Keywords
ACC/AHA Task Force Members
Glenn N. Levine, MD, FACC, FAHA, Chair
Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect
Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair
Sana M. Al-Khatib, MD, MHS, FACC, FAHA
Kim K. Birtcher, MS, PharmD, AACC
Biykem Bozkurt, MD, PhD, FACC, FAHA
Ralph G. Brindis, MD, MPH, MACC
Joaquin E. Cigarroa, MD, FACC
Lesley H. Curtis, PhD, FAHA
Lee A. Fleisher, MD, FACC, FAHA
Federico Gentile, MD, FACC
Samuel Gidding, MD, FAHA
Mark A. Hlatky, MD, FACC
John Ikonomidis, MD, PhD, FAHA
José Joglar, MD, FACC, FAHA
Susan J. Pressler, PhD, RN, FAHA
Duminda N. Wijeysundera, MD, PhD
Table of Contents
- Preamble ....................................................................e156
- 1.Introduction ...............................................................e159
- 1.1.Methodology and Evidence Review .................e159
- 1.2.Organization of the Writing Committee .............e159
- 1.3.Document Review and Approval ........................e159
- 1.4.Scope of the Guideline ........................................e159
- 1.1.
- 2.General Principles ......................................................e160
- 2.1.Definitions: Terms and Classification ................e160
- 2.2.Epidemiology and Demographics ......................e160
- 2.3.Initial Evaluation of Patients With Syncope..........e162
- 2.3.1.History and Physical Examination: Recommendation ........................................e162
- 2.3.2.Electrocardiography: Recommendation..............e163
- 2.3.3.Risk Assessment: Recommendations ..........e163
- 2.3.4.Disposition After Initial Evaluation: Recommendations .....................................e165
- 2.3.1.
- 2.1.
- 3.Additional Evaluation and Diagnosis ......................e167
- 3.1.Blood Testing: Recommendations ..................e167
- 3.2.Cardiovascular Testing: Recommendations .....e168
- 3.2.1.Cardiac Imaging: Recommendations .........e168
- 3.2.2.Stress Testing: Recommendation .............e169
- 3.2.3.Cardiac Monitoring: Recommendations......e169
- 3.2.4.In-Hospital Telemetry: Recommendation ......e171
- 3.2.5.Electrophysiological Study: Recommendations .......................................e171
- 3.2.6.Tilt-Table Testing: Recommendations.......e172
- 3.2.1.
- 3.3.Neurological Testing: Recommendations ........e173
- 3.3.1.Autonomic Evaluation: Recommendation.........e173
- 3.3.2.Neurological and Imaging Diagnostics: Recommendations .....................................e174
- 3.3.1.
- 3.1.
- 4.Management of Cardiovascular Conditions ............e175
- 4.1.Arrhythmic Conditions: Recommendations .....e175
- 4.1.1.Bradycardia: Recommendation .................e175
- 4.1.2.Supraventricular Tachycardia: Recommendations ...................................e175
- 4.1.3.Ventricular Arrhythmia: Recommendation...e176
- 4.1.1.
- 4.2.Structural Conditions: Recommendations .......e176
- 4.2.1.Ischemic and Nonischemic Cardiomyopathy: Recommendation ..........e176
- 4.2.2.Valvular Heart Disease: Recommendation........e176
- 4.2.3.Hypertrophic Cardiomyopathy: Recommendation .....................................e177
- 4.2.4.Arrhythmogenic Right Ventricular Cardiomyopathy: Recommendations .........e177
- 4.2.5.Cardiac Sarcoidosis: Recommendations.....e177
- 4.2.1.
- 4.3.Inheritable Arrhythmic Conditions: Recommendations ........................................e178
- 4.3.1.Brugada Syndrome: Recommendations......e178
- 4.3.2.Short-QT Syndrome: Recommendation.......e179
- 4.3.3.Long-QT Syndrome: Recommendations...........e179
- 4.3.4.Catecholaminergic Polymorphic Ventricular Tachycardia: Recommendations...............e180
- 4.3.5.Early Repolarization Pattern: Recommendations............................................e180
- 4.3.1.
- 4.1.
- 5.Reflex Conditions: Recommendations ...................e181
- 5.1.Vasovagal Syncope: Recommendations ...........e181
- 5.2.Pacemakers in Vasovagal Syncope: Recommendation .........................................e182
- 5.3.Carotid Sinus Syndrome: Recommendations .......e183
- 5.4.Other Reflex Conditions ..............................e183
- 5.1.
