckman KJ,
    2. Gallastegui JL,
    3. Bauman JL,
    4. et al
    . The predictive value of electrophysiologic studies in untreated patients with Wolff-Parkinson-White syndrome. J Am Coll Cardiol. 1990;15:640–7.
    OpenUrlCrossRefPubMed
  204. 204.
    1. Pappone C,
    2. Vicedomini G,
    3. Manguso F,
    4. et al
    . Risk of malignant arrhythmias in initially symptomatic patients with Wolff-Parkinson-White syndrome: results of a prospective long-term electrophysiological follow-up study. Circulation. 2012;125:661–8.
    OpenUrlAbstract/FREE Full Text
  205. 205.
    1. Rinne C,
    2. Klein GJ,
    3. Sharma AD,
    4. et al
    . Relation between clinical presentation and induced arrhythmias in the Wolff-Parkinson-White syndrome. Am J Cardiol. 1987;60:576–9.
    OpenUrlCrossRefPubMed
  206. 206.
    1. Brembilla-Perrot B,
    2. Holban I,
    3. Houriez P,
    4. et al
    . Influence of age on the potential risk of sudden death in asymptomatic Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol. 2001;24:1514–8.
    OpenUrlCrossRefPubMed
  207. 207.
    1. Pappone C,
    2. Santinelli V,
    3. Manguso F,
    4. et al
    . A randomized study of prophylactic catheter ablation in asymptomatic patients with the Wolff-Parkinson-White syndrome. N Engl J Med. 2003;349:1803–11.
    OpenUrlCrossRefPubMed
  208. 208.
    1. Pappone C,
    2. Santinelli V,
    3. Rosanio S,
    4. et al
    . Usefulness of invasive electrophysiologic testing to stratify the risk of arrhythmic events in asymptomatic patients with Wolff-Parkinson-White pattern: results from a large prospective long-term follow-up study. J Am Coll Cardiol. 2003;41:239–44.
    OpenUrlCrossRefPubMed
  209. 209.
    1. Epstein AE,
    2. Miles WM,
    3. Benditt DG,
    4. et al
    . Personal and public safety issues related to arrhythmias that may affect consciousness: implications for regulation and physician recommendations. A medical/scientific statement from the American Heart Association and the North American Society of Pacing and Electrophysiology. Circulation. 1996;94:1147–66.
    OpenUrlFREE Full Text
  210. 210.
    1. Klein GJ,
    2. Yee R,
    3. Sharma AD
    . Longitudinal electrophysiologic assessment of asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern. N Engl J Med. 1989;320:1229–33.
    OpenUrlCrossRefPubMed
  211. 211.
    1. Leitch JW,
    2. Klein GJ,
    3. Yee R,
    4. et al
    . Prognostic value of electrophysiology testing in asymptomatic patients with Wolff-Parkinson-White pattern. Circulation. 1990;82:1718–23.
    OpenUrlAbstract/FREE Full Text
  212. 212.
    1. Milstein S,
    2. Sharma AD,
    3. Klein GJ
    . Electrophysiologic profile of asymptomatic Wolff-Parkinson-White pattern. Am J Cardiol. 1986;57:1097–100.
    OpenUrlCrossRefPubMed
  213. 213.
    1. Satoh M,
    2. Aizawa Y,
    3. Funazaki T,
    4. et al
    . Electrophysiologic evaluation of asymptomatic patients with the Wolff-Parkinson-White pattern. Pacing Clin Electrophysiol. 1989;12:413–20.
    OpenUrlCrossRefPubMed
  214. 214.↵
    1. Havránek S,
    2. Simek J,
    3. St’ovícek P,
    4. et al
    . Distribution of mean cycle length in cavo-tricuspid isthmus dependent atrial flutter. Physiol Res. 2012;61:43–51.
    OpenUrlPubMed
  215. 215.↵
    1. Waldo AL,
    2. Feld GK
    . Inter-relationships of atrial fibrillation and atrial flutter mechanisms and clinical implications. J Am Coll Cardiol. 2008;51:779–86.
