2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia
A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society
This article has a correction. Please see:
- Table of Contents
- 1. Introduction
- 2. General Principles
- 3. Sinus Tachyarrhythmias
- 4. Nonsinus Focal Atrial Tachycardia and MAT
- 5. Atrioventricular Nodal Reentrant Tachycardia
- 6. Manifest and Concealed Accessory Pathways
- 7. Atrial Flutter
- 8. Junctional Tachycardia
- 9. Special Populations
- 10. Quality-of-Life Considerations
- 11. Cost-Effectiveness
- 12. Shared Decision Making
- 13. Evidence Gaps and Future Research Needs
- Presidents and Staff
- Figures & Tables
- Supplemental Materials
- Info & Metrics
- 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
Table of Contents
1.1. Methodology and Evidence Review e508
1.2. Organization of the GWC e510
1.3. Document Review and Approval e510
1.4. Scope of the Guideline e510
General Principles e510
2.1. Mechanisms and Definitions e510
2.2. Epidemiology, Demographics, and Public Health Impact e510
2.3. Evaluation of the Patient With Suspected or Documented SVT e511
2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms e511
2.3.2. Evaluation of the ECG e514
2.4. Principles of Medical Therapy e515
2.4.1. Acute Treatment: Recommendations e515
2.4.2. Ongoing Management: Recommendations e517
2.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation e518
2.5.1. Mapping With Multiple and Roving Electrodes e518
2.5.2. Tools to Facilitate Ablation, Including 3-Dimensional Electroanatomic Mapping e518
2.5.3. Mapping and Ablation With No or Minimal Radiation e519
2.5.4. Ablation Energy Sources e519
Sinus Tachyarrhythmias e520
3.1. Physiological Sinus Tachycardia e521
3.2. Inappropriate Sinus Tachycardia e521
3.2.1. Acute Treatment e521
3.2.2. Ongoing Management: Recommendations e521
Nonsinus Focal Atrial Tachycardia and MAT e523
4.1. Focal Atrial Tachycardia e523
4.1.1. Acute Treatment: Recommendations e526
4.1.2. Ongoing Management: Recommendations e527
4.2. Multifocal Atrial Tachycardia e527
4.2.1. Acute Treatment: Recommendation e531
4.2.2. Ongoing Management: Recommendations e531
Atrioventricular Nodal Reentrant Tachycardia e531
5.1. Acute Treatment: Recommendations e532
5.2. Ongoing Management: Recommendations e533
Manifest and Concealed Accessory Pathways e534
6.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways e535
6.1.1. Acute Treatment: Recommendations e535
6.1.2. Ongoing Management: Recommendations e536
6.2. Management of Asymptomatic Pre-Excitation e537
6.2.1. PICOTS Critical Questions e537
6.2.2. Asymptomatic Patients With Pre-Excitation: Recommendations e538
6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations e539
Atrial Flutter e539
7.1. Cavotricuspid Isthmus–Dependent Atrial Flutter e539
7.2. Non–Isthmus-Dependent Atrial Flutters e540
7.3. Acute Treatment: Recommendations e541
7.4. Ongoing Management: Recommendations e542
Junctional Tachycardia e544
8.1. Acute Treatment: Recommendations e544
8.2. Ongoing Management: Recommendations e545
Special Populations e545
9.1. Pediatrics e545
9.2. Patients With Adult Congenital Heart Disease e549
9.2.1. Clinical Features e549
9.2.2. Acute Treatment: Recommendations e550
9.2.3. Ongoing Management: Recommendations e551
9.3. Pregnancy e553
9.3.1. Acute Treatment: Recommendations e553
9.3.2. Ongoing Management: Recommendations e554
9.4. SVT in Older Populations e555
9.4.1. Acute Treatment and Ongoing Management: Recommendation e555
Quality-of-Life Considerations e555
Shared Decision Making e556
Evidence Gaps and Future Research Needs e556
Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, based on systematic methods to evaluate and classify evidence, provide a cornerstone of quality cardiovascular care.
In response to reports from the Institute of Medicine1,2 and a mandate to evaluate new knowledge and maintain relevance at the point of care, the ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) modified its methodology.3–5 The relationships between guidelines, data standards, appropriate use criteria, and performance measures are addressed elsewhere.4
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.
Guideline Writing Committee (GWC) members review the literature; weigh the quality of evidence for or against particular tests, treatments, or procedures; and estimate expected health outcomes. In developing recommendations, the GWC uses evidence-based methodologies that are based on all available data.4–6 Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort studies, systematic reviews, and expert opinion. Only selected references are cited.
The Task Force recognizes the need for objective, independent Evidence Review Committees (ERCs) that include methodologists, epidemiologists, clinicians, and biostatisticians who systematically survey, abstract, and assess the evidence to address key clinical questions posed in the PICOTS format (P=population, I=intervention, C=comparator, O=outcome, T=timing, S=setting).4,5 Practical considerations, including time and resource constraints, limit the ERCs to evidence that is relevant to key clinical questions and lends itself to systematic review and analysis that could affect the strength of corresponding recommendations. Recommendations developed by the GWC on the basis of the systematic review are marked “SR”.
Guideline-Directed Medical Therapy
The term guideline-directed medical therapy refers to care defined mainly by ACC/AHA Class I recommendations. For these and all recommended drug treatment regimens, the reader should confirm dosage with product insert material and carefully evaluate for contraindications and interactions. Recommendations are limited to treatments, drugs, and devices approved for clinical use in the United States.
Class of Recommendation and Level of Evidence
The Class of Recommendation (COR; ie, the strength of the recommendation) encompasses the anticipated magnitude and certainty of benefit in proportion to risk. The Level of Evidence (LOE) rates evidence supporting the effect of the intervention on the basis of the type, quality, quantity, and consistency of data from clinical trials and other reports (Table 1).5,7 Unless otherwise stated, recommendations are sequenced by COR and then by LOE. Where comparative data exist, preferred strategies take precedence. When >1 drug, strategy, or therapy exists within the same COR and LOE and no comparative data are available, options are listed alphabetically. Each recommendation is followed by supplemental text linked to supporting references and evidence tables.
Relationships With Industry and Other Entities
The ACC and AHA sponsor the guidelines without commercial support, and members volunteer their time. The Task Force zealously avoids actual, potential, or perceived conflicts of interest that might arise through relationships with industry or other entities (RWI). All GWC members and reviewers are required to disclose current industry relationships or personal interests from 12 months before initiation of the writing effort. Management of RWI involves selecting a balanced GWC and assuring that the chair and a majority of committee members have no relevant RWI (Appendix 1). Members are restricted with regard to writing or voting on sections to which their RWI apply. For transparency, members’ comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is also available online. The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds representing different geographic regions, sexes, ethnicities, intellectual perspectives/biases, and scopes of clinical practice, and by inviting organizations and professional societies with related interests and expertise to participate as partners or collaborators.
Individualizing Care in Patients With Associated Conditions and Comorbidities
Managing patients with multiple conditions can be complex, especially when recommendations applicable to coexisting illnesses are discordant or interacting.8 The guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances. The recommendations should not replace clinical judgment.
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.