- 6.Orthostatic Hypotension: Recommendations .......e183
- 6.1.Neurogenic Orthostatic Hypotension: Recommendations .......................................e183
- 6.2.Dehydration and Drugs: Recommendations.......e185
- 6.1.
- 7.Orthostatic Intolerance .........................................e186
- 8.Pseudosyncope: Recommendations .....................e186
- 9.Uncommon Conditions Associated With Syncope ....e187
- 10.Age, Lifestyle, and Special Populations: Recommendations ...............................................e188
- 10.1.Pediatric Syncope: Recommendations ........e188
- 10.2.Adult Congenital Heart Disease: Recommendations .....................................e190
- 10.3.Geriatric Patients: Recommendations ........e191
- 10.4.Driving and Syncope: Recommendation ......e192
- 10.5.Athletes: Recommendations ......................e193
- 10.1.
- 11.Quality of Life and Healthcare Cost of Syncope .....e194
- 11.1.Impact of Syncope on Quality of Life .........e194
- 11.2.Healthcare Costs Associated With Syncope .....e194
- 11.1.
- 12.Emerging Technology, Evidence Gaps, and Future Directions ...............................................................e194
- 12.1.Definition, Classification, and Epidemiology...e194
- 12.2.Risk Stratification and Clinical Outcomes ....e194
- 12.3.Evaluation and Diagnosis ............................e195
- 12.4.Management of Specific Conditions ............e195
- 12.5.Special Populations ....................................e195
- 12.1.
- References ..............................................................e196
- Appendix 1.
- Author Relationships With Industry and Other Entities (Relevant) ......................................e210
- Appendix 2.
- Reviewer Relationships With Industry and Other Entities (Comprehensive) ............................e212
- Appendix 3.
- Abbreviations ......................................................e217
Preamble
Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines (guidelines) with recommendations to improve cardiovascular health. These guidelines, which are based on systematic methods to evaluate and classify evidence, provide a cornerstone for quality cardiovascular care. The ACC and AHA sponsor the development and publication of guidelines without commercial support, and members of each organization volunteer their time to the writing and review efforts. Guidelines are official policy of the ACC and AHA.
Intended Use
Practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular disease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organizations may have a global impact. Although guidelines may be used to inform regulatory or payer decisions, their intent is to improve patients’ quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances and should not replace clinical judgment.
Clinical Implementation
Guideline-recommended management is effective only when followed by healthcare providers and patients. Adherence to recommendations can be enhanced by shared decision making between healthcare providers and patients, with patient engagement in selecting interventions based on individual values, preferences, and associated conditions and comorbidities.
Methodology and Modernization
The ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) continuously reviews, updates, and modifies guideline methodology on the basis of published standards from organizations including the Institute of Medicine
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and on the basis of internal re-evaluation. Similarly, the presentation and delivery of guidelines are re-evaluated and modified on the basis of evolving technologies and other factors to facilitate optimal dissemination of information at the point of care to healthcare professionals. Given time constraints of busy healthcare providers and the need to limit text, the current guideline format delineates that each recommendation be supported by limited text (ideally, <250 words) and hyperlinks to supportive evidence summary tables. Ongoing efforts to further limit text are underway. Recognizing the importance of cost-value considerations in certain guidelines, when appropriate and feasible, an analysis of the value of a drug, device, or intervention may be performed in accordance with the ACC/AHA methodology.3
- Anderson J.L.
- Heidenreich P.A.
- Barnett P.G.
- et al.
ACC/AHA statement on cost/value methodology in clinical practice guidelines and performance measures: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures and Task Force on Practice Guidelines.
J Am Coll Cardiol. 2014; 63: 2304-2322
To ensure that guideline recommendations remain current, new data are reviewed on an ongoing basis, with full guideline revisions commissioned in approximately 6-year cycles. Publication of new, potentially practice-changing study results that are relevant to an existing or new drug, device, or management strategy will prompt evaluation by the Task Force, in consultation with the relevant guideline writing committee, to determine whether a focused update should be commissioned. For additional information and policies regarding guideline development, we encourage readers to consult the ACC/AHA guideline methodology manual
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and other methodology articles.5
, - Halperin J.L.
- Levine G.N.
- Al-Khatib S.M.
