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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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
WRITING COMMITTEE MEMBERS*
Richard L. Page, MD, FACC, FAHA, FHRS, Chair
Jos A. Joglar, MD, FACC, FAHA, FHRS, Vice Chair
Mary A. Caldwell, RN, MBA, PhD, FAHA
Stephen C. Hammill, MD, FACC, FHRS
Hugh Calkins, MD, FACC, FAHA, FHRS*
Julia H. Indik, MD, PhD, FACC, FAHA, FHRS
Jamie B. Conti, MD, FACC*
Bruce D. Lindsay, MD, FACC, FHRS*
Barbara J. Deal, MD
Brian Olshansky, MD, FACC, FAHA, FHRS*
N.A. Mark Estes III, MD, FACC, FAHA, FHRS*
Andrea M. Russo, MD, FACC, FHRS*
Michael E. Field, MD, FACC, FHRS
Win-Kuang Shen, MD, FACC, FAHA, FHRS
Zachary D. Goldberger, MD, MS, FACC, FAHA, FHRS Cynthia M. Tracy, MD, FACC
Sana M. Al-Khatib, MD, MHS, FACC, FAHA, FHRS, Evidence Review Committee Chair
ACC/AHA TASK FORCE MEMBERS
Jonathan L. Halperin, MD, FACC, FAHA, Chair
Glenn N. Levine, MD, FACC, FAHA, Chair-Elect
Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair
Nancy M. Albert, PhD, RN, FAHA
Mark A. Hlatky, MD, FACC
Sana M. Al-Khatib, MD, MHS, FACC, FAHA
John Ikonomidis, MD, PhD, FAHA
Kim K. Birtcher, PharmD, AACC
Jose Joglar, MD, FACC, FAHA
Biykem Bozkurt, MD, PhD, FACC, FAHA
Richard J. Kovacs, MD, FACC, FAHA
Ralph G. Brindis, MD, MPH, MACC
E. Magnus Ohman, MD, FACC
Joaquin E. Cigarroa, MD, FACC
Susan J. Pressler, PhD, RN, FAHA
Lesley H. Curtis, PhD, FAHA
Frank W. Sellke, MD, FACC, FAHA
Lee A. Fleisher, MD, FACC, FAHA
Win-Kuang Shen, MD, FACC, FAHA
Federico Gentile, MD, FACC
Duminda N. Wijeysundera, MD, PhD
Samuel Gidding, MD, FAHA

*Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with
industry and other entities may apply; see Appendix 1 for recusal information.
ACC/AHA Representative.
HRS Representative.
ACC/AHA Task Force on Performance Measures Liaison.
ACC/AHA Task Force on Clinical Practice Guidelines Liaison.
Former Task Force member; current member during this writing effort.
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 online-only Author Comprehensive Relationships Data Supplement is available with this article at
http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000310/-/DC1.
The online-only Data Supplement files are available with this article at
http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000310/-/DC2.

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2015 ACC/AHA/HRS SVT Guideline: Executive Summary
The American College of Cardiology requests that this document be cited as follows: Page RL, Joglar JA, Al-Khatib SM, 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. 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. 2015;132:000-000.
This article is copublished in 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 (my.americanheart.org), and the Heart Rhythm Society (www.hrsonline.org). A copy of the document is available at
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Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the
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(Circulation. 2015;132:000000.)
2015 by the American College of Cardiology Foundation, the American Heart Association, Inc., and the Heart Rhythm Society.
Circulation is available at http://circ.ahajournals.org
DOI: 10.1161/CIR.0000000000000310

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Table of Contents
Preamble.................................................................................................................................................................. 5
1. Introduction ......................................................................................................................................................... 8
1.1. Methodology and Evidence Review............................................................................................................. 8
1.2. Organization of the GWC ............................................................................................................................ 9
1.3. Document Review and Approval ................................................................................................................. 9
1.4. Scope of the Guideline ................................................................................................................................. 9
2. General Principles ............................................................................................................................................. 10
2.1. Mechanisms and Definitions ...................................................................................................................... 10
2.2. Epidemiology, Demographics, and Public Health Impact ......................................................................... 12
2.3. Evaluation of the Patient With Suspected or Documented SVT ................................................................ 12
2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms ..................................... 12
2.3.2. Evaluation of the ECG ........................................................................................................................ 13
2.4. Principles of Medical Therapy ................................................................................................................... 15
2.4.1. Acute Treatment: Recommendations .................................................................................................. 15
2.4.2. Ongoing Management: Recommendations ......................................................................................... 16
2.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation .................................................. 18
3. Sinus Tachyarrhythmias .................................................................................................................................... 19
3.1. Physiological Sinus Tachycardia................................................................................................................ 19
3.2. Inappropriate Sinus Tachycardia ................................................................................................................ 20
3.2.1. Acute Treatment .................................................................................................................................. 20
3.2.2. Ongoing Management: Recommendations ......................................................................................... 20
4. Nonsinus Focal Atrial Tachycardia and MAT .................................................................................................. 21
4.1. Focal AT..................................................................................................................................................... 21
4.1.1. Acute Treatment: Recommendations .................................................................................................. 22
4.1.2. Ongoing Management: Recommendations ......................................................................................... 23
4.2. Multifocal Atrial Tachycardia .................................................................................................................... 24
4.2.1. Acute Treatment: Recommendation ................................................................................................... 24
4.2.2. Ongoing Management: Recommendations ......................................................................................... 24
5. Atrioventricular Nodal Reentrant Tachycardia ................................................................................................. 25
5.1. Acute Treatment: Recommendations ......................................................................................................... 25
5.2. Ongoing Management: Recommendations ................................................................................................ 26
6. Manifest and Concealed Accessory Pathways .................................................................................................. 28
6.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways....................... 29
6.1.1. Acute Treatment: Recommendations .................................................................................................. 29
6.1.2. Ongoing Management: Recommendations ......................................................................................... 32
6.2. Management of Asymptomatic Pre-Excitation .......................................................................................... 33
6.2.1. PICOTS Critical Questions ................................................................................................................. 33
6.2.2. Asymptomatic Patients With Pre-Excitation: Recommendations ....................................................... 34
6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations ..... 34
7. Atrial Flutter ...................................................................................................................................................... 34
7.1. Cavotricuspid Isthmus-Dependent Atrial Flutter ....................................................................................... 34
7.2. NonIsthmus-Dependent Atrial Flutters .................................................................................................... 35
7.3. Acute Treatment: Recommendations ......................................................................................................... 35
7.4. Ongoing Management: Recommendations ................................................................................................ 36
8. Junctional Tachycardia...................................................................................................................................... 37
8.1. Acute Treatment: Recommendations ......................................................................................................... 38
8.2. Ongoing Management: Recommendations ................................................................................................ 38
9. Special Populations ........................................................................................................................................... 39
9.1. Pediatrics .................................................................................................................................................... 39
9.2. Patients With Adult Congenital Heart Disease .......................................................................................... 41
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9.2.1. Clinical Features ................................................................................................................................. 41

9.2.2. Acute Treatment: Recommendations .................................................................................................. 41
9.2.3. Ongoing Management: Recommendations ......................................................................................... 43
9.3. Pregnancy ................................................................................................................................................... 44
9.3.1. Acute Treatment: Recommendations .................................................................................................. 45
9.3.2. Ongoing Management: Recommendations ......................................................................................... 45
9.4. SVT in Older Populations .......................................................................................................................... 45
9.4.1. Acute Treatment and Ongoing Management: Recommendation ........................................................ 45
10. Quality-of-Life Considerations ....................................................................................................................... 46
11. Cost-Effectiveness........................................................................................................................................... 46
12. Shared Decision Making ................................................................................................................................. 46
Appendix 1. Author Relationships With Industry and Other Entities (Relevant) ................................................. 48
Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) ............................................. 51

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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 Medicine (1, 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.
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Class of Recommendation and Level of Evidence

The Class of Recommendation (COR; i.e., 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.