    OpenUrlCrossRefPubMed
  216. 216.↵
    1. Pérez FJ,
    2. Schubert CM,
    3. Parvez B,
    4. et al
    . Long-term outcomes after catheter ablation of cavo-tricuspid isthmus dependent atrial flutter: a meta-analysis. Circ Arrhythm Electrophysiol. 2009;2:393–401.
    OpenUrlAbstract/FREE Full Text
  217. 217.↵
    1. Ellis K,
    2. Wazni O,
    3. Marrouche N,
    4. et al
    . Incidence of atrial fibrillation post-cavotricuspid isthmus ablation in patients with typical atrial flutter: left-atrial size as an independent predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol. 2007;18:799–802.
    OpenUrlCrossRefPubMed
  218. 218.↵
    1. Hsieh M-H,
    2. Tai C-T,
    3. Chiang C-E,
    4. et al
    . Recurrent atrial flutter and atrial fibrillation after catheter ablation of the cavotricuspid isthmus: a very long-term follow-up of 333 patients. J Interv Card Electrophysiol. 2002;7:225–31.
    OpenUrlCrossRefPubMed
  219. 219.↵
    1. Tai CT,
    2. Chen SA,
    3. Chiang CE,
    4. et al
    . Long-term outcome of radiofrequency catheter ablation for typical atrial flutter: risk prediction of recurrent arrhythmias. J Cardiovasc Electrophysiol. 1998;9:115–21.
    OpenUrlCrossRefPubMed
  220. 220.↵
    1. Paydak H,
    2. Kall JG,
    3. Burke MC,
    4. et al
    . Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course. Circulation. 1998;98:315–22.
    OpenUrlAbstract/FREE Full Text
  221. 221.↵
    1. Chinitz JS,
    2. Gerstenfeld EP,
    3. Marchlinski FE,
    4. et al
    . Atrial fibrillation is common after ablation of isolated atrial flutter during long-term follow-up. Heart Rhythm. 2007;4:1029–33.
    OpenUrlCrossRefPubMed
  222. 222.↵
    1. Teh AW,
    2. Medi C,
    3. Lee G,
    4. et al
    . Long-term outcome following ablation of atrial flutter occurring late after atrial septal defect repair. Pacing Clin Electrophysiol. 2011;34:431–5.
    OpenUrlCrossRefPubMed
  223. 223.↵
    1. Gerstenfeld EP,
    2. Callans DJ,
    3. Dixit S,
    4. et al
    . Mechanisms of organized left atrial tachycardias occurring after pulmonary vein isolation. Circulation. 2004;110:1351–7.
    OpenUrlAbstract/FREE Full Text
  224. 224.↵
    1. Chugh A,
    2. Oral H,
    3. Lemola K,
    4. et al
    . Prevalence, mechanisms, and clinical significance of macroreentrant atrial tachycardia during and following left atrial ablation for atrial fibrillation. Heart Rhythm. 2005;2:464–71.
    OpenUrlCrossRefPubMed
  225. 225.↵
    1. Veenhuyzen GD,
    2. Knecht S,
    3. O’Neill MD,
    4. et al
    . Atrial tachycardias encountered during and after catheter ablation for atrial fibrillation: part I: classification, incidence, management. Pacing Clin Electrophysiol. 2009;32:393–8.
    OpenUrlCrossRefPubMed
  226. 226.↵
    1. Karch MR,
    2. Zrenner B,
    3. Deisenhofer I,
    4. et al
    . Freedom from atrial tachyarrhythmias after catheter ablation of atrial fibrillation: a randomized comparison between 2 current ablation strategies. Circulation. 2005;111:2875–80.
    OpenUrlAbstract/FREE Full Text
  227. 227.↵
    1. Sawhney N,
    2. Anousheh R,
    3. Chen W,
    4. et al
    . Circumferential pulmonary vein ablation with additional linear ablation results in an increased incidence of left atrial flutter compared with segmental pulmonary vein isolation as an initial approach to ablation of paroxysmal atrial fibrillation. Circ Arrhythm Electrophysiol. 2010;3:243–8.
    OpenUrlAbstract/FREE Full Text
  228. 228.↵
    1. Neumann T,
    2. Vogt J,
    3. Schumacher B,
    4. et al
    . Circumferential pulmonary vein isolation with the cryoballoon technique results from a prospective 3-center study. J Am Coll Cardiol. 2008;52:273–8.