- et al.
Further evolution of the ACC/AHA clinical practice guideline recommendation classification system: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines.
J Am Coll Cardiol. 2016; 67: 1572-1574
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, 7
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- Arnett D.K.
- Goodman R.A.
- Halperin J.L.
- et al.
AHA/ACC/HHS strategies to enhance application of clinical practice guidelines in patients with cardiovascular disease and comorbid conditions: from the American Heart Association, American College of Cardiology, and U.S. Department of Health and Human Services.
J Am Coll Cardiol. 2014; 64: 1851-1856
Selection of Writing Committee Members
The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds. Writing committee members represent different geographic regions, sexes, ethnicities, races, intellectual perspectives/biases, and scopes of clinical practice. The Task Force may also invite organizations and professional societies with related interests and expertise to participate as partners, collaborators, or endorsers.
Relationships With Industry and Other Entities
The ACC and AHA have rigorous policies and methods to ensure that guidelines are developed without bias or improper influence. The complete relationships with industry and other entities (RWI) policy can be found online. Appendix 1 of the current document lists writing committee members’ relevant RWI. For the purposes of full transparency, writing committee members’ comprehensive disclosure information is available online, as is comprehensive disclosure information for the Task Force.
Evidence Review and Evidence Review Committees
When developing recommendations, the writing committee uses evidence-based methodologies that are based on all available data.
4
, 5
, - Halperin J.L.
- Levine G.N.
- Al-Khatib S.M.
- et al.
Further evolution of the ACC/AHA clinical practice guideline recommendation classification system: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines.
J Am Coll Cardiol. 2016; 67: 1572-1574
6
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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 key references are cited.An independent evidence review committee (ERC) is commissioned when there are 1 or more questions deemed of utmost clinical importance that merit formal systematic review. This systematic review will determine which patients are most likely to benefit from a drug, device, or treatment strategy and to what degree. Criteria for commissioning an ERC and formal systematic review include: a) the absence of a current authoritative systematic review; b) the feasibility of defining the benefit and risk in a time frame consistent with the writing of a guideline; c) the relevance to a substantial number of patients; and d) the likelihood that the findings can be translated into actionable recommendations. ERC members may include methodologists, epidemiologists, healthcare providers, and biostatisticians. The recommendations developed by the writing committee on the basis of the systematic review are marked with“SR”.
Guideline-Directed Management and Therapy
The term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic testing, and pharmacological and procedural treatments. For these and all recommended drug treatment regimens, the reader should confirm the dosage by reviewing product insert material and evaluate the treatment regimen for contraindications and interactions. The recommendations are limited to drugs, devices, and treatments approved for clinical use in the United States.
Class of Recommendation and Level of Evidence
The Class of Recommendation (COR) indicates the strength of the recommendation, encompassing the estimated magnitude and certainty of benefit in proportion to risk. The Level of Evidence (LOE) rates the quality of scientific evidence that supports the intervention on the basis of the type, quantity, and consistency of data from clinical trials and other sources (Table 1).
4
, 5
, - Halperin J.L.
- Levine G.N.
- Al-Khatib S.M.
- et al.
Further evolution of the ACC/AHA clinical practice guideline recommendation classification system: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines.
J Am Coll Cardiol. 2016; 67: 1572-1574
6
Table 1Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care∗ (Updated August 2015)
 |
Glenn N. Levine, MD, FACC, FAHA
Chair, ACC/AHA Task Force on Clinical Practice Guidelines
1. Introduction
1.1 Methodology and Evidence Review
The recommendations listed in this guideline are, whenever possible, evidence based. An initial extensive evidence review, which included literature 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, was conducted from July to October 2015. Key search words included but were not limited to the following: athletes, autonomic neuropathy, bradycardia, carotid sinus hypersensitivity, carotid sinus syndrome, children, death, dehydration, diagnosis, driving, electrocardiogram, electrophysiological study, epidemiology, falls, implantable loop recorder, mortality, older populations, orthostatic hypotension, pediatrics, psychogenic pseudosyncope, recurrent syncope, risk stratification, supraventricular tachycardia, syncope unit, syncope, tilt-table test, vasovagal syncope, and ventricular arrhythmia. Additional relevant studies published through October 2016, during the guideline writing process, were also considered by the writing committee and added to the evidence tables when appropriate. The finalized evidence tables, included in the Online Data Supplement, summarize the evidence used by the writing committee to formulate recommendations. Lastly, the writing committee reviewed documents related to syncope previously published by the ACC and AHA and other organizations and societies. References selected and published in this document are representative and not all inclusive.