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
Jonathan L. Halperin, MD, FACC, FAHA
Chair, ACC/AHA Task Force on Clinical Practice Guidelines
1.1. Methodology and Evidence Review
The recommendations listed in this guideline are, whenever possible, evidence based. An extensive evidence review was conducted in April 2014 that included literature published through September 2014. Other selected references published through May 2015 were incorporated by the GWC. Literature included was derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. The relevant data are included in evidence tables in the Online Data Supplement. Key search words included but were not limited to the following: ablation therapy (catheter and radiofrequency; fast and slow pathway), accessory pathway (manifest and concealed), antiarrhythmic drugs, atrial fibrillation, atrial tachycardia, atrioventricular nodal reentrant (reentry, reciprocating) tachycardia, atrioventricular reentrant (reentry, reciprocating) tachycardia, beta blockers, calcium channel blockers, cardiac imaging, cardioversion, cost effectiveness, cryotherapy, echocardiography, elderly (aged and older), focal atrial tachycardia, Holter monitor, inappropriate sinus tachycardia, junctional tachycardia, multifocal atrial tachycardia, paroxysmal supraventricular tachycardia, permanent form of junctional reciprocating tachycardia, pre-excitation, pregnancy, quality of life, sinoatrial node, sinus node reentry, sinus tachycardia, supraventricular tachycardia, supraventricular arrhythmia, tachycardia, tachyarrhythmia, vagal maneuvers (Valsalva maneuver), and Wolff-Parkinson-White syndrome. 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.9
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).10 The present guideline addresses other SVTs, including regular narrow–QRS complex tachycardias, as well as other, irregular SVTs (eg, atrial flutter with irregular ventricular response and multifocal atrial tachycardia [MAT]). This guideline supersedes the “2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias.”11 It incorporates new and existing knowledge derived from published clinical trials, basic science, and comprehensive review articles, along with evolving treatment strategies and new drugs. Some recommendations from the earlier guideline have been updated as warranted by new evidence or a better understanding of existing evidence, whereas other inaccurate, irrelevant, or overlapping recommendations were deleted or modified. Whenever possible, we reference data from the acute clinical care environment; however, in some cases, the reference studies from the invasive electrophysiology laboratory inform our understanding of arrhythmia diagnosis and management. 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.
In the current healthcare environment, cost consideration cannot be isolated from shared decision making and patient-centered care. The AHA and ACC have acknowledged the importance of value in health care, calling for eventual development of a Level of Value for practice recommendations in the “2014 ACC/AHA Statement on Cost/Value Methodology in Clinical Practice Guidelines and Performance Measures.”6 Although quality-of-life and cost-effectiveness data were not sufficient to allow for development of specific recommendations, the GWC agreed the data warranted brief discussion (Sections 10 and 11). Throughout this document, and associated with all recommendations and algorithms, the importance of shared decision making should be acknowledged. Each approach, ranging from observation to drug treatment to ablation, must be considered in the setting of a clear discussion with the patient regarding risk, benefit and personal preference. See Section 12 for additional information.
In developing this guideline, the GWC reviewed prior published guidelines and related statements. Table 2 contains a list of guidelines and statements deemed pertinent to this writing effort and is intended for use as a resource, thus obviating the need to repeat existing guideline recommendations.
2. General Principles
2.1. Mechanisms and Definitions
For the purposes of this guideline, SVT is defined as per Table 3, 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.
2.2. Epidemiology, Demographics, and Public Health Impact
The epidemiology of SVT, including its frequency, patterns, causes, and effects, is imprecisely defined because of incomplete data and failure to discriminate among AF, atrial flutter, and other supraventricular arrhythmias. The best available evidence indicates that the prevalence of SVT in the general population is 2.29 per 1000 persons.32 When adjusted by age and sex in the US population, the incidence of paroxysmal supraventricular tachycardia (PSVT) is estimated to be 36 per 100 000 persons per year.32 There are approximately 89 000 new cases per year and 570 000 persons with PSVT.32 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 bpm versus 155 bpm; P=0.0006). Women have twice the risk of men of developing PSVT.32 Individuals >65 years of age have >5 times the risk of younger persons of developing PSVT.32
Patients with PSVT who are referred to specialized centers for management with ablation are younger, have an equal sex distribution, and have a low frequency of cardiovascular disease.33–47 The frequency of atrioventricular nodal reentrant tachycardia (AVNRT) is greater in women than in men. This may be due to an actual higher incidence in women, or it may reflect referral bias. In persons who are middle-aged or older, AVNRT is more common, whereas in adolescents, the prevalence may be more balanced between atrioventricular reentrant tachycardia (AVRT) and AVNRT, or AVRT may be more prevalent.32 The relative frequency of tachycardia mediated by an accessory pathway decreases with age. The incidence of manifest pre-excitation or WPW pattern on ECG tracings in the general population is 0.1% to 0.3%. However, not all patients with manifest ventricular pre-excitation develop PSVT.47–49 The limited data on the public health impact of SVT indicate that the arrhythmia is commonly a reason for emergency department and primary care physician visits but is infrequently the primary reason for hospital admission.11,50,51
2.3. Evaluation of the Patient With Suspected or Documented SVT
2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms
Patients seen in consultation for palpitations often describe symptoms with characteristic features suggestive of SVT that may guide physicians to appropriate testing and a definitive diagnosis. The diagnosis of SVT is often made in the emergency department, but it is common to elicit symptoms suggestive of SVT before initial electrocardiogram/electrocardiographic (ECG) documentation. SVT symptom onset often begins in adulthood; in 1 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.52 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.53 In comparison with AVRT, patients with AVNRT are more likely to be female, with an age of onset >30 years.49,54–56 AVNRT onset has been reported after the age of 50 years in 16% and before the age of 20 years in 18%.57 Among women with SVT and no other cardiovascular disease, the onset of symptoms occurred during childbearing years (eg, 15 to 50 years) in 58%.32 The first onset of SVT occurred in only 3.9% of women during pregnancy, but among women with an established history of SVT, 22% reported that pregnancy exacerbated their symptoms.58
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.53,59 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.60 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%.60 Although this was a pediatric population, it provided symptom data that are likely applicable to adults. 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). In 1 study, the criteria for panic disorder were fulfilled in 67% of patients with SVT that remained unrecognized after their initial evaluation. Physicians attributed symptoms of SVT to panic, anxiety, or stress in 54% of patients, with women more likely to be mislabeled with panic disorder than men.61
When AVNRT and AVRT are compared, symptoms appear to differ substantially. Patients with AVNRT more frequently describe symptoms of “shirt flapping” or “neck pounding”54,62 that may be related to pulsatile reversed flow when the right atrium contracts against a closed tricuspid valve (cannon a-waves). During 1 invasive study of patients with AVNRT and AVRT, both arrhythmias decreased arterial pressure and increased left atrial pressure, but simulation of SVT mechanism by timing the pacing of the atria and ventricles showed significantly higher left atrial pressure in simulated AVNRT than in simulated AVRT.62 Polyuria is particularly common with AVNRT and is related to higher right atrial pressures and elevated levels of atrial natriuretic protein in patients with AVNRT compared with patients who have AVRT or atrial flutter.63
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.64 The rate of AVRT is faster when AVRT is induced during exercise,65 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.66,67 The drop in blood pressure (BP) during SVT is greatest in the first 10 to 30 seconds and somewhat normalizes within 30 to 60 seconds, despite minimal changes in rate.68,69 Shorter ventriculoatrial intervals are associated with a greater mean decrease in BP.69 Studies have demonstrated a relationship between hemodynamic changes and the relative timing of atrial and ventricular activation. In a study of patients with AVNRT with short versus long ventriculoatrial intervals, there was no significant difference in tachycardia cycle length70; however, the induction of typical AVNRT caused a marked initial fall in systemic BP, followed by only partial recovery that resulted in stable hypotension and a reduction in cardiac output due to a decrease in stroke volume. In comparison, atypical AVNRT, having a longer ventriculoatrial interval, exhibited a lesser degree of initial hypotension, a complete recovery of BP, and no significant change in cardiac output.70
The contrasting hemodynamic responses without significant differences in heart rate during SVT confirm that rate alone does not account for these hemodynamic changes. Atrial contraction on a closed valve might impair pulmonary drainage and lead to neural factors that account for these observations. These findings were confirmed in a study performed in the electrophysiological (EP) laboratory: When pacing was used to replicate the timing of ventricular and atrial activation during SVT, the decrease in BP was greatest with simultaneous ventriculoatrial timing, smaller with a short vertriculoatrial interval, and smallest with a long ventriculoatrial interval.71 An increase in central venous pressure followed the same trend. Sympathetic nerve activity increased with all 3 pacing modalities but was most pronounced with simultaneous atrial and ventricular pacing or a short ventriculoatrial interval.