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 http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000310/-/DC1.
Comprehensive disclosure information for the Task Force is available at http://www.acc.org/guidelines/aboutguidelines-and-clinical-documents/guidelines-and-documents-task-forces. 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.
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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 guideline (9) 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

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Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions,
Treatments, or Diagnostic Testing in Patient Care*

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),
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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 http://jaccjacc.acc.org/Clinical_Document/2015_SVT_Evidence_Tables_Data_Supplement.docx.
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 narrowQRS complex tachycardias, as well as other, irregular SVTs (e.g., 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.

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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.
Table 2. Relevant Terms and Definitions
Arrhythmia/Term
Supraventricular
tachycardia (SVT)

Paroxysmal
supraventricular
tachycardia (PSVT)
Atrial fibrillation (AF)

Sinus tachycardia
Physiologic sinus
tachycardia
Inappropriate sinus
tachycardia
Atrial tachycardia (AT)
Focal AT

Sinus node reentry

tachycardia

Multifocal atrial
tachycardia (MAT)
Atrial flutter
Cavotricuspid isthmus
dependent atrial flutter:
typical

Cavotricuspid isthmus
dependent atrial flutter:
reverse typical
Atypical or non
cavotricuspid isthmus
dependent atrial flutter

Definition
An umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of
100 bpm at rest), the mechanism of which involves tissue from the His bundle or above.
These SVTs include inappropriate sinus tachycardia, AT (including focal and multifocal
AT), macroreentrant AT (including typical atrial flutter), junctional tachycardia, AVNRT,
and various forms of accessory pathway-mediated reentrant tachycardias. In this
guideline, the term does not include AF.
A clinical syndrome characterized by the presence of a regular and rapid tachycardia of
abrupt onset and termination. These features are characteristic of AVNRT or AVRT, and,
less frequently, AT. PSVT represents a subset of SVT.
A supraventricular arrhythmia with uncoordinated atrial activation and, consequently,
ineffective atrial contraction. ECG characteristics include: 1) irregular atrial activity, 2)
absence of distinct P waves, and 3) irregular R-R intervals (when atrioventricular
conduction is present). AF is not addressed in this document.
Rhythm arising from the sinus node in which the rate of impulses exceeds 100 bpm.
Appropriate increased sinus rate in response to exercise and other situations that increase
sympathetic tone.
Sinus heart rate >100 bpm at rest, with a mean 24-h heart rate >90 bpm not due to
appropriate physiological responses or primary causes such as hyperthyroidism or anemia.
An SVT arising from a localized atrial site, characterized by regular, organized atrial
activity with discrete P waves and typically an isoelectric segment between P waves. At
times, irregularity is seen, especially at onset (warm-up) and termination (warmdown). Atrial mapping reveals a focal point of origin.
A specific type of focal AT that is due to microreentry arising from the sinus node
complex, characterized by abrupt onset and termination, resulting in a P-wave
morphology that is indistinguishable from sinus rhythm.
An irregular SVT characterized by 3 distinct P-wave morphologies and/or patterns of
atrial activation at different rates. The rhythm is always irregular.
Macroreentrant AT propagating around the tricuspid annulus, proceeding superiorly along
the atrial septum, inferiorly along the right atrial wall, and through the cavotricuspid
isthmus between the tricuspid valve annulus and the Eustachian valve and ridge. This
activation sequence produces predominantly negative "sawtooth" flutter waves on the
ECG in leads 2, 3, and aVF and a late positive deflection in V1. The atrial rate can be
slower than the typical 300 bpm (cycle length 200 ms) in the presence of antiarrhythmic
drugs or scarring. It is also known as "typical atrial flutter" or "cavotricuspid isthmus
dependent atrial flutter" or "counterclockwise atrial flutter."
Macroreentrant AT that propagates around in the direction reverse that of typical atrial
flutter. Flutter waves typically appear positive in the inferior leads and negative in V1.
This type of atrial flutter is also referred to as "reverse typical" atrial flutter or "clockwise
typical atrial flutter.
Macroreentrant ATs that do not involve the cavotricuspid isthmus. A variety of reentrant
circuits may include reentry around the mitral valve annulus or scar tissue within the left
or right atrium. A variety of terms have been applied to these arrhythmias according to the
reentry circuit location, including particular forms, such as "LA flutter" and LA
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Junctional tachycardia
Atrioventricular nodal
reentrant tachycardia
(AVNRT)
Typical AVNRT
Atypical AVNRT

Accessory pathway

Manifest accessory
pathways
Concealed accessory
pathway
Pre-excitation pattern

Asymptomatic preexcitation (isolated preexcitation)

Wolff-Parkinson-White
(WPW) syndrome
Atrioventricular reentrant
tachycardia (AVRT)
Orthodromic AVRT

Antidromic AVRT

macroreentrant tachycardia" or incisional atrial reentrant tachycardia due to reentry around

surgical scars.
A nonreentrant SVT that arises from the AV junction (including the His bundle).
A reentrant tachycardia involving 2 functionally distinct pathways, generally referred to as
"fast" and "slow" pathways. Most commonly, the fast pathway is located near the apex of
Kochs triangle, and the slow pathway inferoposterior to the compact AV node tissue.
Variant pathways have been described, allowing for slow-slow AVNRT.
AVNRT in which a slow pathway serves as the anterograde limb of the circuit and the fast
pathway serves as the retrograde limb (also called slow-fast AVNRT").
AVNRT in which the fast pathway serves as the anterograde limb of the circuit and a slow
pathway serves as the retrograde limb (also called fast-slow AV node reentry) or a slow
pathway serves as the anterograde limb and a second slow pathway serves as the
retrograde limb (also called slow-slow AVNRT).
For the purpose of this guideline, an accessory pathway is defined as an extranodal AV
pathway that connects the myocardium of the atrium to the ventricle across the AV
groove. Accessory pathways can be classified by their location, type of conduction
(decremental or nondecremental), and whether they are capable of conducting
anterogradely, retrogradely, or in both directions. Of note, accessory pathways of other
types (such as atriofascicular, nodo-fascicular, nodo-ventricular, and fasciculoventricular
pathways) are uncommon and are discussed only briefly in this document (Section 7).
A pathway that conducts anterogradely to cause ventricular pre-excitation pattern on the
ECG.
A pathway that conducts only retrogradely and does not affect the ECG pattern during
sinus rhythm.
An ECG pattern reflecting the presence of a manifest accessory pathway connecting the
atrium to the ventricle. Pre-excited ventricular activation over the accessory pathway
competes with the anterograde conduction over the AV node and spreads from the
accessory pathway insertion point in the ventricular myocardium. Depending on the
relative contribution from ventricular activation by the normal AV nodal / His Purkinje
system versus the manifest accessory pathway, a variable degree of pre-excitation, with its
characteristic pattern of a short P-R interval with slurring of the initial upstroke of the
QRS complex (delta wave), is observed. Pre-excitation can be intermittent or not easily
appreciated for some pathways capable of anterograde conduction; this is usually
associated with a low-risk pathway, but exceptions occur.
The abnormal pre-excitation ECG pattern in the absence of documented SVT or
symptoms consistent with SVT.
Syndrome characterized by documented SVT or symptoms consistent with SVT in a
patient with ventricular pre-excitation during sinus rhythm.
A reentrant tachycardia, the electrical pathway of which requires an accessory pathway,
the atrium, atrioventricular node (or second accessory pathway), and ventricle.
An AVRT in which the reentrant impulse uses the accessory pathway in the retrograde
direction from the ventricle to the atrium, and the AV node in the anterograde direction.
The QRS complex is generally narrow or may be wide because of pre-existing bundlebranch block or aberrant conduction.
An AVRT in which the reentrant impulse uses the accessory pathway in the anterograde
direction from the atrium to the ventricle, and the AV node for the retrograde direction.
Occasionally, instead of the AV node, another accessory pathway can be used in the
retrograde direction, which is referred to as pre-excited AVRT. The QRS complex is wide
(maximally pre-excited).
A rare form of nearly incessant orthodromic AVRT involving a slowly conducting,
concealed, usually posteroseptal accessory pathway.