An independent ERC was commissioned to perform a systematic review of clinical questions, the results of which were considered by the writing committee for incorporation into this guideline. The systematic review report “Pacing as a Treatment for Reflex-Mediated (Vasovagal, Situational, or Carotid Sinus Hypersensitivity) Syncope” is published in conjunction with this guideline.
9
- Varosy P.D.
- Chen L.Y.
- Miller A.L.
- et al.
Pacing as a treatment for reflex-mediated (vasovagal, situational, or carotid sinus hypersensitivity) syncope: a systematic review for the 2017 ACC/AHA/HRS guideline for the evaluation and management of syncope: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.
Heart Rhythm. 2017; 14: e255-e269
1.2 Organization of the Writing Committee
The writing committee was composed of clinicians with expertise in caring for patients with syncope, including cardiologists, electrophysiologists, an emergency physician, and a pediatric cardiologist. The writing committee included representatives from the ACC, AHA, Heart Rhythm Society (HRS), American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine.
1.3 Document Review and Approval
This document was reviewed by 2 official reviewers each nominated by the ACC, AHA, and HRS; 1 reviewer each from the American Academy of Neurology, American College of Emergency Physicians and Society for Academic Emergency Medicine, and Pediatric and Congenital Electrophysiology Society; a lay/patient representative; and 25 individual content reviewers. Reviewers’ RWI information was distributed to the writing committee and is published in this document (Appendix 2).
This document was approved for publication by the governing bodies of the ACC, AHA, and HRS and was endorsed by the American College of Emergency Physicians, the Society for Academic Emergency Medicine, and the Pediatric and Congenital Electrophysiology Society.
1.4 Scope of the Guideline
The purpose of this ACC/AHA/HRS guideline is to provide contemporary, accessible, and succinct guidance on the management of adult and pediatric patients with suspected syncope. This guideline is intended to be a practical document for cardiologists, arrhythmia specialists, neurologists, emergency physicians, general internists, geriatric specialists, sports medicine specialists, and other healthcare professionals involved in the care of this very large and heterogeneous population. It is not a review of physiology, pathophysiology, or mechanisms of underlying conditions associated with syncope. The nature of syncope as a symptom required that the writing committee consider numerous conditions for which it can be a symptom, and as much as possible, we have addressed the involvement of syncope only as a presenting symptom. Because of the plausible association of syncope and sudden cardiac death (SCD) in selected populations, this document discusses risk stratification and prevention of SCD when appropriate. The use of the terms selected populations and selected patients in this document is intended to direct healthcare providers to exercise clinical judgment, which is often required during the evaluation and management of patients with syncope. When a recommendation is made to refer a patient to a specialist with expertise for further evaluation, such as in the case of autonomic neurology, adult congenital heart disease (ACHD), older populations, or athletes, the writing committee agreed to make Class IIa recommendations because of the paucity of outcome data. The definition of older populations has been evolving. Age >75 years is used to define older populations or older adults in this document, unless otherwise specified. If a study has defined older adults by a different age cutoff, the relevant age is noted in those specific cases. Finally, the guideline addresses the management of syncope with the patient as a focus, rather than larger aspects of health services, such as syncope management units. The goals of the present guideline are:
- •To define syncope as a symptom, with different causes, in different populations and circumstances.
- •To provide guidance and recommendations on the evaluation and management of patients with suspected syncope in the context of different clinical settings, specific causes, or selected circumstances.
- •To identify key areas in which knowledge is lacking, to foster future collaborative research opportunities and efforts.
In developing this guideline, the writing committee reviewed the evidence to support recommendations in the relevant ACC/AHA guidelines noted in Table 2 and affirms the ongoing validity of the related recommendations in the context of syncope, thus obviating the need to repeat existing guideline recommendations in the present guideline when applicable or when appropriate. Table 2 also contains a list of other statements that may be of interest to the reader.