In a study of 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.72 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.
See Online Data Supplement 1 for additional data on clinical presentation and differential diagnosis on the basis of symptoms.
2.3.2. Evaluation of the ECG
A 12-lead ECG obtained during tachycardia and during sinus rhythm may reveal the etiology of tachycardia. For the patient who describes prior, but not current, symptoms of palpitations, the resting ECG can identify pre-excitation that should prompt a referral to a cardiac electrophysiologist.
A wide-complex tachycardia (QRS duration >120 ms) may represent either VT or a supraventricular rhythm with abnormal conduction. Conduction abnormalities may be due to rate-related aberrant conduction, pre-existing bundle-branch block seen in sinus rhythm, or an accessory pathway that results in pre-excitation (Table 4). The presence of atrioventricular (AV) dissociation (with ventricular rate faster than atrial rate) or fusion complexes–representing dissociation of supraventricular impulses from a ventricular rhythm– provides the diagnosis of VT (Figure 1). Other criteria are useful but not diagnostic. Concordance of the precordial QRS complexes such that all are positive or negative suggests VT or pre-excitation, whereas QRS complexes in tachycardia that are identical to those seen in sinus rhythm are consistent with SVT. Other, more complicated ECG algorithms have been developed to distinguish VT from SVT, such as the Brugada criteria, which rely on an examination of the QRS morphology in the precordial leads,73 and the Vereckei algorithm, which is based on an examination of the QRS complex in lead aVR74 (Table 5). The failure to correctly identify VT can be potentially life threatening, particularly if misdiagnosis results in VT being treated with verapamil or diltiazem. Adenosine is suggested in the “2010 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care–Part 8: Adult Advanced Cardiovascular Life Support” (2010 Adult ACLS guideline)75 if a wide-complex tachycardia is monomorphic, regular, and hemodynamically tolerated, because adenosine may help convert the rhythm to sinus and may help in the diagnosis. When doubt exists, it is safest to assume any wide-complex tachycardia is VT, particularly in patients with known cardiovascular disease, such as prior myocardial infarction.
For a patient presenting in SVT, the 12-lead ECG can potentially identify the arrhythmia mechanism (Figure 7). The tachycardia should first be classified according to whether there is a regular or irregular ventricular rate. An irregular ventricular rate suggests AF, MAT, or atrial flutter with variable AV conduction. When AF is associated with a rapid ventricular response, the irregularity of the ventricular response is less easily detected and can be misdiagnosed as a regular SVT.76 If the atrial rate exceeds the ventricular rate, then atrial flutter or AT (focal or multifocal) is usually present (rare cases of AVNRT with 2:1 conduction have been described77).
If the SVT is regular, this may represent AT with 1:1 conduction or an SVT that involves the 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: Figures 2 and 3) and AVRT (Section 7: Figures 4 and 6). In these reentrant tachycardias, the retrogradely conducted P wave may be difficult to discern, especially if bundle-branch block is present. In typical AVNRT, atrial activation is nearly simultaneous with the QRS, so the terminal portion of the P wave is usually located at the end of the QRS complex, appearing as a narrow and negative deflection in the inferior leads (a pseudo S wave) and a slightly positive deflection at the end of the QRS complex in lead V1 (pseudo R′). In orthodromic AVRT (with anterograde conduction down the AV node), the P wave can usually be seen in the early part of the ST-T segment. In typical forms of AVNRT and AVRT, because the P wave is located closer to the prior QRS complex than the subsequent QRS complex, the tachycardias are referred to as having a “short RP.” They also have a 1:1 relationship between the P wave and QRS complex, except in rare cases of AVNRT in which 2:1 AV block or various degrees of AV block can occur. 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 sinus that is usually seen near the end of or shortly after the T wave (Figure 5). In sinus node reentry tachycardia, a form of focal AT, the P-wave morphology is identical to the P wave in sinus rhythm.
2.4. Principles of Medical Therapy
See Figure 8 for the algorithm for acute treatment of tachycardia of unknown mechanism; Figure 9 for the algorithm for ongoing management of tachycardia of unknown mechanism; Table 6 for acute drug therapy for SVT (intravenous administration); and Table 7 for ongoing drug therapy for SVT (oral administration).
2.4.1. Acute Treatment: Recommendations
Because patients with SVT account for approximately 50 000 emergency department visits each year,81 emergency physicians may be the first to evaluate patients whose tachycardia mechanism is unknown and to have the opportunity to diagnose the mechanism of arrhythmia. It is important to record a 12-lead ECG to differentiate tachycardia mechanisms according to whether the AV node is an obligate component (Section 2.3.2), because treatment that targets the AV node will not reliably terminate tachycardias that are not AV node dependent. Also, if the QRS duration is >120 ms, it is crucial to distinguish VT from SVT with aberrant conduction, pre-existing bundle-branch block, or pre-excitation (Table 4). In particular, the administration of verapamil or diltiazem for treatment of either VT or a pre-excited AF may lead to hemodynamic compromise or may accelerate the ventricular rate and lead to ventricular fibrillation.
2.4.2. Ongoing Management: Recommendations
The recommendations and algorithm (Figure 9) for ongoing management, along with other recommendations and algorithms for specific SVTs that follow, are meant to include consideration of patient preferences and clinical judgment; this may include consideration of consultation with a cardiologist or clinical cardiac electrophyisiologist, as well as patient comfort with possible invasive diagnostic and therapeutic intervention. Recommendations for treatment options (including drug therapy, ablation, or observation) must be considered in the context of frequency and duration of the SVT, along with clinical manifestations, such as symptoms or adverse consequences (eg, development of cardiomyopathy).
2.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation
2.5.1. Mapping With Multiple and Roving Electrodes
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.141 EP studies involve placement of multielectrode catheters in the heart at ≥1 sites in the atria, ventricles, or coronary sinus. Pacing and programmed electrical stimulation may be performed with or without pharmacological provocation. Making a precise and correct diagnosis of the mechanism of SVT is the key to successful outcome, particularly when multiple arrhythmia mechanisms are possible; as such, appropriate diagnostic maneuvers should be performed before proceeding with ablation. By using diagnostic maneuvers during the EP study, the mechanism of SVT can be defined in most cases.80,142 Complications of diagnostic EP studies are rare but can be life threatening.143
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.144 The simplest technique uses several multipole catheters plus a roving catheter that is sequentially positioned in different regions of interest and measures local activation time. Electroanatomic mapping systems and specialized multielectrode catheters, such as circular or multispline catheters, can map simultaneously from multiple sites and improve the speed and resolution of mapping.
2.5.2. Tools to Facilitate Ablation, Including 3-Dimensional Electroanatomic Mapping
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.145 Disadvantages include higher cost, as well as additional training, support, and procedure preparation time. Several studies have demonstrated the advantages of electroanatomic mapping, with success rates comparable to conventional approaches yet with significant reduction in fluoroscopy times.145–148
2.5.3. Mapping and Ablation With No or Minimal Radiation
Fluoroscopy has historically been the primary imaging modality used for EP studies. The use of ionizing radiation puts patient, operator, and laboratory staff at risk of the short- and long-term effects of radiation exposure. 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.147,149–152 Radiation exposure may be further reduced by using robotic or magnetic navigation of catheters that use a 3-dimensional anatomic tracking system superimposed on traditional fluoroscopy imaging. A reduced- fluoroscopy approach is particularly important in pediatric patients and during pregnancy.153,154
2.5.4. Ablation Energy Sources
Radiofrequency current is the most commonly used energy source for SVT ablation.155 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. Published trials, including a meta-analysis comparing radiofrequency ablation with cryoablation for treatment of AVNRT, have shown a higher rate of recurrence with cryoablation but lower risk of permanent AV nodal block.156–158 The rate of AVNRT recurrence with cryoablation depends on the size of the ablation electrode and the endpoint used.156,159 Ultimately, the choice of technology should be made on the basis of an informed discussion between the operator and the patient.