Permanent form of
junctional reciprocating
tachycardia (PJRT)
AF with ventricular pre-excitation caused by conduction over 1 accessory pathway(s).
Pre-excited AF
AF indicates atrial fibrillation; AT, atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reentrant
tachycardia; AVRT, atrioventricular reentrant tachycardia; bpm, beats per minute; ECG, electrocardiogram/
electrocardiographic; LA, left atrial; MAT, multifocal atrial tachycardia; PJRT, permanent form of junctional reciprocating
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tachycardia; PSVT, paroxysmal supraventricular tachycardia; SVT, supraventricular tachycardia; and WPW, WolffParkinson-White.

2.2. Epidemiology, Demographics, and Public Health Impact

The best available evidence indicates that the prevalence of SVT in the general population is 2.25 per 1,000
persons (13). When adjusted by age and sex in the U.S. 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 middleaged 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

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symptoms of shirt flapping or neck pounding (19, 24) that may be related to pulsatile reversed flow when
the atria contract 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 preexcitation 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 bundlebranch 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 ashort 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.
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
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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.

Figure 1. Differential Diagnosis for Adult Narrow QRS Tachycardia

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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 Blomstrm-Lundqvist et al. (12).

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.

2.4.1. Acute Treatment: Recommendations

Because patients with SVT account for approximately 50,000 emergency department visits each year (32),
emergency medicine 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.

COR

LOE

B-R

B-R

B-NR

B-NR

IIa

B-R

IIa

C-LD

Recommendations
1. Vagal maneuvers are recommended for acute treatment in patients with regular
SVT (33-35).
2. Adenosine is recommended for acute treatment in patients with regular SVT (34,
36-43).
3. Synchronized cardioversion is recommended for acute treatment in patients with
hemodynamically unstable SVT when vagal maneuvers or adenosine are ineffective
or not feasible (44).
4. Synchronized cardioversion is recommended for acute treatment in patients with
hemodynamically stable SVT when pharmacological therapy is ineffective or
contraindicated (36, 45).
1. Intravenous diltiazem or verapamil can be effective for acute treatment in
patients with hemodynamically stable SVT (36, 39, 42, 46).
2. Intravenous beta blockers are reasonable for acute treatment in patients with
hemodynamically stable SVT (47).

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Figure 2. Acute Treatment of Regular SVT of Unknown Mechanism

Regular SVT

Vagal maneuvers
and/or IV adenosine
(Class I)
If ineffective
or not feasible

Hemodynamically
stable
Yes
IV beta blockers,
IV diltiazem, or
IV verapamil
(Class IIa)

No
Synchronized
cardioversion*
(Class I)

If ineffective or not feasible

Synchronized
cardioversion*
(Class I)
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.

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
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the context of frequency and duration of the SVT, along with clinical manifestations, such as symptoms or
adverse consequences (e.g., development of cardiomyopathy).

COR

LOE

B-R

B-NR

C-LD

IIa

B-R

IIb

B-R

IIb

B-R

IIb

C-LD

IIb

C-LD

Recommendations
1. Oral beta blockers, diltiazem, or verapamil is useful for ongoing management in
patients with symptomatic SVT who do not have ventricular pre-excitation during
sinus rhythm (48-50).
2. Electrophysiological (EP) study with the option of ablation is useful for the
diagnosis and potential treatment of SVT (51-58).
3. Patients with SVT should be educated on how to perform vagal maneuvers for
ongoing management of SVT (33).
1. Flecainide or propafenone is reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have symptomatic
SVT and are not candidates for, or prefer not to undergo, catheter ablation (48, 5965).
1. Sotalol may be reasonable for ongoing management in patients with symptomatic
SVT who are not candidates for, or prefer not to undergo, catheter ablation (66).
2. Dofetilide may be reasonable for ongoing management in patients with
symptomatic SVT who are not candidates for, or prefer not to undergo, catheter
ablation and in whom beta blockers, diltiazem, flecainide, propafenone, or verapamil
are ineffective or contraindicated (59).
3. Oral amiodarone may be considered for ongoing management in patients with
symptomatic SVT who are not candidates for, or prefer not to undergo, catheter
ablation and in whom beta blockers, diltiazem, dofetilide, flecainide, propafenone,
sotalol, or verapamil are ineffective or contraindicated (67).
4. Oral digoxin may be reasonable for ongoing management in patients with
symptomatic SVT without pre-excitation who are not candidates for, or prefer not to
undergo, catheter ablation (50).

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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); SVT,
supraventricular tachycardia; and VT, ventricular tachycardia.

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
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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 (8184). 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 (e.g., albuterol, salmeterol), and illicit stimulant drugs (e.g.,
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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.
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 that leads to 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

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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.

COR

LOE

C-LD

IIa

B-R

IIb

C-LD

IIb

C-LD

Recommendations
1. Evaluation for and treatment of reversible causes are recommended in patients
with suspected IST (81, 101).
1. Ivabradine is reasonable for ongoing management in patients with symptomatic
IST (85-93).
1. Beta blockers may be considered for ongoing management in patients with
symptomatic IST (87, 89).
2. The combination of beta blockers and ivabradine may be considered for ongoing
management in patients with IST (89).

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.

4.1. Focal AT
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 ATmediated 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 12lead 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.

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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.

COR

LOE

C-LD

C-LD

IIa

B-NR

IIb

C-LD

IIb

C-LD

Recommendations
1. Intravenous beta blockers, diltiazem, or verapamil is useful for acute treatment in
hemodynamically stable patients with focal AT (107, 119-121).
2. Synchronized cardioversion is recommended for acute treatment in patients with
hemodynamically unstable focal AT (44, 122).
1. Adenosine can be useful in the acute setting to either restore sinus rhythm or
diagnose the tachycardia mechanism in patients with suspected focal AT (107, 121,
123).
1. Intravenous amiodarone may be reasonable in the acute setting to either restore
sinus rhythm or slow the ventricular rate in hemodynamically stable patients with
focal AT (120, 124).
2. Ibutilide may be reasonable in the acute setting to restore sinus rhythm in
hemodynamically stable patients with focal AT (120, 124).

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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.

4.1.2. Ongoing Management: Recommendations

COR

LOE

B-NR

IIa

C-LD

IIa

C-LD

Recommendations
1. Catheter ablation is recommended in patients with symptomatic focal AT as an
alternative to pharmacological therapy (104, 107-112, 114-116, 124-126).
1. Oral beta blockers, diltiazem, or verapamil are reasonable for ongoing management
in patients with symptomatic focal AT (107, 119, 120).
2. Flecainide or propafenone can be effective for ongoing management in patients
without structural heart disease or ischemic heart disease who have focal AT (127Page 23 of 74

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IIb

C-LD

131).
1. Oral sotalol or amiodarone may be reasonable for ongoing management in patients
with focal AT (104, 129, 132-136).

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).

4.2. 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

COR

LOE

IIa

C-LD

Recommendation
1. Intravenous metoprolol (141) or verapamil (142, 143) can be useful for acute
treatment in patients with MAT.