Table 2Relevant ACC/AHA Guidelines
| Title | Organization | Publication Year (Reference) |
|---|---|---|
| ACC/AHA guideline policy relevant to the management of syncope | ||
| Supraventricular tachycardia | ACC/AHA/HRS | 2015 10
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. J Am Coll Cardiol. 2016; 67: e27-e115 |
| Valvular heart disease | AHA/ACC | 2014 11 |
| Device-based therapies for cardiac rhythm abnormalities | ACCF/AHA/HRS | 2012 12
2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013; 61: e6-e75 |
| Ventricular arrhythmias and sudden cardiac death | ACC/AHA/ESC | 2006 13 ,
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol. 2006; 48: e247-e346 |
| Other ACC/AHA guidelines of interest | ||
| Hypertension | ACC/AHA | --- |
| Stable ischemic heart disease | ACC/AHA/ACP/AATS/PCNA/SCAI/STS | 2012 and 2014 14 ,
2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2014; 64: 1929-1949 15
2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2012; 60: e44-e164 |
| Atrial fibrillation | AHA/ACC/HRS | 2014 16 |
| Non–ST-elevation acute coronary syndromes | AHA/ACC | 2014 17 |
| Assessment of cardiovascular risk | ACC/AHA | 2013 18 |
| Heart failure | ACC/AHA | 2013 19 , |
| Hypertrophic cardiomyopathy | ACC/AHA | 2011 20
2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic Surgery, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2011; 58: e212-e260 |
| Assessment of cardiovascular risk in asymptomatic adults | ACC/AHA | 2010 21 |
| Adult congenital heart disease | ACC/AHA | 2008 22 ,
ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in collaboration with the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008; 52: e143-e263 |
| Other related references | ||
| Scientific statement on electrocardiographic early repolarization | AHA | 2016 23 |
| Expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope | HRS | 2015 24 |
| Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death | ESC | 2015 and 2013 25 ,
HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm. 2013; 10: 1932-1963 26
2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology. G Ital Cardiol (Rome). 2016; 17: 108-170 |
| Expert consensus statement on the recognition and management of arrhythmias in adult congenital heart disease | PACES/HRS | 2014 27
PACES/HRS expert consensus statement on the recognition and management of arrhythmias in adult congenital heart disease: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Can J Cardiol. 2014; 30: e1-e63 |
| Expert consensus statement on the use of implantable cardioverter-defibrillator therapy in patients who are not included or not well represented in clinical trials | HRS/ACC/AHA | 2014 28 |
| Expert consensus statement on ventricular arrhythmias | EHRA/HRS/APHRS | 2014 29 |
| Expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes | HRS/EHRA/APHRS | 2013 25
HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm. 2013; 10: 1932-1963 |
| Guidelines for the diagnosis and management of syncope | ESC | 2009 30 |
AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; ACCF, American College of Cardiology Foundation; ACP, American College of Physicians; AHA, American Heart Association; APHRS, Asia Pacific Heart Rhythm Society; EHRA, European Heart Rhythm Association; ESC, European Society of Cardiology; HRS, Heart Rhythm Society; PACES, Pediatric and Congenital Electrophysiology Society; PCNA, Preventive Cardiovascular Nurses Association; SCAI, Society for Cardiovascular Angiography and Interventions; and STS, Society of Thoracic Surgeons.
∗ Revisions to the current documents are being prepared, with publication expected in 2017.
2. General Principles
2.1 Definitions: Terms and Classification
For the purpose of this guideline, definitions of syncope and relevant terms are provided in Table 3.
