2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary
2015; Lippincott Williams & Wilkins; Volume: 133; Issue: 14 Linguagem: Inglês
10.1161/cir.0000000000000310
ISSN1524-4539
AutoresRichard L. Page, José A. Joglar, Mary A. Caldwell, Hugh Calkins, Jamie B. Conti, Barbara J. Deal, N.A. Mark Estes, Michael E. Field, Zachary D. Goldberger, Stephen C. Hammill, Julia H. Indik, Bruce D. Lindsay, Brian Olshansky, Andrea M. Russo, Win-Kuang Shen, Cynthia M. Tracy, Sana M. Al‐Khatib,
Tópico(s)Atrial Fibrillation Management and Outcomes
ResumoHomeCirculationVol. 133, No. 142015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUB2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive SummaryA Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society Richard L. Page, MD, FACC, FAHA, FHRS, Chair José A. Joglar, MD, FACC, FAHA, FHRS, Vice Chair Mary A. Caldwell, RN, MBA, PhD, FAHA Hugh Calkins, MD, FACC, FAHA, FHRS Jamie B. Conti, MD, FACC Barbara J. Deal, MD N.A. Mark EstesIII, MD, FACC, FAHA, FHRS Michael E. Field, MD, FACC, FHRS Zachary D. Goldberger, MD, MS, FACC, FAHA, FHRS Stephen C. Hammill, MD, FACC, FHRS Julia H. Indik, MD, PhD, FACC, FAHA, FHRS Bruce D. Lindsay, MD, FACC, FHRS Brian Olshansky, MD, FACC, FAHA, FHRS Andrea M. Russo, MD, FACC, FHRS Win-Kuang Shen, MD, FACC, FAHA, FHRS Cynthia M. Tracy, and MD, FACC Sana M. Al-KhatibMD, MHS, FACC, FAHA, FHRSEvidence Review Committee Chair‡ Richard L. PageRichard L. Page , José A. JoglarJosé A. Joglar , Mary A. CaldwellMary A. Caldwell , Hugh CalkinsHugh Calkins *, †, ‡, §, ‖, ¶ , Jamie B. ContiJamie B. Conti *, †, ‡, §, ‖, ¶ , Barbara J. DealBarbara J. Deal *, †, ‡, §, ‖, ¶ , N.A. Mark EstesIIIN.A. Mark EstesIII *, †, ‡, §, ‖, ¶ , Michael E. FieldMichael E. Field *, †, ‡, §, ‖, ¶ , Zachary D. GoldbergerZachary D. Goldberger *, †, ‡, §, ‖, ¶ , Stephen C. HammillStephen C. Hammill *, †, ‡, §, ‖, ¶ , Julia H. IndikJulia H. Indik *, †, ‡, §, ‖, ¶ , Bruce D. LindsayBruce D. Lindsay *, †, ‡, §, ‖, ¶ , Brian OlshanskyBrian Olshansky *, †, ‡, §, ‖, ¶ , Andrea M. RussoAndrea M. Russo *, †, ‡, §, ‖, ¶ , Win-Kuang ShenWin-Kuang Shen *, †, ‡, §, ‖, ¶ , Cynthia M. TracyCynthia M. Tracy *, †, ‡, §, ‖, ¶ , and Sana M. Al-KhatibSana M. Al-Khatib and Evidence Review Committee Chair‡ Originally published23 Sep 2015https://doi.org/10.1161/CIR.0000000000000310Circulation. 2016;133:e471–e505is corrected byCorrection to: 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm SocietyOther version(s) of this articleYou are viewing the most recent version of this article. Previous versions: September 23, 2015: Previous Version 1 Table of ContentsPreamble e472Introduction e4731.1. Methodology and Evidence Review e4731.2. Organization of the GWC e4731.3. Document Review and Approval e4741.4. Scope of the Guideline e474General Principles e4752.1. Mechanisms and Definitions e4752.2. Epidemiology, Demographics, and Public Health Impact e4752.3. Evaluation of the Patient With Suspected or Documented SVT e4762.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms e4762.3.2. Evaluation of the ECG e4772.4. Principles of Medical Therapy e4782.4.1. Acute Treatment: Recommendations e4782.4.2. Ongoing Management: Recommendations e4792.5. Basic Principles of Electrophysiological Study, Mapping, and Ablation e479Sinus Tachyarrhythmias e4803.1. Physiological Sinus Tachycardia e4803.2. Inappropriate Sinus Tachycardia e4803.2.1. Acute Treatment e4803.2.2. Ongoing Management: Recommendations e480Nonsinus Focal Atrial Tachycardia and MAT e4814.1. Focal Atrial Tachycardia e4814.1.1. Acute Treatment: Recommendations e4814.1.2. Ongoing Management: Recommendations e4824.2. Multifocal Atrial Tachycardia e4824.2.1. Acute Treatment: Recommendation e4824.2.2. Ongoing Management: Recommendations e482Atrioventricular Nodal Reentrant Tachycardia e4825.1. Acute Treatment: Recommendations e4825.2. Ongoing Management: Recommendations e483Manifest and Concealed Accessory Pathways e4836.1. Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways e4846.1.1. Acute Treatment: Recommendations e4846.1.2. Ongoing Management: Recommendations e4846.2. Management of Asymptomatic Pre-Excitation e4846.2.1. PICOTS Critical Questions e4846.2.2. Asymptomatic Patients With Pre-Excitation: Recommendations e4856.3. Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations e485Atrial Flutter e4857.1. Cavotricuspid Isthmus-Dependent Atrial Flutter e4857.2. Non–Isthmus-Dependent Atrial Flutters e4867.3. Acute Treatment: Recommendations e4867.4. Ongoing Management: Recommendations e487Junctional Tachycardia e4878.1. Acute Treatment: Recommendations e4878.2. Ongoing Management: Recommendations e487Special Populations e4879.1. Pediatrics e4879.2. Patients With Adult Congenital Heart Disease e4899.2.1. Clinical Features e4899.2.2. Acute Treatment: Recommendations e4909.2.3. Ongoing Management: Recommendations e4909.3. Pregnancy e4909.3.1. Acute Treatment: Recommendations e4909.3.2. Ongoing Management: Recommendations e4919.4. SVT in Older Populations e4919.4.1. Acute Treatment and Ongoing Management: Recommendation e491Quality-of-Life Considerations e491Cost-Effectiveness e491Shared Decision Making e491References e492Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e501Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) e502PreambleSince 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.4Intended UsePractice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations may have a broader target. Although guidelines may inform regulatory or payer decisions, they are intended to improve quality of care in the interest of patients.Evidence ReviewGuideline 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 TherapyThe 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 EvidenceThe 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.Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care*Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care*Relationships With Industry and Other EntitiesThe 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 ComorbiditiesManaging patients with multiple conditions can be complex, especially when recommendations applicable to coexisting illnesses are discordant or interacting.8 The guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances. The recommendations should not replace clinical judgment.Clinical ImplementationManagement 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.PolicyThe 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.3,5The reader is encouraged to consult the full-text guideline9 for additional guidance and details with regard to SVT because the executive summary contains limited information.Jonathan L. Halperin, MD, FACC, FAHAChair, ACC/AHA Task Force on Clinical Practice Guidelines1. Introduction1.1. Methodology and Evidence ReviewThe recommendations listed in this guideline are, whenever possible, evidence based. An extensive evidence review was conducted in April 2014 that included literature published through September 2014. Other selected references published through May 2015 were incorporated by the GWC. Literature included was derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. The relevant search terms and data are included in evidence tables in the Online Data Supplement. Additionally, the GWC reviewed documents related to supraventricular tachycardia (SVT) previously published by the ACC, AHA, and Heart Rhythm Society (HRS). References selected and published in this document are representative and not all-inclusive.An independent ERC was commissioned to perform a systematic review of key clinical questions, the results of which were considered by the GWC for incorporation into this guideline. The systematic review report on the management of asymptomatic patients with Wolff-Parkinson-White (WPW) syndrome is published in conjunction with this guideline.101.2. Organization of the GWCThe 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 ApprovalThis 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 GuidelineThe purpose of this joint ACC/AHA/HRS document is to provide a contemporary guideline for the management of adults with all types of SVT other than atrial fibrillation (AF). Although AF is, strictly speaking, an SVT, the term SVT generally does not refer to AF. AF is addressed in the 2014 ACC/AHA/HRS Guideline for the Management of Atrial Fibrillation (2014 AF guideline).11 The present guideline addresses other SVTs, including regular narrow–QRS complex tachycardias, as well as other, irregular SVTs (eg, atrial flutter with irregular ventricular response and multifocal atrial tachycardia [MAT]). This guideline supersedes the "2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias."12 Although this document is aimed at the adult population (≥18 years of age) and offers no specific recommendations for pediatric patients, as per the reference list, we examined literature that included pediatric patients. In some cases, the data from noninfant pediatric patients helped inform this guideline.2. General Principles2.1. Mechanisms and DefinitionsFor the purposes of this guideline, SVT is defined as per Table 2, which provides definitions and the mechanism(s) of each type of SVT. The term SVT does not generally include AF, and this document does not discuss the management of AF.Table 2. Relevant Terms and DefinitionsArrhythmia/TermDefinitionSupraventricular tachycardia (SVT)An umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of 100 bpm at rest), the mechanism of which involves tissue from the His bundle or above. These SVTs include inappropriate sinus tachycardia, AT (including focal and multifocal AT), macroreentrant AT (including typical atrial flutter), junctional tachycardia, AVNRT, and various forms of accessory pathway-mediated reentrant tachycardias. In this guideline, the term does not include AF.Paroxysmal supraventricular tachycardia (PSVT)A clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination. These features are characteristic of AVNRT or AVRT, and, less frequently, AT. PSVT represents a subset of SVT.Atrial fibrillation (AF)A supraventricular arrhythmia with uncoordinated atrial activation and, consequently, ineffective atrial contraction. ECG characteristics include: 1) irregular atrial activity, 2) absence of distinct P waves, and 3) irregular R-R intervals (when atrioventricular conduction is present). AF is not addressed in this document.Sinus tachycardiaRhythm arising from the sinus node in which the rate of impulses exceeds 100 bpm. • Physiologic sinus tachycardiaAppropriate increased sinus rate in response to exercise and other situations that increase sympathetic tone. • Inappropriate sinus tachycardiaSinus heart rate >100 bpm at rest, with a mean 24-h heart rate >90 bpm not due to appropriate physiological responses or primary causes such as hyperthyroidism or anemia.Atrial tachycardia (AT) • Focal ATAn SVT arising from a localized atrial site, characterized by regular, organized atrial activity with discrete P waves and typically an isoelectric segment between P waves. At times, irregularity is seen, especially at onset ("warm-up") and termination ("warm-down"). Atrial mapping reveals a focal point of origin. • Sinus node reentry tachycardiaA specific type of focal AT that is due to microreentry arising from the sinus node complex, characterized by abrupt onset and termination, resulting in a P-wave morphology that is indistinguishable from sinus rhythm. • Multifocal atrial tachycardia (MAT)An irregular SVT characterized by ≥3 distinct P-wave morphologies and/or patterns of atrial activation at different rates. The rhythm is always irregular.Atrial flutter • Cavotricuspid isthmus–dependent atrial flutter: typicalMacroreentrant AT propagating around the tricuspid annulus, proceeding superiorly along the atrial septum, inferiorly along the right atrial wall, and through the cavotricuspid isthmus between the tricuspid valve annulus and the Eustachian valve and ridge. This activation sequence produces predominantly negative "sawtooth" flutter waves on the ECG in leads 2, 3, and aVF and a late positive deflection in V1. The atrial rate can be slower than the typical 300 bpm (cycle length 200 ms) in the presence of antiarrhythmic drugs or scarring. It is also known as "typical atrial flutter" or "cavotricuspid isthmus–dependent atrial flutter" or "counterclockwise atrial flutter." • Cavotricuspid isthmus–dependent atrial flutter: reverse typicalMacroreentrant AT that propagates around in the direction reverse that of typical atrial flutter. Flutter waves typically appear positive in the inferior leads and negative in V1. This type of atrial flutter is also referred to as "reverse typical" atrial flutter or "clockwise typical atrial flutter." • Atypical or non–cavotricuspid isthmus–dependent atrial flutterMacroreentrant ATs that do not involve the cavotricuspid isthmus. A variety of reentrant circuits may include reentry around the mitral valve annulus or scar tissue within the left or right atrium. A variety of terms have been applied to these arrhythmias according to the reentry circuit location, including particular forms, such as "LA flutter" and "LA macroreentrant tachycardia" or incisional atrial reentrant tachycardia due to reentry around surgical scars.Junctional tachycardiaA nonreentrant SVT that arises from the AV junction (including the His bundle).Atrioventricular nodal reentrant tachycardia (AVNRT)A reentrant tachycardia involving 2 functionally distinct pathways, generally referred to as "fast" and "slow" pathways. Most commonly, the fast pathway is located near the apex of Koch's triangle, and the slow pathway inferoposterior to the compact AV node tissue. Variant pathways have been described, allowing for "slow-slow" AVNRT. • Typical AVNRTAVNRT in which a slow pathway serves as the anterograde limb of the circuit and the fast pathway serves as the retrograde limb (also called "slow-fast AVNRT"). • Atypical AVNRTAVNRT in which the fast pathway serves as the anterograde limb of the circuit and a slow pathway serves as the retrograde limb (also called "fast-slow AV node reentry") or a slow pathway serves as the anterograde limb and a second slow pathway serves as the retrograde limb (also called "slow-slow AVNRT").Accessory pathwayFor the purpose of this guideline, an accessory pathway is defined as an extranodal AV pathway that connects the myocardium of the atrium to the ventricle across the AV groove. Accessory pathways can be classified by their location, type of conduction (decremental or nondecremental), and whether they are capable of conducting anterogradely, retrogradely, or in both directions. Of note, accessory pathways of other types (such as atriofascicular, nodo-fascicular, nodo-ventricular, and fasciculoventricular pathways) are uncommon and are discussed only briefly in this document (Section 7). • Manifest accessory pathwaysA pathway that conducts anterogradely to cause ventricular pre-excitation pattern on the ECG. • Concealed accessory pathwayA pathway that conducts only retrogradely and does not affect the ECG pattern during sinus rhythm. • Pre-excitation patternAn ECG pattern reflecting the presence of a manifest accessory pathway connecting the atrium to the ventricle. Pre-excited ventricular activation over the accessory pathway competes with the anterograde conduction over the AV node and spreads from the accessory pathway insertion point in the ventricular myocardium. Depending on the relative contribution from ventricular activation by the normal AV nodal/His Purkinje system versus the manifest accessory pathway, a variable degree of pre-excitation, with its characteristic pattern of a short P-R interval with slurring of the initial upstroke of the QRS complex (delta wave), is observed. Pre-excitation can be intermittent or not easily appreciated for some pathways capable of anterograde conduction; this is usually associated with a low-risk pathway, but exceptions occur. • Asymptomatic pre-excitation (isolated pre-excitation)The abnormal pre-excitation ECG pattern in the absence of documented SVT or symptoms consistent with SVT. • Wolff-Parkinson-White (WPW) syndromeSyndrome characterized by documented SVT or symptoms consistent with SVT in a patient with ventricular pre-excitation during sinus rhythm.Atrioventricular reentrant tachycardia (AVRT)A reentrant tachycardia, the electrical pathway of which requires an accessory pathway, the atrium, atrioventricular node (or second accessory pathway), and ventricle. • Orthodromic AVRTAn AVRT in which the reentrant impulse uses the accessory pathway in the retrograde direction from the ventricle to the atrium, and the AV node in the anterograde direction. The QRS complex is generally narrow or may be wide because of pre-existing bundle-branch block or aberrant conduction. • Antidromic AVRTAn AVRT in which the reentrant impulse uses the accessory pathway in the anterograde direction from the atrium to the ventricle, and the AV node for the retrograde direction. Occasionally, instead of the AV node, another accessory pathway can be used in the retrograde direction, which is referred to as pre-excited AVRT. The QRS complex is wide (maximally pre-excited).Permanent form of junctional reciprocating tachycardia (PJRT)A rare form of nearly incessant orthodromic AVRT involving a slowly conducting, concealed, usually posteroseptal accessory pathway.Pre-excited AFAF with ventricular pre-excitation caused by conduction over ≥1 accessory pathway(s).AF indicates atrial fibrillation; AT, atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; bpm, beats per minute; ECG, electrocardiogram/electrocardiographic; LA, left atrial; MAT, multifocal atrial tachycardia; PJRT, permanent form of junctional reciprocating tachycardia; PSVT, paroxysmal supraventricular tachycardia; SVT, supraventricular tachycardia; and WPW, Wolff-Parkinson-White.2.2. Epidemiology, Demographics, and Public Health ImpactThe best available evidence indicates that the prevalence of SVT in the general population is 2.29 per 1000 persons.13 When adjusted by age and sex in the US population, the incidence of paroxysmal supraventricular tachycardia (PSVT) is estimated to be 36 per 100 000 persons per year.13 There are approximately 89 000 new cases per year and 570 000 persons with PSVT.13 Compared with patients with cardiovascular disease, those with PSVT without any cardiovascular disease are younger (37 versus 69 years; P=0.0002) and have faster PSVT (186 versus 155 bpm; P=0.0006). Women have twice the risk of men of developing PSVT.13 Individuals >65 years of age have >5 times the risk of younger persons of developing PSVT.13Atrioventricular nodal reentrant tachycardia (AVNRT) is more common in persons who are middle-aged or