3. Sinus Tachyarrhythmias
In normal individuals, the sinus rate at rest is generally between 50 bpm and 90 bpm, reflecting vagal tone.160–163 Sinus tachycardia refers to the circumstance in which the sinus rate exceeds 100 bpm. Sinus tachycardia may be appropriate in response to physiological stimuli or other exogenous factors or may be inappropriate when the heart rate exceeds what would be expected for physical activity or other circumstances. On the ECG, the P wave is upright in leads I, II, and aVF and is biphasic in lead V1. As the sinus rate increases, activation arises from more superior aspects of the right atrium, resulting in a larger-amplitude P wave in the inferior leads.
3.1. Physiological Sinus Tachycardia
Sinus tachycardia is regarded as physiological when it is the result of appropriate autonomic influences, such as in the setting of physical activity or emotional responses. Physiological sinus tachycardia may result from pathological causes, including infection with fever, dehydration, anemia, heart failure, and hyperthyroidism, in addition to exogenous substances, including caffeine, drugs with a beta-agonist effect (eg, albuterol, salmeterol), and illicit stimulant drugs (eg, amphetamines, cocaine). In these cases, tachycardia is expected to resolve with correction of the underlying cause.
3.2. Inappropriate Sinus Tachycardia
Inappropriate sinus tachycardia (IST) is defined as sinus tachycardia that is unexplained by physiological demands at rest, with minimal exertion, or during recovery from exercise. 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.160 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 and drugs of abuse. Anxiety is also an important trigger, and patients with IST may have associated anxiety disorders.160 Structural heart disease, such as cardiomyopathies, must also be excluded, though the development of a cardiomyopathy secondary to sinus tachycardia is extremely rare.164,165 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, which results in slowing of the heart rate. On the basis of the results of 2 large, randomized, placebo-controlled trials, this drug was recently approved by the FDA for use in patients with systolic heart failure. In the BEAUTIFUL (Morbidity-Mortality Evaluation of the If Inhibitor Ivabradine in Patients With Coronary Disease and Left-Ventricular Dysfunction) study,166 10 917 patients with coronary disease and a left ventricular ejection fraction <40% were randomized to ivabradine or placebo. In the SHIFT (Systolic Heart Failure Treatment With the If Inhibitor Ivabradine) trial,167 6558 patients with a left ventricular ejection fraction ≤35% were randomized to ivabradine or placebo. In both of these trials, therapy with ivabradine resulted in additional heart rate reductions of 6 to 8 bpm and proved to be generally safe. 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.168–176
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.177–183 Ablation is typically performed with 3-dimensional electroanatomic or noncontact mapping techniques targeting sites of early activation with isoproterenol infusion, with or without use of intracardiac ultrasound–guided mapping to image the crista terminalis. Nonetheless, symptoms commonly recur after several months, with IST recurrence in up to 27% and overall symptomatic recurrence (IST or non-IST AT) in 45% of patients.177,179,180,182 Complications can be significant and may include symptomatic sinus or junctional bradycardia necessitating pacemaker placement, phrenic nerve injury with paralysis of the right hemidiaphragm, and significant facial and upper-extremity swelling caused by narrowing of the superior vena cava/RA junction, which may rarely result in superior vena cava syndrome. 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. Even more aggressive surgical methods to ablate or denervate the sinus node have been described, further highlighting the risks that highly symptomatic patients are willing to accept to find relief.184 Effective patient communication is key for these patients.
4. Nonsinus Focal Atrial Tachycardia and MAT
4.1. Focal Atrial Tachycardia
Focal AT is characterized as a fast rhythm from a discrete origin, discharging at a rate that is generally regular, and conducting in a centrifugal manner throughout the atrial tissue. Focal AT represents approximately 3% to 17% of the patients referred for SVT ablation.49,122,186 The demographics of focal AT in the adult population will continue to change as SVTs are increasingly ablated at a younger age.
Focal AT can be sustained or nonsustained. The atrial rate during focal AT is usually between 100 and 250 bpm.186 Presence and severity of symptoms during focal AT are variable among patients. Focal AT in the adult population is usually associated with a benign prognosis, although AT-mediated cardiomyopathy has been reported in up to 10% of patients referred for ablation of incessant SVT.187,188 Nonsustained focal AT is common and often does not require treatment.
The diagnosis of focal AT is suspected when the ECG criteria are met (Section 2). Algorithms have been developed to estimate the origin of the focal AT from the P-wave morphology recorded on a standard 12-lead ECG.189,190 In general, a positive P wave in lead V1 and negative P waves in leads I and aVL are correlated to ATs arising from the left atrium. Positive P waves in leads II, III, and aVF suggest that the origin of AT is from the cranial portion of either atria. Shorter P-wave duration is correlated to AT arising from the paraseptal tissue versus the right or left atrial free wall.191 The precise location of the focal AT is ultimately confirmed by mapping during EP studies when successful ablation is achieved.123–127,192–196 Focal AT has been localized to the crista terminalis, right or left atrial free wall or appendage, tricuspid or mitral annulus, paraseptal or paranodal areas, pulmonary veins, coronary sinus, and coronary cusps, but it originates more frequently from the right atrium than from the left atrium.197,198
The underlying mechanism of focal AT can be automatic, triggered activity, or microreentry, but methods to distinguish the mechanism through pharmacological testing or EP study are of modest value because of limited sensitivity and specificity.123,199,200 An automatic AT can be transiently suppressed by adenosine or by overdrive pacing and may be terminated by beta blockers, diltiazem, or verapamil. Whereas a triggered AT can be terminated by adenosine or overdrive pacing, its response to beta blockers, diltiazem, or verapamil may be variable. A microreentrant AT can be induced and terminated by programmed stimulation, but its response to adenosine, beta blockers, diltiazem, or verapamil may depend on the location of the microreentrant circuit; the tachycardia can be terminated by these drugs if the microreentrant circuit involves tissue around the sinus node, whereas microreentrant ATs from other locations generally will not be terminated by these drugs.
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. Sinus node reentry is characterized by paroxysmal episodes of tachycardia, generally 100 bpm to 150 bpm.201–203 Confirmation of the reentrant mechanism requires an EP study. Induction of sinus node reentrant tachycardia during programmed stimulation, demonstration of entrainment, and localization of the tachycardia origin in the region of the sinus node are necessary to confirm the diagnosis.
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.204,205 The design or execution of these studies is frequently suboptimal because of the poorly defined inclusion criteria or variable clinical settings. Several studies included a mix of patients with congenital or postoperative AT, and some of these patients likely had macroreentrant AT. In many reports, the response to intravenous drug therapy was evaluated by EP study rather than in the clinical environment.123,200,204–207 In the clinical setting, if the diagnosis is uncertain, vagal maneuvers may be attempted to better identify the mechanism of SVT.
Digoxin has not been well studied for focal AT. Intravenous class Ic drugs (eg, flecainide, propafenone) may be moderately effective in treating focal AT in the acute setting, as reported in earlier, small observational studies, although intravenous forms of IC drugs are not available in the United States. In patients with an implanted cardiac pacing device, it may be possible to perform overdrive pacing through the device, although close monitoring is required to prevent any significant adverse effect, such as pacing-induced AF or other atrial arrhythmias. Equipment should be available to provide support for cardioversion of AF if needed.