4.2.2. Ongoing Management: Recommendations

COR
IIa

LOE
B-NR

Recommendations
1. Oral verapamil (Level of Evidence: B-NR) or diltiazem (Level of Evidence: C-LD) is

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C-LD
IIa

C-LD

reasonable for ongoing management in patients with recurrent symptomatic MAT

(144, 145) .
2. Metoprolol is reasonable for ongoing management in patients with recurrent
symptomatic MAT (140, 141, 145).

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.
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

COR

LOE

B-R

B-R

B-NR

B-NR

IIa

B-R

IIb

C-LD

IIb

C-LD

Recommendations
1. Vagal maneuvers are recommended for acute treatment in patients with AVNRT
(33-35, 146, 147).
2. Adenosine is recommended for acute treatment in patients with AVNRT (37, 41, 43,
148).
3. Synchronized cardioversion should be performed for acute treatment in
hemodynamically unstable patients with AVNRT when adenosine and vagal
maneuvers do not terminate the tachycardia or are not feasible (44, 122).
4. Synchronized cardioversion is recommended for acute treatment in
hemodynamically stable patients with AVNRT when pharmacological therapy does
not terminate the tachycardia or is contraindicated (36, 45).
1. Intravenous beta blockers, diltiazem, or verapamil are reasonable for acute
treatment in hemodynamically stable patients with AVNRT (47, 149-152).
1. Oral beta blockers, diltiazem, or verapamil may be reasonable for acute treatment
in hemodynamically stable patients with AVNRT (153, 154).
2. Intravenous amiodarone may be considered for acute treatment in
hemodynamically stable patients with AVNRT when other therapies are ineffective or
contraindicated (67).

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Figure 6. Acute Treatment of AVNRT

AVNRT

Vagal maneuvers
and/or IV adenosine
(Class I)
Oral beta blockers,
diltiazem, or
verapamil may be
reasonable for
acute treatment in
hemodynamically
stable patients with
AVNRT (Class IIb)

If ineffective

Hemodynamically
stable
No

Yes

IV beta blockers,
IV diltiazem, or
IV verapamil
(Class IIa)

If ineffective
or not feasible

Synchronized
cardioversion*
(Class I)

If ineffective
or not feasible
IV amiodarone
(Class IIb)
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.

5.2. Ongoing Management: Recommendations

COR

LOE

B-R

B-NR

B-R

IIa

B-R

Recommendations
1. Oral verapamil or diltiazem is recommended for ongoing management in patients
with AVNRT who are not candidates for, or prefer not to undergo, catheter ablation
(49, 50, 155, 156).
2. Catheter ablation of the slow pathway is recommended in patients with AVNRT
(51-58, 157-161).
3. Oral beta blockers are recommended for ongoing management in patients with
AVNRT who are not candidates for, or prefer not to undergo, catheter ablation
(50).
1. Flecainide or propafenone is reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have AVNRT and
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IIa

B-NR

IIb

B-R

IIb

B-R

IIb

C-LD

are not candidates for, or prefer not to undergo, catheter ablation and in whom beta
blockers, diltiazem, or verapamil are ineffective or contraindicated (48, 59-66, 153,
154, 162, 163).
2. Clinical follow-up without pharmacological therapy or ablation is reasonable for
ongoing management in minimally symptomatic patients with AVNRT (156).
1. Oral sotalol or dofetilide may be reasonable for ongoing management in patients
with AVNRT who are not candidates for, or prefer not to undergo, catheter ablation
(59, 66).
2. Oral digoxin or amiodarone may be reasonable for ongoing treatment of AVNRT
in patients who are not candidates for, or prefer not to undergo, catheter ablation
(50, 67).
3. Self-administered (pill-in-the-pocket) acute doses of oral beta blockers,
diltiazem, or verapamil may be reasonable for ongoing management in patients with
infrequent, well-tolerated episodes of AVNRT (153, 154).

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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).

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.

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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 pre-excited 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 (165169).

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.

6.1.1. Acute Treatment: Recommendations

COR

LOE

B-R

B-R

B-NR

B-NR

B-NR

C-LD

IIa

B-R
C-LD

Recommendations
1. Vagal maneuvers are recommended for acute treatment in patients with
orthodromic AVRT (43, 147, 170, 171).
2. Adenosine is beneficial for acute treatment in patients with orthodromic AVRT (43,
172, 173).
3. Synchronized cardioversion should be performed for acute treatment in
hemodynamically unstable patients with AVRT if vagal maneuvers or adenosine are
ineffective or not feasible (170, 174, 175).
4. Synchronized cardioversion is recommended for acute treatment in
hemodynamically stable patients with AVRT when pharmacological therapy is
ineffective or contraindicated (36, 45).
5. Synchronized cardioversion should be performed for acute treatment in
hemodynamically unstable patients with pre-excited AF (44, 170).
6. Ibutilide (176) or intravenous procainamide (177) is beneficial for acute treatment
in patients with pre-excited AF who are hemodynamically stable.
1. Intravenous diltiazem, verapamil (43, 172, 178, 179) (Level of Evidence: B-R) or beta
blockers (180) (Level of Evidence: C-LD) can be effective for acute treatment in
patients with orthodromic AVRT who do not have pre-excitation on their resting ECG
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IIb

B-R

III:
Harm

C-LD

during sinus rhythm.

1. Intravenous beta blockers, diltiazem, or verapamil might be considered for acute
treatment in patients with orthodromic AVRT who have pre-excitation on their
resting ECG and have not responded to other therapies (43, 178, 179, 181).
1. Intravenous digoxin, intravenous amiodarone, intravenous or oral beta blockers,
diltiazem, and verapamil are potentially harmful for acute treatment in patients with
pre-excited AF (181-186).

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Figure 8. Acute Treatment of Orthodromic AVRT

Orthodromic AVRT

Vagal maneuvers
and/or IV adenosine
(Class I)
If ineffective
or not feasible

Hemodynamically
stable
Yes

No

Synchronized
cardioversion
(Class I)

Pre-excitation
on resting
ECG
Yes

IV beta blockers,
IV diltiazem, or
IV verapamil
(Class IIb)

No

IV beta blockers,
IV diltiazem, or
IV verapamil
(Class IIa)

If ineffective or not feasible

Synchronized
Cardioversion*
(Class I)
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.

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6.1.2. Ongoing Management: Recommendations

COR

LOE

B-NR

C-LD

IIa

B-R

IIb

B-R

IIb

C-LD

IIb

C-LD

IIb

C-LD

III:
Harm

C-LD

Recommendations
1. Catheter ablation of the accessory pathway is recommended in patients with
AVRT and/or pre-excited AF (55, 165, 187-193).
2. Oral beta blockers, diltiazem, or verapamil are indicated for ongoing management
of AVRT in patients without pre-excitation on their resting ECG (48, 194).
1. Oral flecainide or propafenone is reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have AVRT and/or
pre-excited AF and are not candidates for, or prefer not to undergo, catheter
ablation (60, 61, 64, 65, 195).
1. Oral dofetilide or sotalol may be reasonable for ongoing management in patients
with AVRT and/or pre-excited AF who are not candidates for, or prefer not to
undergo, catheter ablation (99,106).
2. Oral amiodarone may be considered for ongoing management in patients with
AVRT and/or pre-excited AF who are not candidates for, or prefer not to undergo,
catheter ablation and in whom beta blockers, diltiazem, flecainide, propafenone, and
verapamil are ineffective or contraindicated (196, 197).
3. Oral beta blockers, diltiazem, or verapamil may be reasonable for ongoing
management of orthodromic AVRT in patients with pre-excitation on their resting
ECG who are not candidates for, or prefer not to undergo, catheter ablation (48,
194).
4. Oral digoxin may be reasonable for ongoing management of orthodromic AVRT
in patients without pre-excitation on their resting ECG who are not candidates for,
or prefer not to undergo, catheter ablation (198).
1. Oral digoxin is potentially harmful for ongoing management in patients with
AVRT or AF and pre-excitation on their resting ECG (182).