Table 3Relevant Terms and Definitions
| Term | Definition/Comments and References |
|---|---|
| Syncope | A symptom that presents with an abrupt, transient, complete loss of consciousness, associated with inability to maintain postural tone, with rapid and spontaneous recovery. The presumed mechanism is cerebral hypoperfusion. 24 , 30 There should not be clinical features of other nonsyncope causes of loss of consciousness, such as seizure, antecedent head trauma, or apparent loss of consciousness (i.e., pseudosyncope).24 , 30 |
| Loss of consciousness | A cognitive state in which one lacks awareness of oneself and one's situation, with an inability to respond to stimuli. |
| Transient loss of consciousness | Self-limited loss of consciousness 30 can be divided into syncope and nonsyncope conditions. Nonsyncope conditions include but are not limited to seizures, hypoglycemia, metabolic conditions, drug or alcohol intoxication, and concussion due to head trauma. The underlying mechanism of syncope is presumed to be cerebral hypoperfusion, whereas nonsyncope conditions are attributed to different mechanisms. |
| Presyncope(near-syncope) | The symptoms before syncope. These symptoms could include extreme lightheadedness; visual sensations, such as “tunnel vision” or “graying out”; and variable degrees of altered consciousness without complete loss of consciousness. Presyncope could progress to syncope, or it could abort without syncope. |
| Unexplained syncope (syncope of undetermined etiology) | Syncope for which a cause is undetermined after an initial evaluation that is deemed appropriate by the experienced healthcare provider. The initial evaluation includes but is not limited to a thorough history, physical examination, and ECG. |
| Orthostatic intolerance | A syndrome consisting of a constellation of symptoms that include frequent, recurrent, or persistent lightheadedness, palpitations, tremulousness, generalized weakness, blurred vision, exercise intolerance, and fatigue upon standing. These symptoms can occur with or without orthostatic tachycardia, OH, or syncope. 24 Individuals with orthostatic intolerance have ≥1 of these symptoms associated with reduced ability to maintain upright posture. |
| Orthostatic tachycardia | A sustained increase in heart rate of ≥30 bpm within 10 min of moving from a recumbent to a quiet (nonexertional) standing position (or ≥40 bpm in individuals 12–19 y of age). 24 , 30 , 31 |
| Orthostatic hypotension (OH) | A drop in systolic BP of ≥20 mm Hg or diastolic BP of ≥10 mm Hg with assumption of an upright posture. 31 |
| • Initial (immediate) OH | A transient BP decrease within 15 s after standing, with presyncope or syncope. 31 , 32 |
| • Classic OH | A sustained reduction of systolic BP of ≥20 mm Hg or diastolic BP of ≥10 mm Hg within 3 min of assuming upright posture. 31 |
| • Delayed OH | A sustained reduction of systolic BP of ≥20 mm Hg (or 30 mm Hg in patients with supine hypertension) or diastolic BP of ≥10 mm Hg that takes >3 min of upright posture to develop. The fall in BP is usually gradual until reaching the threshold. 31 |
| • Neurogenic OH | A subtype of OH that is due to dysfunction of the autonomic nervous system and not solely due to environmental triggers (e.g., dehydration or drugs). 33 , 34 Neurogenic OH is due to lesions involving the central or peripheral autonomic nerves. |
| Cardiac (cardiovascular) syncope | Syncope caused by bradycardia, tachycardia, or hypotension due to low cardiac index, blood flow obstruction, vasodilatation, or acute vascular dissection. 35 , 36 |
| Noncardiac syncope | Syncope due to noncardiac causes, which include reflex syncope, OH, volume depletion, dehydration, and blood loss. 35 |
| Reflex (neurally mediated) syncope | Syncope due to a reflex that causes vasodilation, bradycardia, or both. 24 , 30 , 31 |
| • Vasovagal syncope (VVS) | The most common form of reflex syncope mediated by the vasovagal reflex. VVS: 1) may occur with upright posture (standing or seated or with exposure to emotional stress, pain, or medical settings; 2) typically is characterized by diaphoresis, warmth, nausea, and pallor; 3) is associated with vasodepressor hypotension and/or inappropriate bradycardia; and 4) is often followed by fatigue. Typical features may be absent in older patients. 24 VVS is often preceded by identifiable triggers and/or by a characteristic prodrome. The diagnosis is made primarily on the basis of a thorough history, physical examination, and eyewitness observation, if available. |
| • Carotid sinus syndrome | Reflex syncope associated with carotid sinus hypersensitivity. 30 Carotid sinus hypersensitivity is present when a pause ≥3 s and/or a decrease of systolic pressure ≥50 mm Hg occurs upon stimulation of the carotid sinus. It occurs more frequently in older patients. Carotid sinus hypersensitivity can be associated with varying degrees of symptoms. Carotid sinus syndrome is defined when syncope occurs in the presence of carotid sinus hypersensitivity. |
| • Situational syncope | Reflex syncope associated with a specific action, such as coughing, laughing, swallowing, micturition, or defecation. These syncope events are closely associated with specific physical functions. |
| Postural (orthostatic) tachycardia syndrome (POTS) | A clinical syndrome usually characterized by all of the following: 1) frequent symptoms that occur with standing (e.g., lightheadedness, palpitations, tremulousness, generalized weakness, blurred vision, exercise intolerance, and fatigue); and 2) an increase in heart rate of ≥30 bpm during a positional change from supine to standing (or ≥40 bpm in those 12–19 y of age); and 3) the absence of OH (>20 mm Hg reduction in systolic BP). Symptoms associated with POTS include those that occur with standing (e.g., lightheadedness, palpitations); those not associated with particular postures (e.g., bloating, nausea, diarrhea, abdominal pain); and those that are systemic (e.g., fatigue, sleep disturbance, migraine headaches). 37 The standing heart rate is often >120 bpm.31 , 38 , 39 , 40 , 41 , 42 |
| Psychogenic pseudosyncope | A syndrome of apparent but not true loss of consciousness that may occur in the absence of identifiable cardiac, reflex, neurological, or metabolic causes. 30 |
BP indicates blood pressure; ECG, electrocardiogram; OH, orthostatic hypotension; POTS, postural tachycardia syndrome; and VVS, vasovagal syncope.