4.1.2. Ongoing Management: Recommendations
4.2. Multifocal Atrial Tachycardia
MAT is defined as a rapid, irregular rhythm with at least 3 distinct morphologies of P waves on the surface ECG. It may be difficult to distinguish MAT from AF on physical examination or even on a single ECG tracing, so a 12-lead ECG is indicated to confirm the diagnosis. On the ECG, the atrial rate is >100 bpm (or >90 bpm, as defined in at least 1 report220). Unlike AF, there is a distinct isoelectric period between P waves. The P-P, P-R, and R-R intervals are variable. The mechanism of MAT is not well established. Although it is assumed that the variability of P-wave morphology implies a multifocal origin, there are very few mapping studies of MAT.221 Similarly, the variability of the P-R interval may relate to decremental conduction through the AV node, as opposed to the origin of the P wave. Occasional responsiveness to verapamil suggests a triggered mechanism, but data are limited.222
MAT is commonly associated with underlying conditions, including pulmonary disease, pulmonary hypertension, coronary disease, and valvular heart disease,223 as well as hypomagnesemia and theophylline therapy.224 The first-line treatment is management of the underlying condition. Intravenous magnesium may also be helpful in patients with normal magnesium levels.225 Antiarrhythmic medications in general are not helpful in suppression of multifocal AT.226 Management often involves slowing conduction at the AV nodal level to control heart rate. Verapamil has been shown to have some efficacy in patients with MAT who do not have ventricular dysfunction, sinus node dysfunction, or AV block227,228; although diltiazem has not been studied, it may provide a class effect with similar mechanism to verapamil. Beta blockers can be used with caution to treat MAT in the absence of respiratory decompensation, sinus node dysfunction, or AV block.229,230 Amiodarone has been reported to be useful in 1 report.231 Cardioversion is not useful in MAT.223
4.2.1. Acute Treatment: Recommendation
4.2.2. Ongoing Management: Recommendations
5. Atrioventricular Nodal Reentrant Tachycardia
AVNRT is the most common SVT. It is usually seen in young adults without structural heart disease or ischemic heart disease, and >60% of cases are observed in women.49 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).54 The anatomic substrate of AVNRT is dual AV nodal physiology (Table 3).
AVNRT is often well tolerated and is rarely life threatening. Patients will typically present with the sudden onset of palpitations and possibly with shortness of breath, dizziness, and neck pulsations. Syncope is a rare manifestation of AVNRT. AVNRT may occur spontaneously or on provocation with exertion, coffee, tea, or alcohol.
5.1. Acute Treatment: Recommendations
5.2. Ongoing Management: Recommendations
6. Manifest and Concealed Accessory Pathways
Accessory pathways can be manifest or concealed; 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. Typically, pathways directly connect the atrium and ventricle, bypassing the normal conduction through the AV node and His Purkinje system. The pathways are considered manifest if they conduct in the anterograde direction, demonstrating pre-excitation with a delta wave on the ECG. Manifest pathways occur in 0.1% to 0.3% of the population and may conduct in both the anterograde and retrograde directions or, less commonly, only in the anterograde direction.252 Concealed pathways conduct only in the retrograde direction and therefore do not cause pre-excitation on the standard 12-lead ECG.
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. Other SVTs, such as AVNRT, AT, and atrial flutter, can also conduct rapidly over a manifest accessory pathway; in these instances, the pathway is considered a “bystander” because it is not part of the tachycardia circuit. Most accessory pathways have conduction properties similar to the myocardium and do not demonstrate decremental conduction. A unique form of AVRT involves a concealed accessory pathway, usually located in the posteroseptal region, with retrograde decremental conduction properties resulting in a form of orthodromic reentrant tachycardia termed PJRT. This tachycardia has deeply inverted retrograde P waves in leads II, III, and aVF, with a long RP interval due to the location and decremental conduction properties of the accessory pathway (Figure 6). The incessant nature of PJRT may result in tachycardia-induced cardiomyopathy that usually resolves after successful treatment. Another unusual accessory pathway is the atriofascicular fiber (also called a Mahaim fiber) that connects the right atrium to a fascicle of the distal right bundle branch and has decremental anterograde conduction while not allowing conduction in the retrograde direction; this pathway can allow reentrant tachycardia with a circuit that involves anterograde conduction over the accessory pathway with characteristic left bundle-branch block morphology and retrograde conduction through the AV node/His Purkinje system. Other rare accessory pathway connections that may participate in reentrant tachycardia are nodofascicular pathways (connecting the AV node to a fascicle) and nodoventricular pathways (connecting the AV node to the ventricular myocardium). Fasciculoventricular pathways, connecting a fascicle to the proximal right or left bundle branch, have also been described, although they have never been reported to participate in tachycardia. An EP study is necessary to establish the diagnosis of these rare accessory pathways.
The diagnosis of WPW syndrome is reserved for patients who demonstrate ventricular pre-excitation on their resting ECG that participates in arrhythmias. 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%.253,254 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.254–258 Antiarrhythmic drug treatment of patients with orthodromic AVRT can be directed at either the accessory pathway or the AV node, as both are key portions of the reentrant circuit. AV nodal–blocking agents may be contraindicated in patients at risk of rapid conduction down the accessory pathway during AF. Catheter ablation strategies target the accessory pathway, with high success rates.
6.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways
6.1.1. Acute Treatment: Recommendations
6.1.2. Ongoing Management: Recommendations
6.2. Management of Asymptomatic Pre-Excitation
6.2.1. PICOTS Critical Questions
See the ERC systematic review report, “Risk Stratification for Arrhythmic Events in Patients With Asymptomatic Pre-Excitation” for the complete evidence review on the management of asymptomatic pre-excitation,9 and see Online Data Supplements 13, 14, and 15 for additional data on asymptomatic pre-excitation, which were reproduced directly from the ERC’s systematic review. These recommendations have been designated with the notation SR to emphasize the rigor of support from the ERC’s systematic review. PICOTS Question 1 did not provide adequate data for a recommendation; the other 3 PICOTS questions are addressed in the recommendations in Section 6.2.2.
As noted in Section 1.1, the recommendations in Section 6.3 are based on a separately commissioned systematic review of the available evidence, the results of which were used to frame our decision making. Full details are provided in the ERC’s systematic review report.9 The following 4 questions were considered by the ERC:
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?
What is the usefulness of invasive EP study (without catheter ablation of the accessory pathway) versus no testing for predicting arrhythmic events (including SCD) in patients with asymptomatic pre-excitation?
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?
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
6.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations
7. Atrial Flutter
See Figure 17 for a schematic depicting classification of atrial flutter/ATs; Figure 18 for the algorithm for acute treatment of atrial flutter; and Figure 19 for the algorithm for ongoing management of atrial flutter.