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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).

6.2. 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 preexcitation (10), and see Online Data Supplements 13, 14, and 15 for additional data on asymptomatic preexcitation (http://jaccjacc.acc.org/Clinical_Document/2015_SVT_Evidence_Tables_Data_Supplement.docx),
which were reproduced directly from the ERCs systematic review. These recommendations have been
designated with the notation SR to emphasize the rigor of support from the ERCs 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 preexcitation?

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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

COR

LOE
B-NR SR

I
C-LD SR
IIa

B-NR SR

IIa

B-NR SR

IIa

B-NR SR

IIa

B-NR SR

Recommendations
1. In asymptomatic patients with pre-excitation, the findings of abrupt loss of
conduction over a manifest pathway during exercise testing in sinus rhythm (199202) (Level of Evidence: B-NR) SR or intermittent loss of pre-excitation during ECG or
ambulatory monitoring (202) (Level of Evidence: C-LD) SR are useful to identify
patients at low risk of rapid conduction over the pathway.
1. An EP study is reasonable in asymptomatic patients with pre-excitation to riskstratify for arrhythmic events (165, 167, 203-206).
2. Catheter ablation of the accessory pathway is reasonable in asymptomatic patients
with pre-excitation if an EP study identifies a high risk of arrhythmic events,
including rapidly conducting pre-excited AF (165, 207, 208).
3. Catheter ablation of the accessory pathway is reasonable in asymptomatic patients
if the presence of pre-excitation precludes specific employment (such as with pilots)
(55, 165, 187-193, 207-209).
4. Observation, without further evaluation or treatment, is reasonable in
asymptomatic patients with pre-excitation (206, 210-213).

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

Recommendations
COR

LOE
B-NR

I
C-LD
I

B-NR

Recommendations
1. In symptomatic patients with pre-excitation, the findings of abrupt loss of
conduction over the pathway during exercise testing in sinus rhythm (199-202) (Level
of Evidence: B-NR) or intermittent loss of pre-excitation during ECG or ambulatory
monitoring (202) (Level of Evidence: C-LD) are useful for identifying patients at low
risk of developing rapid conduction over the pathway.
2. An EP study is useful in symptomatic patients with pre-excitation to risk-stratify
for life-threatening arrhythmic events (165, 167, 203-205).

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.

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
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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. NonIsthmus-Dependent Atrial Flutters

Nonisthmus-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 nonCTI-dependent flutter requires more extensive mapping than does ablation of
CTI-dependent flutter, and success rates are lower (Online Data SupplementAppendix 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

COR

LOE

B-R

B-NR

B-NR

C-LD

B-NR

IIa

B-R

Recommendations
1. Oral dofetilide or intravenous ibutilide is useful for acute pharmacological
cardioversion in patients with atrial flutter (229-236).
2. Intravenous or oral beta blockers, diltiazem, or verapamil are useful for acute rate
control in patients with atrial flutter who are hemodynamically stable (237-244).
3. Elective synchronized cardioversion is indicated in stable patients with welltolerated atrial flutter when a rhythm-control strategy is pursued (245-247).
4. Synchronized cardioversion is recommended for acute treatment of patients with
atrial flutter who are hemodynamically unstable and do not respond to
pharmacological therapies (122, 170, 245, 248).
5. Rapid atrial pacing is useful for acute conversion of atrial flutter in patients who
have pacing wires in place as part of a permanent pacemaker or implantable
cardioverter-defibrillator or for temporary atrial pacing after cardiac surgery (249253).
6. Acute antithrombotic therapy is recommended in patients with atrial flutter to
align with recommended antithrombotic therapy for patients with AF (254).
1. Intravenous amiodarone can be useful for acute control of the ventricular rate (in
the absence of pre-excitation) in patients with atrial flutter and systolic heart failure,
when beta blockers are contraindicated or ineffective (240, 255, 256).

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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.

7.4. Ongoing Management: Recommendations

COR

LOE

B-R

C-LD

C-LD

B-NR

IIa

B-R

IIa

B-NR

IIa

C-LD

IIa

C-LD

Recommendations
1. Catheter ablation of the CTI is useful in patients with atrial flutter that is either
symptomatic or refractory to pharmacological rate control (155, 257-260).
2. Beta blockers, diltiazem, or verapamil are useful to control the ventricular rate in
patients with hemodynamically tolerated atrial flutter (237-239).
3. Catheter ablation is useful in patients with recurrent symptomatic nonCTIdependent flutter after failure of at least 1 antiarrhythmic agent (261, 262).
4. Ongoing management with antithrombotic therapy is recommended in patients
with atrial flutter to align with recommended antithrombotic therapy for patients
with AF (254).
1. The following drugs can be useful to maintain sinus rhythm in patients with
symptomatic, recurrent atrial flutter, with the drug choice depending on underlying
heart disease and comorbidities:
a. Amiodarone (263)
b. Dofetilide (236, 264)
c. Sotalol (265)
2. Catheter ablation is reasonable in patients with CTI-dependent atrial flutter that
occurs as the result of flecainide, propafenone, or amiodarone used for treatment of
AF (266-269).
3. Catheter ablation of the CTI is reasonable in patients undergoing catheter
ablation of AF who also have a history of documented clinical or induced CTIdependent atrial flutter (269, 270).
4. Catheter ablation is reasonable in patients with recurrent symptomatic nonCTIPage 36 of 74

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IIb

B-R

IIb

C-LD

dependent flutter as primary therapy, before therapeutic trials of antiarrhythmic

drugs, after carefully weighing potential risks and benefits of treatment options
(271).
1. Flecainide or propafenone may be considered to maintain sinus rhythm in
patients without structural heart disease or ischemic heart disease who have
symptomatic recurrent atrial flutter (272-274).
2. Catheter ablation may be reasonable for asymptomatic patients with recurrent
atrial flutter (54, 216, 257).

Figure 11. Ongoing Management of Atrial Flutter

Atrial flutter

Treatment
strategy

Rate control

Rhythm control*
Options to consider

Beta blockers,
diltiazem, or
verapamil
(Class I)

Catheter ablation
(Class I)

Amiodarone,
dofetilide, or
sotalol
(Class IIa)

Flecainide or
propafenone
(in the absence
of SHD)
(Class IIb)

If ineffective
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 nodalblocking agents to reduce risk of 1:1 conduction during atrial flutter.
AV indicates atrioventricular; SHD, structural heart disease (including ischemic heart disease).

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.

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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 adults (275); 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 toxicity (276) or myocardial infarction (277, 278).
Treatment of this rhythm centers on addressing the underlying condition.

8.1. Acute Treatment: Recommendations

COR

LOE

IIa

C-LD

IIa

C-LD

Recommendations
1. Intravenous beta blockers are reasonable for acute treatment in patients with
symptomatic junctional tachycardia (275).
2. Intravenous diltiazem, procainamide, or verapamil is reasonable for acute
treatment in patients with junctional tachycardia (279).

8.2. Ongoing Management: Recommendations

COR

LOE

IIa

C-LD

IIa

C-LD

IIb

C-LD

IIb

C-LD

Recommendations
1. Oral beta blockers are reasonable for ongoing management in patients with
junctional tachycardia (275).
2. Oral diltiazem or verapamil is reasonable for ongoing management in patients with
junctional tachycardia (279).
1. Flecainide or propafenone may be reasonable for ongoing management in patients
without structural heart disease or ischemic heart disease who have junctional
tachycardia (280, 281).
2. Catheter ablation may be reasonable in patients with junctional tachycardia when
medical therapy is not effective or contraindicated (282-288).