∗ These definitions are derived from previously published definitions from scientific investigations, guidelines, expert consensus statements, and Webster dictionary after obtaining consensus from the WC.
Table 4Historical Characteristics Associated With Increased Probability of Cardiac and Noncardiac Causes of Syncope
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| More often associated with cardiac causes of syncope |
| • Older age (>60 y) |
| • Male sex |
| • Presence of known ischemic heart disease, structural heart disease, previous arrhythmias, or reduced ventricular function |
| • Brief prodrome, such as palpitations, or sudden loss of consciousness without prodrome |
| • Syncope during exertion |
| • Syncope in the supine position |
| • Low number of syncope episodes (1 or 2) |
| • Abnormal cardiac examination |
| • Family history of inheritable conditions or premature SCD (<50 y of age) |
| • Presence of known congenital heart disease |
| More often associated with noncardiac causes of syncope |
| • Younger age |
| • No known cardiac disease |
| • Syncope only in the standing position |
| • Positional change from supine or sitting to standing |
| • Presence of prodrome: nausea, vomiting, feeling warmth |
| • Presence of specific triggers: dehydration, pain, distressful stimulus, medical environment |
| • Situational triggers: cough, laugh, micturition, defecation, deglutition |
| • Frequent recurrence and prolonged history of syncope with similar characteristics |
SCD indicates sudden cardiac death.
2.2 Epidemiology and Demographics
Syncope has many causes and clinical presentations; the incidence depends on the population being evaluated. Estimates of isolated or recurrent syncope may be inaccurate and underestimated because epidemiological data have not been collected in a consistent fashion or because a consistent definition has not been used. Interpretation of the symptoms varies among the patients, observers, and healthcare providers. The evaluation is further obscured by inaccuracy of data collection and by improper diagnosis.
Studies of syncope report prevalence rates as high as 41%, with recurrent syncope occurring in 13.5%.
43
In a cross section of 1,925 randomly selected residents of Olmsted County, Minnesota, with a median age of 62 years (all age >45 years), 364 reported an episode of syncope in their lifetime; the estimated prevalence of syncope was 19%. Females reported a higher prevalence of syncope (22% versus 15%, p<0.001).44
The incidence follows a trimodal distribution in both sexes, with the first episode common around 20, 60, or 80 years of age and the third peak occurring 5 to 7 years earlier in males.45
Predictors of recurrent syncope in older adults are aortic stenosis, impaired renal function, atrioventricular (AV) or left bundle-branch block, male sex, chronic obstructive pulmonary disorder, heart failure (HF), atrial fibrillation (AF), advancing age, and orthostatic medications,45
with a sharp increase in incidence after 70 years of age.35
Reflex syncope was most common (21%), followed by cardiac syncope (9%) and orthostatic hypotension (OH) (9%), with the cause of syncope unknown in 37%.35
In patients with New York Heart Association class III–IV HF, syncope is present in 12% to 14% of patients.46
, 47
In older adults, there is a greater risk of hospitalization and death related to syncope. The National Hospital Ambulatory Medical Care Survey reported 6.7 million episodes of syncope in the emergency department (ED), or 0.77% of all ED patients. Among patients >80 years of age, 58% were admitted to hospital.
48
The prevalence of syncope as a presenting symptom to the ED ranged from 0.8% to 2.4% in multiple studies in both academic and community settings.49
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Older institutionalized patients have a 7% annual incidence of syncope, a 23% overall prevalence, and a 30% 2-year recurrence rate.