7.1. Cavotricuspid Isthmus–Dependent Atrial Flutter
Atrial flutter is a macroreentrant atrial arrhythmia characterized by regular atrial rate and constant P-wave morphology. When the atrial flutter circuit involves the cavotricuspid isthmus (CTI), it is labeled CTI-dependent atrial flutter. When CTI-dependent flutter involves a circuit that rotates around the tricuspid valve in a counterclockwise direction (up the septum and down the free wall), it is called “typical”; less commonly, the CTI-dependent flutter circuit rotates in a clockwise direction (sometimes called “reverse typical”).203 Counterclockwise CTI-dependent atrial flutter is characterized electrocardiographically by dominant negative flutter waves in the inferior leads (so-called “sawtooth waves”) and a positive P wave in lead V1 at atrial rates of 250 bpm to 350 bpm (Figure 17). Clockwise isthmus-dependent flutter shows the opposite pattern (ie, positive flutter waves in the inferior leads and wide, negative flutter waves in lead V1) (Figure 17). 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.310
Atrial flutter can occur in clinical settings similar to those associated with AF, and atrial flutter can be triggered by AT or AF.121,311 It is common for AF and atrial flutter to coexist in the same patient. After CTI ablation, 22% to 50% of patients have been reported to develop AF after a mean follow-up of 14 to 30 months, although 1 study reported a much higher rate of AF development, with 82% of patients treated by catheter ablation for atrial flutter manifesting AF within 5 years.312 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.121,312–316
Atrial flutter may result from antiarrhythmic therapy of AF, particularly when flecainide, propafenone, or amiodarone is used for treatment of AF.317,318 In those patients with atrial flutter resulting from antiarrhythmic therapy of AF, ablation of the CTI-dependent flutter may prevent recurrent flutter while antiarrhythmic therapy for AF is continued.318
Patients with atrial flutter are thought to have the same risk of thromboembolism as patients with AF; therefore, recommendations for anticoagulation mirror those for patients with AF.10,121,314 Similarly, the recommendations for anticoagulation with regard to either pharmacological or electrical cardioversion of patients with atrial flutter are the same as those for patients with AF, as discussed in the 2014 AF guideline (Section 6.1).10
7.2. Non–Isthmus-Dependent Atrial Flutters
Non–isthmus-dependent atrial flutter or atypical flutter describes macroreentrant ATs that are not dependent on conduction through the CTI. A variety of circuits have been described, including a path around the mitral annulus (perimitral flutter), re-entry involving the left atrial roof, and re-entry around regions of scarring in the right or left atrium. Non–isthmus-dependent atrial flutters often occur in patients with atrial scarring from prior heart surgery or ablation but also may occur in any form of heart disease or may be idiopathic.134,140,319 Non–isthmus-dependent atrial flutters can coexist with CTI-dependent flutter or involve the presence of multiple atrial re-entry circuits.133,320 The reentrant circuits are classified as either macroreentrant AT (large; often several centimeters or longer in diameter) or microreentrant AT (≤2 cm in diameter), which may be indistinguishable from focal AT.321
In the presence of substantial atrial disease, prior surgery, or prior radiofrequency catheter ablation, the ECG flutter-wave morphology is not a reliable predictor of whether the flutter circuit involves the CTI. Although an ECG with a typical flutter appearance has good predictive value for CTI-dependent flutter in a patient who has not undergone prior catheter ablation of AF, the ECG appearance is less useful in predicting the flutter circuit in a patient who has previously undergone AF ablation.322–325 The presence of a positive or biphasic (but dominantly positive) deflection in V1, accompanied by deflections in other leads inconsistent with typical counterclockwise atrial flutter, suggests the presence of an atypical flutter (Figure 17). Definitive diagnosis requires EP study and intracardiac mapping.326
Catheter ablation of non–CTI-dependent flutter requires more extensive mapping than does ablation of CTI-dependent flutter, and success rates are lower (Table 8). The location of the circuit determines ablation approach and risks.
The substrate for macroreentrant atrial arrhythmias after cardiac surgery is atrial scarring from atriotomy incisions and cannulation sites and from the underlying myopathic process of the valve disease itself; this is sometimes referred to as incisional atrial reentrant tachycardia. The location of the reentrant circuit depends on the type of surgical approach, and common populations include patients who have undergone mitral valve surgery or have a repaired atrial septal defect.327–330 These arrhythmias are also common after surgical or catheter ablation for AF.331,332 Both single- and dual-loop circuits, as well as focal ATs, can be present. It is useful to review the procedural notes to identify the location of atrial incisions or prior ablation that can assist with future mapping and ablation.
The development of a microreentrant or macroreentrant left AT after AF ablation occurs in approximately 5% of patients.330,333,334 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.333–338 Non–reentrant focal arrhythmias often originate at lesion edges or reconnected segments of prior isolated pulmonary veins.333 Reisolation of the pulmonary vein and ablation of any nonpulmonary vein foci are often effective in treating these arrhythmias. Detailed activation and entrainment mapping of the tachycardia during a second procedure result in effective ablation in approximately 90% of patients.335 Although right atrial CTI-dependent flutter may also occur, most of the tachycardias originate in the left atrium.
As with all types of atrial flutter, it may be very difficult to achieve rate control in patients with post–AF ablation non–CTI-dependent flutter (far more so than in patients with preablation AF). When the ventricular response cannot be controlled with common rate-control medications, attempts at restoration of sinus rhythm with pharmacological therapy and cardioversion are often required. Many of the atrial flutters that are observed during the first 3 months after catheter ablation or after cardiac surgery will not recur later on. For this reason, it is advised that attempts at ablation of atrial flutter after AF ablation be deferred until after the 3-month waiting period.339 Rarely, pharmacological therapy and attempts at rhythm control with antiarrhythmic drug therapy fail to adequately control atrial flutter during the 3 months after AF ablation. In this situation, early repeat ablation is warranted.
7.3. Acute Treatment: Recommendations
7.4. Ongoing Management: Recommendations
8. Junctional Tachycardia
Junctional tachycardia is a rapid, occasionally irregular, narrow-complex tachycardia (with rates typically of 120 bpm to 220 bpm) (Figure 20). AV dissociation (often isorhythmic) may be seen, and when present, excludes the misdiagnosis of AVRT and makes AVNRT highly unlikely. Other SVTs are often misdiagnosed and misclassified as junctional tachycardia because of the frequent absence of demonstrable P waves in reentrant rhythms. Furthermore, when 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).388
Junctional tachycardia is uncommon in adults388; 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. Adults with junctional tachycardia typically have a relatively benign course, whereas infants and children with acquired or congenital junctional tachycardia have a high rate of death due to heart failure or an uncontrollable, incessant tachyarrhythmia.
There are data to support the use of beta blockers, diltiazem, flecainide, procainamide, propafenone, and verapamil for the treatment of junctional tachycardia (see recommendations and references in Sections 8.1 and 8.2). The efficacy of amiodarone has been reported only in pediatric patients.389,390 Digoxin has not been well established as chronic therapy for junctional tachycardia.
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 toxicity391 or myocardial infarction.392,393 Treatment of this rhythm centers on addressing the underlying condition. In addition, there is some evidence that beta blockers,394 intravenous adenosine, or verapamil395 can terminate an accelerated junctional arrhythmia. A transient junction rhythm may be seen after slow-pathway ablation for AVNRT.396
8.1. Acute Treatment: Recommendations
8.2. Ongoing Management: Recommendations
9. Special Populations
As discussed in the Scope (Section 1.4), the present document is aimed at the adult population (≥18 years of age) and offers no specific recommendations for pediatric patients. Nevertheless, a brief discussion of SVT in pediatric patients is included below, highlighting major considerations with regard to SVT in younger patients, including adolescent patients.