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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).

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 pathwaymediated 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).

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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, 165168). Pharmacological therapy of SVT in childhood is largely based on practice patterns because RCTs of
antiarrhythmic medications in children are lacking. AV nodalblocking 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 35C, atrial overdrive pacing, and procainamide or
amiodarone infusions (309-313). In general, postoperative junctional tachycardia resolves and does not require
ongoing therapy.

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

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 pathwaymediated 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 indepth 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

COR

LOE

C-LD

B-NR

C-LD

Recommendations
1. Acute antithrombotic therapy is recommended in ACHD patients who have AT or
atrial flutter to align with recommended antithrombotic therapy for patients with AF
(254).
2. Synchronized cardioversion is recommended for acute treatment in ACHD patients
and SVT who are hemodynamically unstable (170, 332).
3. Intravenous diltiazem or esmolol (with extra caution used for either agent, observing
for the development of hypotension) is recommended for acute treatment in ACHD
patients and SVT who are hemodynamically stable (333, 334).
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B-NR

IIa

B-NR

IIa

B-NR

IIa

B-NR

IIb

B-NR

4. Intravenous adenosine is recommended for acute treatment in ACHD patients and

SVT (121, 335-337).
1. Intravenous ibutilide or procainamide can be effective for acute treatment in
patients and atrial flutter who are hemodynamically stable (338-340).
2. Atrial pacing can be effective for acute treatment in ACHD patients and SVT who
are hemodynamically stable and anticoagulated as per current guidelines for
antithrombotic therapy in patients with AF (338, 341-344).
3. Elective synchronized cardioversion can be useful for acute termination of AT or
atrial flutter in ACHD patients when acute pharmacological therapy is ineffective or
contraindicated (332).
1. Oral dofetilide or sotalol may be reasonable for acute treatment in ACHD patients
and AT and/or atrial flutter who are hemodynamically stable (345, 346).

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Figure 13. Acute Treatment of SVT in ACHD Patients

SVT in ACHD pts,

undefined mechanism

Hemodynamically
stable
Yes

No
IV adenosine and/or
synchronized cardioversion
(Class I)

IV adenosine
(Class I)
If ineffective

If ineffective

Treatment
strategy

Rate control

IV diltiazem or
IV esmolol
(Class I)

Rhythm control

Synchronized
cardioversion*
(Class IIa)

IV ibutilide,
IV procainamide, or
atrial pacing
(Class IIa)

Dofetilide or
sotalol
(Class IIb)

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.

9.2.3. Ongoing Management: Recommendations

COR

LOE

C-LD

C-LD

Recommendations
1. Ongoing management with antithrombotic therapy is recommended in ACHD
patients and AT or atrial flutter to align with recommended antithrombotic
therapy for patients with AF (254).
2. Assessment of associated hemodynamic abnormalities for potential repair of
structural defects is recommended in ACHD patients as part of therapy for SVT
(347, 348).
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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

IIa

B-NR

IIa

B-NR

IIa

B-NR

IIa

B-NR

IIb

B-NR

IIb

B-NR

IIb

B-NR

III:
Harm

B-NR

1. Preoperative catheter ablation or intraoperative surgical ablation of accessory

pathways or AT is reasonable in patients with SVT who are undergoing surgical
repair of Ebstein anomaly (349-355).
2. Oral beta blockers or sotalol therapy can be useful for prevention of recurrent
AT or atrial flutter in ACHD patients (135, 323, 356).
3. Catheter ablation is reasonable for treatment of recurrent symptomatic SVT in
ACHD patients (222, 325, 326, 328, 331, 357-361).
4. Surgical ablation of AT or atrial flutter can be effective in ACHD undergoing
planned surgical repair (362-373).
1. Atrial pacing may be reasonable to decrease recurrences of AT or atrial flutter
in ACHD patients and sinus node dysfunction (344, 374, 375).
2. Oral dofetilide may be reasonable for prevention of recurrent AT or atrial
flutter in ACHD patients (323, 346, 376, 377).
3. Amiodarone may be reasonable for prevention of recurrent AT or atrial flutter
in ACHD patients for whom other medications and catheter ablation are
ineffective or contraindicated (323).
1. Flecainide should not be administered for treatment of SVT in ACHD patients
with significant ventricular dysfunction (298).

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.

9.3. 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
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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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

COR

LOE

C-LD

C-LD

C-LD

IIa

C-LD

IIb

C-LD

IIb

C-LD

IIb

C-LD

Recommendations
1. Vagal maneuvers are recommended for acute treatment in pregnant patients with
SVT (147, 380).
2. Adenosine is recommended for acute treatment in pregnant patients with SVT (380).
3. Synchronized cardioversion is recommended for acute treatment in pregnant
patients with hemodynamically unstable SVT when pharmacological therapy is
ineffective or contraindicated (380).
1. Intravenous metoprolol or propranolol is reasonable for acute treatment in pregnant
patients with SVT when adenosine is ineffective or contraindicated (380).
1. Intravenous verapamil may be reasonable for acute treatment in pregnant patients
with SVT when adenosine and beta blockers are ineffective or contraindicated (380).
2. Intravenous procainamide may be reasonable for acute treatment in pregnant
patients with SVT (381).
3. Intravenous amiodarone may be considered for acute treatment in pregnant patients
with potentially life-threatening SVT when other therapies are ineffective or
contraindicated (382, 383).

9.3.2. Ongoing Management: Recommendations

COR

LOE

IIa

C-LD

IIb

C-LD

IIb

C-LD

Recommendations
1. The following drugs, alone or in combination, can be effective for ongoing
management in pregnant patients with highly symptomatic SVT:
a. Digoxin (382, 384)
b. Flecainide (382, 384)
c. Metoprolol (382, 385)
d. Propafenone (382)
e. Propranolol (382, 385)
f. Sotalol (382, 384)
g. Verapamil (382)
1. Catheter ablation may be reasonable in pregnant patients with highly symptomatic,
recurrent, drug-refractory SVT with efforts toward minimizing radiation exposure
(386, 387).
2. Oral amiodarone may be considered for ongoing management in pregnant patients
when treatment of highly symptomatic, recurrent SVT is required and other therapies
are ineffective or contraindicated (382, 383).

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
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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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.

COR

LOE

B-NR

Recommendation
1. Diagnostic and therapeutic approaches to SVT should be individualized in patients
more than 75 years of age to incorporate age, comorbid illness, physical and cognitive
functions, patient preferences, and severity of symptoms (27, 28, 388-396).

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 (e.g., 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 most
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.

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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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, Publication Manager, Science, Education, and Quality
American College of Cardiology/American Heart Association
Lisa Bradfield, CAE, Director, Science 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.
Key Words: AHA Scientific Statements Tachycardia, Supraventricular Tachycardia, Atrioventricular
Nodal Reentry Wolff-Parkinson-White Syndrome Catheter Ablation Tachycardia, Ectopic Atrial
Tachycardia, Ectopic Junctional Atrial Flutter Anti-Arrhythmia Agents Accessory Atrioventricular
Bundle; Valsalva Maneuver Tachycardia, Reciprocating Electric Countershock Heart Defects, Congenital
Death, Sudden Electrophysiologic Techniques, Cardiac Sinus Tachycardia

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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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)
Committee
Member

Employment

Richard L.
Page (Chair)

University of Wisconsin
School of Medicine and
Public HealthChair,
Department of Medicine
University of Texas
Southwestern Medical
CenterProfessor of
Internal Medicine;
Program Director,
Clinical Cardiac
Electrophysiology
Duke Clinical Research
InstituteAssociate
Professor of Medicine
University of California
San FranciscoAssistant
Professor (Retired)
Johns Hopkins Hospital
Professor of Medicine,
Director of
Electrophysiology

Jos A. Joglar
(Vice Chair)

Sana M. AlKhatib
Mary A.
Caldwell
Hugh Calkins

Consultant

Speakers
Bureau

Ownership/
Partnership/
Principal

Personal
Research

None

None

None

None

Institutional,
Organizational,
or Other
Financial Benefit
None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

Atricure
Boehringer
Ingelheim
DaiichiSankyo

None

None

St. Jude
Medical

None

None

All Sections
except 2.4,
5.2, 6.1.2,
9.3.2, and 9.4.