    OpenUrlCrossRefPubMed
  229. 229.
    1. Ellenbogen KA,
    2. Stambler BS,
    3. Wood MA,
    4. et al
    . Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: a dose-response study. J Am Coll Cardiol. 1996;28:130–6.
    OpenUrlCrossRefPubMed
  230. 230.
    1. Suttorp MJ,
    2. Kingma JH,
    3. Jessurun ER,
    4. et al
    . The value of class IC antiarrhythmic drugs for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. J Am Coll Cardiol. 1990;16:1722–7.
    OpenUrlCrossRefPubMed
  231. 231.
    1. Stambler BS,
    2. Wood MA,
    3. Ellenbogen KA,
    4. et al
    . Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or fibrillation. Ibutilide Repeat Dose Study Investigators. Circulation. 1996;94:1613–21.
    OpenUrlAbstract/FREE Full Text
  232. 232.
    1. Kingma JH,
    2. Suttorp MJ
    . Acute pharmacologic conversion of atrial fibrillation and flutter: the role of flecainide, propafenone, and verapamil. Am J Cardiol. 1992;70:56A–60A.
    OpenUrlCrossRefPubMed
  233. 233.
    1. Vos MA,
    2. Golitsyn SR,
    3. Stangl K,
    4. et al
    . Superiority of ibutilide (a new class III agent) over DL-sotalol in converting atrial flutter and atrial fibrillation. The Ibutilide/Sotalol Comparator Study Group. Heart. 1998;79:568–75.
    OpenUrlAbstract/FREE Full Text
  234. 234.
    1. Volgman AS,
    2. Carberry PA,
    3. Stambler B,
    4. et al
    . Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation. J Am Coll Cardiol. 1998;31:1414–9.
    OpenUrlCrossRefPubMed
  235. 235.
    1. Steinwender C,
    2. Hönig S,
    3. Kypta A,
    4. et al
    . Pre-injection of magnesium sulfate enhances the efficacy of ibutilide for the conversion of typical but not of atypical persistent atrial flutter. Int J Cardiol. 2010;141:260–5.
    OpenUrlCrossRefPubMed
  236. 236.
    1. Singh S,
    2. Zoble RG,
    3. Yellen L,
    4. et al
    . Efficacy and safety of oral dofetilide in converting to and maintaining sinus rhythm in patients with chronic atrial fibrillation or atrial flutter: the symptomatic atrial fibrillation investigative research on dofetilide (SAFIRE-D) study. Circulation. 2000;102:2385–90.
    OpenUrlAbstract/FREE Full Text
  237. 237.
    1. Blackshear JL,
    2. Stambler BS,
    3. Strauss WE,
    4. et al
    . Control of heart rate during transition from intravenous to oral diltiazem in atrial fibrillation or flutter. Am J Cardiol. 1996;78:1246–50.
    OpenUrlCrossRefPubMed
  238. 238.
    1. Singh BN,
    2. Hecht HS,
    3. Nademanee K,
    4. et al
    . Electrophysiologic and hemodynamic effects of slow-channel blocking drugs. Prog Cardiovasc Dis. 1982;25:103–32.
    OpenUrlCrossRefPubMed
  239. 239.
    1. Akhtar M,
    2. Tchou P,
    3. Jazayeri M
    . Use of calcium channel entry blockers in the treatment of cardiac arrhythmias. Circulation. 1989;80:IV31–9.
    OpenUrlPubMed
  240. 240.
    1. Delle Karth G,
    2. Geppert A,
    3. Neunteufl T,
    4. et al
    . Amiodarone versus diltiazem for rate control in critically ill patients with atrial tachyarrhythmias. Crit Care Med. 2001;29:1149–53.
    OpenUrlCrossRefPubMed
  241. 241.
    1. Ellenbogen KA,
    2. Dias VC,
    3. Plumb VJ,
    4. et al
    . A placebo-controlled trial of continuous intravenous diltiazem infusion for 24-hour heart rate control during atrial fibrillation and atrial flutter: a multicenter study. J Am Coll Cardiol. 1991;18:891–7.
    OpenUrlCrossRefPubMed
  242. 242.
    1. Ellenbogen KA,
    2. Dias VC,