SVT in young patients varies significantly from SVT in adult patients in terms of mechanism, risk of developing heart failure or cardiac arrest, risks associated with interventional therapy, natural history, and psychosocial impact. Approximately half of pediatric SVT presents in the first 4 months of life, with age-related peaks in occurrence subsequently at 5 to 8 years and after 13 years. Accessory pathway–mediated tachycardia accounts for >70% of SVT in infants, decreasing to approximately 55% in adolescents.56,407–409 AVNRT increases with age, from 9% to 13% of SVT in infants, to 30% to 50% of SVT in teenagers. After 12 years of age, women are more likely to have AVNRT than men, and overall SVT is less frequent among African American and Hispanic patients than in the general pediatric population.56 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. Symptoms of SVT vary with age: gastrointestinal or respiratory findings in infants, chest or abdominal pain in the younger child, and palpitations in the adolescent. 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.410
Pre-excitation is present in 20% to 35% of children with SVT. 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.60,254–257 The risk of cardiac arrest is higher in patients with AVRT precipitating AF, short accessory connection refractory periods, and posteroseptal accessory pathways.60,254–257 Notably, the absence of prior symptoms does not preclude risk because cardiac arrest may be the initial manifestation of pre-excitation.254,257,411 Risk stratification, such as with ambulatory 24-hour monitoring or treadmill exercise testing, is often considered for children with pre-excitation to assess persistence of pre-excitation.412
Pharmacological therapy of SVT in childhood is largely based on practice patterns because RCTs of antiarrhythmic medications in children are lacking. AV nodal–blocking drugs are widely used for the most common arrhythmias, AVRT, and AVNRT. Higher initial doses of adenosine are needed in children than in adults, with children receiving from 150 mcg/kg to 250 mcg/kg.413–415 Digoxin and propranolol have similar efficacy in infants with SVT without pre-excitation.416 Digoxin is avoided in the presence of pre-excitation because its use in infancy has been associated with SCD or ventricular fibrillation.417,418 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, ischemic heart disease, or ventricular dysfunction, flecainide is not used as a first-line medication in children.419
Catheter ablation can be successfully performed in children of all ages, with acute success rates comparable to those reported in adults.281,282,420,421 Success rates are influenced by the presence of structural heart disease or ischemic heart disease and are highest in left-sided accessory pathways and lowest for AT. 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.281,420–422 The implications of complications, including AV block requiring pacing, perforation, and coronary artery or mitral valve injury, are profound in young patients.423–425 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.426 Increased institutional experience, advanced mapping techniques, and use of cryoablation have reduced the incidence of complications, as well as the radiation exposure associated with the procedure. 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. Recurrence rates for SVT after successful procedures are higher than reported in large adult series, ranging from 7% to 17%; whether this reflects technical differences, natural history, or more long-term follow-up is unclear.427–429 Recurrence is highest among right-sided accessory pathways, particularly anteroseptal or multiple pathways, and in AT in the setting of complex congenital heart disease.427–429
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.130 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.130 Postoperative junctional tachycardia occurs in 2% to 10% of young patients undergoing intracardiac surgery, particularly for ventricular or AV septal defects, tetralogy of Fallot, transposition of the great arteries, and Norwood procedures.430,431 Treatment includes sedation with muscle relaxation, limitation of inotropic medications, reduction of core temperature to 34 to 35°C, atrial overdrive pacing, and procainamide or amiodarone infusions.416,432–435 In general, postoperative junctional tachycardia resolves and does not require ongoing therapy.
Although this guideline focuses on adults, it should be noted that SVT may occur in the fetus and, if sustained, may put the fetus at risk of cardiovascular collapse manifested by hydrops. Mothers require safety monitoring by adult cardiologists during treatment. The most common mechanisms for fetal SVT are AVRT and atrial flutter.436 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. Flecainide, sotalol, and digoxin, alone or in combination, have demonstrated arrhythmia termination rates of 60% to 90%, depending on whether hydrops is present.437,438 In cases refractory to the aforementioned drugs, maternal oral loading for 2 to 7 days with amiodarone may prove lifesaving.439 Treatment of fetal SVT has provided safety data for treatment of arrhythmias in women during pregnancy, as addressed in Section 9.3.
9.2. Patients With Adult Congenital Heart Disease
See Figure 22 for the algorithm for acute treatment of non–pre-excited SVT in adult congenital heart disease (ACHD) patients; and Figure 23 for the algorithm for ongoing management of non–pre-excited SVT in ACHD patients.
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.440–444 The most common mechanism of SVT in ACHD patients is macroreentrant AT (also called flutter), which accounts for at least 75% of SVT and frequently involves the CTI. Focal AT, AVNRT, and accessory pathway–mediated tachycardia each account for less than about 8% of SVT, whereas the incidence of AF is about 10% and increases with age.133,445–449 AT occurs in 20% to 45% of adults with Ebstein anomaly, single-ventricle/Fontan procedures, tetralogy of Fallot, transposition of the great arteries, and atrial septal defects.449–451
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. The ventricular rate during SVT may be slowed because of variable AV conduction, which can result in a delay in recognizing tachycardia and the development of congestive failure. Recognition of severe forms of congenital heart disease, including unrepaired or palliated defects, cyanotic heart disease, single or systemic right ventricles, or Ebstein anomaly, is essential to decision making during SVT treatment. In certain conditions, the presence of cyanosis or severe ventricular dysfunction requires consideration of high-risk cardioversion with resuscitation measures at hand; usually, this decision is made at centers with specialized expertise. Management of ACHD patients should be undertaken only in collaboration with a cardiologist who has specialized training or experience in managing such patients.
RCTs assessing antiarrhythmic medication efficacy are lacking. Beta-blocking medications offer the advantages of outpatient medication initiation and may provide protection from tachycardia-mediated hypotension or ischemia. Risks of proarrhythmia are increased with the use of sotalol, ibutilide, dofetilide, and particularly flecainide and require in-hospital initiation. Flecainide is associated with increased risk of SCD419 and is reserved for patients without ventricular dysfunction who do not respond to other therapy. Sinus node dysfunction may contribute to the development of atrial arrhythmias and may become exacerbated with antiarrhythmic medications. Atrial antibradycardia pacing to maintain a consistent physiological heart rate may decrease the frequency of tachycardia episodes and may improve functional capacity.364,370,371 Atrial antitachycardia pacing to terminate atrial reentry tachycardia is an effective approach when feasible.364,370,371
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.452–457 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. Because the CTI is involved in >60% of atrial reentry circuits, an initial strategy targeting this region is often used. Highest success rates are achieved in patients with atrial septal defects, approaching 90% to 100%, although subsequent AF has been reported in 11% to 30% of patients within 3 years.330,449,458 Because of the need for sophisticated knowledge of anatomy, advanced mapping capability, cardiac anesthesia with careful periprocedural monitoring, and repeat ablations, such patients should be referred to centers with extensive experience in complex congenital heart disease ablations.
The development of atrial arrhythmias in ACHD patients is often an indicator of progressive hemodynamic changes, which require in-depth functional and hemodynamic assessment. Intervention for residual hemodynamic/structural defects may need to be planned as part of chronic arrhythmia management. Patients with Ebstein anomaly or repaired tetralogy of Fallot may have significant pulmonary regurgitation, tricuspid regurgitation, or both, which might benefit from reoperation. In some settings, integration of operative ablation techniques with hemodynamic repair may be optimal.
9.2.2. Acute Treatment: Recommendations
9.2.3. Ongoing Management: Recommendations
Pregnancy may confer an increased susceptibility to a variety of arrhythmias, even in the absence of underlying heart disease.513 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.514 An important consideration is that adverse maternal and fetal outcomes have been reported as a result of SVT in pregnancy.515 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. Experience with use of drugs in pregnancy also comes from treating a variety of maternal and fetal conditions, not maternal SVT alone. Although all medications have potential side effects to both the mother and the fetus at any stage of pregnancy, if possible, drugs should be avoided in the first trimester, when risk of congenital malformations is greatest. The lowest recommended dose should be used initially, accompanied by regular monitoring of clinical response.
9.3.1. Acute Treatment: Recommendations
9.3.2. Ongoing Management: Recommendations
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.49 Atypical atrial flutter and macroreentrant AT are on the rise as consequences of increasing AF ablation in this patient population, yet there are limited outcome data from RCTs for this segment of the population. Therapeutic decisions should be balanced between the overall risks and benefits of the invasive nature of ablation versus long-term commitment to pharmacological therapy.