Boston
Scientific
Medtronic
St. Jude
Medical
None

None

All Sections
except 2.4,
6.1.2, 9.3.2,
and 9.4.

None

None

Jamie B.
Conti

University of Florida
Professor of Medicine,
Chief of Cardiovascular
Medicine

None

None

None

Medtronic

Barbara J.
Deal

Feinberg School of
Medicine, Northwestern
UniversityProfessor of
Pediatrics; Ann & Robert
H. Lurie Childrens
Hospital of Chicago

None

None

None

None

Page 48 of 74

Expert
Witness

Voting
Recusals by
Section*

None

None

Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary

N.A. Mark
Estes III

Michael E.
Field

Zachary D.
Goldberger

Stephen C.
Hammill
Julia H. Indik

Bruce D.
Lindsay

Brian
Olshansky

Division Head,
Cardiology
Tufts University School
of MedicineProfessor
of Medicine

University of Wisconsin
School of Medicine and
Public HealthAssistant
Professor of Medicine,
Director of Cardiac
Arrhythmia Service
University of Washington
School of Medicine
Assistant Professor of
Medicine
Mayo ClinicProfessor
Emeritus of Medicine
University of Arizona
Associate Professor of
Medicine
Cleveland Clinic
FoundationProfessor of
Cardiology

University of Iowa
HospitalsProfessor
Emeritus of Medicine;
Mercy Hospital Mason
CityElectrophysiologist

Boston
Scientific
Medtronic
St. Jude
Medical
None

None

None

Boston
Scientific

None

All Sections
except 2.4,
5.2, 6.1.2,
9.3.2, and 9.4.

None

Boston
Scientific
Medtronic
St. Jude
Medical
None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

Biosense
Webster
Boston
Scientific
CardioInsight
Medtronic
BioControl
Biotronik
BoehringerIngelheim
Boston
ScientificGuidant
DaiichiSankyo
Medtronic
Sanofiaventis

None

None

None

Boston
Scientific
Medtronic
St. Jude
Medical

None

All Sections
except 2.4,
5.2, 6.1.2,
9.3.2, and 9.4.

None

None

Amarin
(DSMB)
Boston
Scientific
(DSMB)
Sanofiaventis
(DSMB)

Boston
Scientific

None

All Sections
except 2.4 and
9.4.

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2015 ACC/AHA/HRS SVT Guideline: Executive Summary
None
None
Cooper Medical School of Biotronik
None
All Sections
Medtronic
Biotronik
Rowan University
except 2.4,
Boston
Boston
Professor of Medicine;
5.2, 6.1.2,
Scientific
Scientific
Cooper University
9.3.2, and 9.4.
Medtronic
HospitalDirector,
St. Jude
Electrophysiology and
Medical
Arrhythmia Services
Win-Kuang
Mayo Clinic Arizona
None
None
None
None
None
None
None
Shen
Professor of Medicine;
Chair, Division of
Cardiovascular Diseases
Cynthia M.
George Washington
None
None
None
None
None
None
None
Tracy
UniversityProfessor of
Medicine; Associate
Director Division of
Cardiology, Director of
Cardiac Services
This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships
were reviewed and updated in conjunction with all meetings and/or conference calls of the writing committee during the document development process. The table does
not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents
ownership of 5% of the voting stock or share of the business entity, or ownership of $5,000 of the fair market value of the business entity; or if funds received by the
person from the business entity exceed 5% of the persons gross income for the previous year. Relationships that exist with no financial benefit are also included for the
purpose of transparency. Relationships in this table are modest unless otherwise noted.
Andrea M.
Russo

According to the ACC/AHA, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or
asset, topic, or issue addressed in the document; or b) the company/entity (with whom the relationship exists) makes a drug, drug class, or device addressed in the
document, or makes a competing drug or device addressed in the document; or c) the person or a member of the persons household, has a reasonable potential for
financial, professional or other personal gain or loss as a result of the issues/content addressed in the document.
*Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry and other entities may apply.
Significant relationship.
No financial benefit.
ACC indicates American College of Cardiology; AHA, American Heart Association; DSMB, data safety monitoring board; and HRS, Heart Rhythm Society.

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2015 ACC/AHA/HRS SVT Guideline: Executive Summary

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)
Reviewer

Representation

Employment

Eugene H.
Chung

Official
ReviewerHRS

Timm L.
Dickfeld

Official
ReviewerHRS

Samuel S.
Gidding

Official
Reviewer
ACC/AHA Task
Force on Clinical
Practice
Guidelines
Official
ReviewerACC
Board of Trustees

University of North
Carolina School of
MedicineAssociate
Professor of Medicine
University of
Maryland School of
MedicineAssociate
Professor of Medicine;
Baltimore Veterans
Affairs Medical
CenterDirector,
Electrophysiology
Nemours Cardiac
CenterDivision
Chief of Cardiology;
Jefferson Medical
CollegeProfessor of
Pediatrics
Krannert Institute of
Cardiology
Professor of Clinical
Medicine

Richard J.
Kovacs

Consultant

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

Institutional,
Organizational,
or Other
Financial Benefit
Zoll Medical

Expert
Witness

None

None

None

None

None

Biosense
Webster

None

None

Biosense
Webster*
General
Electric*

None

None

None

None

None

None

None

None

Biomedical
Systems*

None

None

Siemens

AstraZeneca
(DSMB)
MED Institute*
Eli Lilly
(DSMB)*
Teva
Pharmaceuticals
CarioNet*

None

Byron K.
Lee

Official
ReviewerAHA

University of
California San
FranciscoProfessor
of Medicine

Biotronik
Boston Scientific
St. Jude Medical

None

None

Zoll Medical*

Gregory F.
Michaud

Official
ReviewerAHA

Harvard Medical
SchoolAssistant
Professor

Boston Scientific
Medtronic
St. Jude Medical

None

None

Biosense
Webster*
Boston

Page 51 of 74

None

Defendant,
Boehringer
Ingelheimer,
2013

None

Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary
Reviewer

Representation

Simone
Musco

Official
ReviewerACC
Board of
Governors

Mohan N.
Viswanatha
n

Official
ReviewerAHA

Seshadri
Balaji

Content Reviewer

Nancy C.
Berg

Content
ReviewerACC
Electrophysiolog
y Section
Content
ReviewerACC
Electrophysiolog
y Section
Content Reviewer

Noel G.
Boyle

A. John
Camm

Employment

The International
Heart Institute of
Montana
Foundation
Cardiology Research
Investigator
University of
Washington School of
MedicineAssistant
Professor of Medicine
Oregon Health and
Science University
Professor of Pediatrics
and Pediatric
Cardiology, Director
of Pacing and
Electrophysiology
Allina Health System

University of
California Los
AngelesClinical
Professor of Medicine
St. Georges
University of
LondonProfessor of
Clinical Cardiology