older, whereas in adolescents the prevalence may be more balanced between atrioventricular reentrant tachycardia (AVRT) and AVNRT, or AVRT may be more prevalent.13 The relative frequency of tachycardia mediated by an accessory pathway decreases with age. The incidence of manifest pre-excitation or WPW pattern on electrocardiogram/electrocardiographic (ECG) tracings in the general population is 0.1% to 0.3%. However, not all patients with manifest ventricular pre-excitation develop PSVT.14–162.3. Evaluation of the Patient With Suspected or Documented SVT2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of SymptomsThe diagnosis of SVT is often made in the emergency department, but it is common to elicit symptoms suggestive of SVT before initial electrocardiographic documentation. SVT symptom onset often begins in adulthood; in one study in adults, the mean age of symptom onset was 32±18 years of age for AVNRT, versus 23±14 years of age for AVRT.17 In contrast, in a study conducted in pediatric populations, the mean ages of symptom onset of AVRT and AVNRT were 8 and 11 years, respectively.18 In comparison with AVRT, patients with AVNRT are more likely to be female, with an age of onset >30 years.16,19–21SVT has an impact on quality of life, which varies according to the frequency of episodes, the duration of SVT, and whether symptoms occur not only with exercise but also at rest.18,22 In 1 retrospective study in which the records of patients <21 years of age with WPW pattern on the ECG were reviewed, 64% of patients had symptoms at presentation, and an additional 20% developed symptoms during follow-up.23 Modes of presentation included documented SVT in 38%, palpitations in 22%, chest pain in 5%, syncope in 4%, AF in 0.4%, and sudden cardiac death (SCD) in 0.2%.23 A confounding factor in diagnosing SVT is the need to differentiate symptoms of SVT from symptoms of panic and anxiety disorders or any condition of heightened awareness of sinus tachycardia (such as postural orthostatic tachycardia syndrome). When AVNRT and AVRT are compared, symptoms appear to differ substantially. Patients with AVNRT more frequently describe symptoms of "shirt flapping" or "neck pounding"19,24 that may be related to pulsatile reversed flow when the right atrium contracts against a closed tricuspid valve (cannon a-waves).True syncope is infrequent with SVT, but complaints of light-headedness are common. In patients with WPW syndrome, syncope should be taken seriously but is not necessarily associated with increased risk of SCD.25 The rate of AVRT is faster when AVRT is induced during exercise,26 yet the rate alone does not explain symptoms of near-syncope. Elderly patients with AVNRT are more prone to syncope or near-syncope than are younger patients, but the tachycardia rate is generally slower in the elderly.27,28In a study on the relationship of SVT with driving, 57% of patients with SVT experienced an episode while driving, and 24% of these considered it to be an obstacle to driving.29 This sentiment was most common in patients who had experienced syncope or near-syncope. Among patients who experienced SVT while driving, 77% felt fatigue, 50% had symptoms of near-syncope, and 14% experienced syncope. Women had more symptoms in each category.2.3.2. Evaluation of the ECGA 12-lead ECG obtained during tachycardia and during sinus rhythm may reveal the etiology of tachycardia. For the patient who describes prior, but not current, symptoms of palpitations, the resting ECG can identify pre-excitation that should prompt a referral to a cardiac electrophysiologist.For a patient presenting in SVT, the 12-lead ECG can potentially identify the arrhythmia mechanism (Figure 1). If the SVT is regular, this may represent AT with 1:1 conduction or an SVT that involves the atrioventricular (AV) node. Junctional tachycardias, which originate in the AV junction (including the His bundle), can be regular or irregular, with variable conduction to the atria. SVTs that involve the AV node as a required component of the tachycardia reentrant circuit include AVNRT (Section 6) and AVRT (Section 7). In these reentrant tachycardias, the retrogradely conducted P wave may be difficult to discern, especially if bundle-branch block is present. In typical AVNRT, atrial activation is nearly simultaneous with the QRS, so the terminal portion of the P wave is usually located at the end of the QRS complex, appearing as a narrow and negative deflection in the inferior leads (a pseudo S wave) and a slightly positive deflection at the end of the QRS complex in lead V1 (pseudo R′). In orthodromic AVRT (with anterograde conduction down the AV node), the P wave can usua
Referência(s)