10. Quality-of-Life Considerations
Patients with SVT may experience recurring symptoms that negatively impact their quality of life. Episodes of tachycardia can cause lightheadedness and syncope, which can become an obstacle to the performance of usual activities of daily living (eg, driving).72 However, there are minimal data on the effect of treatment on the quality of life for patients with SVT. In 1 study that evaluated patients with SVT who underwent ablation or received medical therapy, questionnaires such as the 36-Item Short-Form Health Survey revealed improved quality-of-life scores in several categories, including physical role functioning (perceived disability from physical limitations), general health perceptions (perceived physical and mental health), and emotional role functioning (perceived disability from emotional limitations).540 These improvements, measured at 1 to 5 years of follow-up, were greater in patients who underwent ablation than in those treated with medical therapy. Other literature, using domains from the 36-Item Short-Form Health Survey541–543 and other quality- of-life questionnaires,544–546 suggests that quality of life is improved after ablation for PSVT. However, these data carry important limitations, particularly a lack of an appropriate control group, small sample sizes, and referral bias. Furthermore, patients affected by PSVT carry different experiences. Therefore, firm conclusions cannot be drawn about the effect on quality of life provided by medical or ablation therapy, and no recommendations are provided.
See Online Data Supplement 22 for additional data on quality-of-life considerations.
Given the rising costs of health care, there is a growing enthusiasm for incorporating economic appraisals of available therapies and resources into guidelines. The “2014 ACC/AHA Statement on Cost/Value Methodology in Clinical Practice Guidelines and Performance Measures”6 called for development of Level of Value categories to accompany COR and LOE in future guidelines. Although basing recommendations on a cost-effectiveness approach to therapy is an important goal for the current and future healthcare economy, it also poses considerable challenges. For example, the cost of therapy, available technology, and practice patterns are highly dynamic, and there may be some cost associated with unintended harm or complications that result from any intervention. Furthermore, the approach toward evaluating the burden of cost in the literature is based on varied perspectives (eg, individual, third party, stakeholder, societal).
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.105 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.547
These studies, along with other older literature, favor catheter ablation over medical therapy as the more cost-effective approach to treating PSVT and atrial flutter. However, the results of these studies were based on cost data and practice patterns that do not apply to the current environment and practice. Therefore, no recommendations are provided.
See Online Data Supplement 23 for additional data on cost-effectiveness.
12. Shared Decision Making
It is important that the patient be included in clinical decision-making processes, with consideration of his/her preferences and goals for therapy, as well as his/her unique physical, psychological, and social situation. In selected cases, personalized, self-directed interventions can be developed in partnership with the patient, such as vagal maneuvers and “pill-in-the-pocket” drug therapy.
Shared decision making is especially important for patients with SVT. As seen in this guideline, SVT treatment can be nuanced and requires expert knowledge of EP processes and treatment options. Treatment options are highly specific to the exact type of arrhythmia and can depend on certain characteristics of a particular arrhythmia (eg, whether there is pre-excitation). 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. This involves a clear explanation of the risks and benefits of each recommendation, including how other comorbidities may impact each treatment option. Discussions with other physicians and healthcare providers caring for the patient will provide the broadest picture available. A full discussion about decisions for subsequent care and any further instructions is important to reinforce these issues before the patient leaves the healthcare setting. 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.
13. Evidence Gaps and Future Research Needs
SVTs, even with the exclusion of AF, are among the most common arrhythmias that require medical intervention. The decade before the publication of the “2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias”11 was characterized by major shifts in understanding of the mechanism for SVT, as well as a sea change in management (because of catheter ablation). Since the early 2000s, there have been many iterative but important advances in pharmacological and invasive management for SVT. Catheter ablation is even better established, with a high degree of success and low complication rate, especially for the most common types of SVT, such as AVNRT and AVRT. Drug options, on the other hand, are relatively unchanged since publication of the 2003 guideline, perhaps relating to ongoing concern about potential adverse side effects of antiarrhythmic agents.
Areas of uncertainty remain, including interventions for which advanced technology is less important. For example, vagal maneuvers are recommended in many circumstances as first-line intervention in patients with SVT, but they are often ineffective. Furthermore, there is great variation in the way these maneuvers are administered. Therefore, research on the best technique of vagal maneuvers, with dissemination of the findings, is necessary. Clinical trials on antiarrhythmic drugs for SVT have been limited, and data are often extrapolated from studies that primarily focused on management of patients with AF. The efficacy of a variety of drugs is likely to differ according to the tachycardia mechanism, and therefore differentiating the best drug for each individual arrhythmia is necessary; for example, the efficacy of class III agents might be markedly different in patients with AF than in patients with atrial flutter. Limited data exist on the optimal management of less common types of SVTs, such as junctional tachycardia and multifocal AT. Therefore, in view of significant gaps that remain with regard to optimal management of patients with SVT, we must consider the role of electronic medical records, registries, and national datasets to better acquire observational data when trials are not available or feasible. Multicenter registry studies would allow for expansion of our knowledge on the best pharmacological and nonpharmacological approaches to treat these arrhythmias. In collaboration with national societies, the National Institutes of Health, and the US Food and Drug Administration, registries could be developed across selected centers to gather important information on safety and long-term outcomes where data are lacking (just as such registries are being developed for AF ablation). Mandatory postmarket surveillance data collection on new drugs for SVT could also be considered by the US Food and Drug Administration as a condition for drug approval.
The mechanism and primary etiology of IST remains to be defined—advances here would provide a first step on finding better therapies for this disorder. It should be noted that medical advances have resulted in an increase in the number of patients with SVT in specific populations, such as in patients after ablation (especially AF), ACHD patients, and patients of advanced age. As the numbers of these often-complicated patients grow, opportunities arise to perform clinical research to guide future recommendations.
New pharmacological therapies are needed, especially for SVT in patients for whom ablation is not an option or has been unsuccessful. Newer drugs that selectively target atrial channels currently under investigation for patients with AF should be investigated for management of AT. Both mapping and ablation techniques need to be further investigated to maximize the likelihood of successful ablation with minimal risk. In the outpatient setting, the added value of new personal monitoring and implantable devices needs to be assessed, and studies of the impact of shared decision making with patients on outcomes are needed for personal monitoring innovations. Finally, we encourage investigation of quality-of-life improvement strategies, in addition to cost-effectiveness studies, for the management of SVT.
Presidents and Staff
American College of Cardiology
Kim A. Williams, Sr, MD, FACC, FAHA, President
Shalom Jacobovitz, Chief Executive Officer
William J. Oetgen, MD, MBA, FACC, Executive Vice President, Science, Education, and Quality
Amelia Scholtz, PhD, Publications Manager, Science, Education, and Quality
American College of Cardiology/American Heart Association
Lisa Bradfield, CAE, Director, Guidelines and Clinical Policy
Abdul R. Abdullah, MD, Associate Science and Medicine Advisor
Alexa Papaila, Project Manager, Science and Clinical Policy
American Heart Association
Mark A. Creager, MD, FACC, FAHA, President
Nancy Brown, Chief Executive Officer
Rose Marie Robertson, MD, FAHA, Chief Science Officer
Gayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice President, Office of Science Operations
Marco Di Buono, PhD, Vice President, Science, Research, and Professional Education
Jody Hundley, Production Manager, Scientific Publications, Office of Science Operations
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.
This document was approved by the American College of Cardiology Board of Trustees and Executive Committee, the American Heart Association Science Advisory and Coordinating Committee, and the Heart Rhythm Society Board of Trustees in August 2015 and the American Heart Association Executive Committee in September 2015.
The Author Comprehensive Relationships Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000311/-/DC1.
The Data Supplement files are available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000311/-/DC2.
The American Heart Association requests that this document be cited as follows: Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NAM 3rd, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen W-K, Tracy CM, Al-Khatib SM. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2016;133;e506-e574. doi: 10.1161/CIR.0000000000000311.
This article has been copublished in the Journal of the American College of Cardiology and HeartRhythm Journal.
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- © 2016 by the American College of Cardiology Foundation, the American Heart Association, Inc., and the Heart Rhythm Society.
- 1.↵Committee on Standards for Developing Trustworthy Clinical Practice Guidelines, Institute of Medicine (US). Clinical Practice Guidelines We Can Trust. Washington, DC: National Academies Press, 2011.
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