Consultant

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

Institutional,
Organizational,
or Other
Financial Benefit

Expert
Witness

None

BristolMyers
Squibb
Sanofiaventis

None

Scientific*
St. Jude
Medical*
None

Biosense
Webster
Siemens
St. Jude Medical
None

None

None

Medtronic*

None

None

None

None

Medtronic*

None

None

None

None

None

None

None

None

None

None

None

None

None

None

Bayer*
Biotronik
Boehringer
Ingelheim
Boston Scientific
ChanRx
Daiichi-Sankyo
Medtronic
Menarini
Mitsubishi

Pfizer

None

None

None

None

Page 52 of 74

None

None

Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary
Reviewer

Representation

Robert M.
Campbell

Content
ReviewerACC
Adult Congenital
and Pediatric
Cardiology
Section

Susan P.
Etheridge

Content
ReviewerACC
Adult Congenital
and Pediatric
Cardiology
Section
Content Reviewer

Paul A.
Friedman

Bulent
Gorenek

Content
ReviewerACC
Electrophysiolog
y Section

Jonathan L.
Halperin

Content
Reviewer
ACC/AHA Task

Employment

Sibley Heart Center

CardiologyDirector,
Chief of Cardiac
Services; Emory
University School of
MedicineDivision
Director of Pediatric
Cardiology, Professor
of Pediatrics
University of Utah
Training Program
Director

Mayo Clinic
Professor of Medicine;
Cardiovascular
Implantable Device
LaboratoryDirector
Eskisehir Osmangazi
UniversityProfessor
and Vice Director,
Cardiology
Department
Mt. Sinai Medical
Professor of Medicine

Consultant

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

Institutional,
Organizational,
or Other
Financial Benefit

Expert
Witness

Novartis
Richmond
Pharmacology*
Sanofi-aventis
Servier
Pharmaceuticals*
St. Jude Medical
Takeda
Pharmaceuticals
Xention
None

None

None

None

None

None

None

None

None

None

None

None

NeoChord

None

None

Biotronik
Medtronic
St. Jude
Medical

Preventice
Sorin*

None

None

None

None

None

None

None

AstraZeneca
Bayer Healthcare
Biotronik

None

None

None

None

None

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Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary
Reviewer

Representation

Employment

Force on Clinical
Practice
Guidelines

Warren M.
Jackman

Content Reviewer

G. Neal
Kay

Content Reviewer

George J.
Klein

Content Reviewer

Bradley P.
Knight

Content Reviewer

John D.
Kugler

Content Reviewer

Fred M.
Kusumoto
Glenn N.

Content Reviewer
Content

University of
Oklahoma Health
Sciences Center
George Lynn Cross
Research Professor
Emeritus; Heart
Rhythm Institute
Senior Scientific
Advisor
University of
AlabamaProfessor
Emeritus
London Health
Sciences Center
Chief of Cardiology
Northwestern
UniversityProfessor
of Cardiology

University of
Nebraska Medical
CenterDivision
Chief of Pediatric
Cardiology
Mayo Clinic
Professor of Medicine
Baylor College of

Consultant

Boehringer
Ingelheim
Boston Scientific
Daiichi-Sankyo
Johnson &
Johnson
Medtronic
Pfizer
Biosense
Webster*
Boston
Scientific*
VytronUS*

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

Institutional,
Organizational,
or Other
Financial Benefit

Expert
Witness

AtriCure*
Biosense
Webster*
Biotronik*
Boston
Scientific*

None

None

None

None

None

None

None

None

None

None

Biotronik
Boston Scientific
Medtronic
Boston Scientific
Medtronic

None

None

None

None

None

Biosense
Webster
Biotronik
Boston
Scientific
Medtronic

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

None

Page 54 of 74

Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary
Reviewer

Levine

Marco A.
Mercader

Representation

Employment

Reviewer
ACC/AHA Task
Force on Clinical
Practice
Guidelines
Content Reviewer

MedicineProfessor
of Medicine; Director,
Cardiac Care Unit

William M.
Miles

Content Reviewer

Fred
Morady

Content Reviewer

Melvin M.
Scheinman

Content Reviewer

Sarah A.
Spinler

Content Reviewer

George Washington
UniversityAssociate
Professor of Medicine
University of
FloridaProfessor of
Medicine, Silverstein
Chair for
Cardiovascular
Education, Director of
the Clinical Cardiac
Electrophysiology
Fellowship Program
University of
MichiganMcKay
Professor of
Cardiovascular
Disease
University of
California San
FranciscoProfessor
of Medicine

University of the
Sciences, Philadelphia
College of
PharmacyProfessor
of Clinical Pharmacy

Consultant

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

Institutional,
Organizational,
or Other
Financial Benefit

Expert
Witness

None

None

None

None

None

None

None

None

None

None

Medtronic
(DSMB)

None

None

None

None

None

None

None

Amgen
Biosense
Webster
Biotronik*
Boston
Scientific*
Gilead Sciences
Janssen
Pharmaceuticals
Medtronic
St. Jude Medical
Portola
Pharmaceuticals

None

None

None

None

None

None

None

None

None

None

Page 55 of 74

Page RL, et al.

2015 ACC/AHA/HRS SVT Guideline: Executive Summary
Reviewer

Representation

Employment

Consultant

Speakers
Bureau

Ownership/
Partnership
/ Principal

Personal
Research

William G.
Stevenson

Content Reviewer

St. Jude Medical

None

None

None

Albert L.
Waldo

Content Reviewer

Brigham and
Womens Hospital
Director, Clinical
Cardiac
Electrophysiology
Program
University Hospitals
Associate Chief of
Cardiovascular
Medicine for
Academic Affairs;
Case Western Reserve
University School of
MedicineProfessor
of Medicine

AtriCure
Biosense
Webster*
CardioInsight
ChanRx
Daiichi-Sankyo
Gilead Sciences
Pfizer
St. Jude
Medical*
Biosense
Webster

BristolMyers
Squibb*
Janssen
Pharmaceut
icals
Pfizer*

None

Gilead
Sciences*

Institutional,
Organizational,
or Other
Financial Benefit
None

Expert
Witness

None

None

None

None
None
None
None
None
Harvard Medical
SchoolProfessor of
Pediatrics; Boston
Childrens Hospital
Chief, Division of
Cardiac
Electrophysiology
None
None
Richard C.
Content Reviewer University of Texas
None
None
None
Boehringer
Wu
Southwestern Medical
Ingelheim
CenterProfessor of
Janssen
Internal Medicine,
Pharmaceutic
Director of Cardiac
al
Electrophysiology Lab
Medtronic
This table represents the relationships of reviewers with industry and other entities that were disclosed at the time of peer review and determined to be relevant to this
document. It does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the
interest represents ownership of 5% of the voting stock or share of the business entity, or ownership of $5,000 of the fair market value of the business entity; or if
funds received by the person from the business entity exceed 5% of the persons gross income for the previous year. A relationship is considered to be modest if it is less
than significant under the preceding definition. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this
table are modest unless otherwise noted. Names are listed in alphabetical order within each category of review.
Edward
Walsh

Content Reviewer

According to the ACC/AHA, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or
asset, topic, or issue addressed in the document; or b) the company/entity (with whom the relationship exists) makes a drug, drug class, or device addressed in the
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2015 ACC/AHA/HRS SVT Guideline: Executive Summary
document, or makes a competing drug or device addressed in the document; or c) the person or a member of the persons household, has a reasonable potential for
financial, professional or other personal gain or loss as a result of the issues/content addressed in the document.
*Significant relationship.
No financial benefit.
ACC indicates American College of Cardiology; AHA, American Heart Association; DSMB, data safety monitoring board; and HRS, Heart Rhythm Society.

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