56
The incidence of syncope in older adults may overlap with falls, so it may be difficult to distinguish one from the other. Older adults are predisposed to falls when syncope occurs, with a 1-year fall rate of 38% among fainters versus 18.3% among nonfainters.57
2.3 Initial Evaluation of Patients With Syncope
The time interval between the index syncopal event and the initial evaluation can vary significantly according to the medical necessity for evaluation and the patient’s effort in seeking evaluation. The clinical setting in which the initial evaluation takes place also varies. The patient could seek evaluation in an outpatient setting with a generalist or a specialist or in the ED at a hospital. The recommendations in the present section are intended for consideration under the general principles of what constitutes GDMT during initial evaluation, regardless of the clinical setting. These general principles for the initial evaluation are shown in Figure 1. Additional evaluation is discussed in subsequent sections according to the outcomes of initial evaluation or in the presence of specific disease conditions.
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2.3.1 History and Physical Examination: Recommendation
Tabled
1Recommendation for History and Physical Examination
| COR | LOE | Recommendation |
|---|---|---|
| I | B-NR | A detailed history and physical examination should be performed in patients with syncope. 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 |
| See Online Data Supplement 1. | The history should aim to identify the prognosis, diagnosis, reversible or ameliorable factors, comorbidities, medication use, and patient and family needs. Cardiac syncope carries a significantly worse prognosis than does neurally mediated syncope. Prognostic factors generally separate neurally mediated from cardiac syncope and are described in Section 2.3.3. The diagnostic history focuses on the situations in which syncope occurs, prodromal symptoms that provide physiological insight, patient’s self-report, bystander observations of the event and vital signs, and post-event symptoms. Video recordings are helpful when available. Time relationship to meals and physical activities and duration of the prodrome are helpful in differentiating neurally mediated syncope from cardiac syncope. Comorbidities and medication use are particularly important factors in older patients. A history of past medical conditions should be obtained, particularly with regard to the existence of preexisting cardiovascular disease. 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 A family history should be obtained, with particular emphasis on histories of syncope or sudden unexplained death (or drowning). Historical characteristics associated with, though not diagnostic of, cardiac and noncardiac syncope are summarized in Table 4.The physical examination should include determination of orthostatic blood pressure and heart rate changes in lying and sitting positions, on immediate standing, and after 3 minutes of upright posture. 31 Careful attention should be paid to heart rate and rhythm, as well the presence of murmurs, gallops, or rubs that would indicate the presence of structural heart disease. A basic neurological examination should be performed, looking for focal defects or other abnormalities that would suggest need for further neurological evaluation or referral. | |
2.3.2 Electrocardiography: Recommendation
Tabled
1Recommendation for Electrocardiography
| COR | LOE | Recommendation |
|---|---|---|
| I | B-NR | In the initial evaluation of patients with syncope, a resting 12-lead electrocardiogram (ECG) is useful. 76 |
| See Online Data Supplement 2. | ECG is widely available and inexpensive and can provide information about the potential and specific cause of the syncope episode (e.g., bradyarrhythmia with sinus pauses or high-grade conduction block; ventricular tachyarrhythmia). It may demonstrate an underlying arrhythmogenic substrate for syncope or SCD. Subsets of patients with Wolff-Parkinson-White syndrome, Brugada syndrome, long-QT syndrome (LQTS), hypertrophic cardiomyopathy (HCM), or arrhythmogenic right ventricular cardiomyopathy (ARVC) have characteristic ECG features, which can prompt the decision to pursue further evaluation. Despite the benefit of identifying a likely cause or potential clue about the cause of syncope from the ECG, prospective studies did not conclude that ECG findings significantly affected subsequent management. 73 , 77 , 78 , 79 , 80 The prognostic value of an abnormal ECG in patients with syncope has been questioned, as well.69 , 81 However, a multicenter, prospective, observational study76 concluded that the presence of AF, intraventricular conduction disturbances, voltage criteria for left ventricular (LV) hypertrophy, and ventricular pacing were associated with increased risk of death from all causes at 1 year. | |
2.3.3 Risk Assessment: Recommendations
Syncope is a symptom that can be due to various causes, ranging from benign to life-threatening conditions. Risk stratification during initial evaluation is important for guiding the treatment and preventing long-term morbidity and mortality. However, risk stratification schemes for short- and long-term clinical outcomes are limited by the inclusion of all patients with syncope, without regard to the presence or absence of underlying medical conditions associated with syncope. For example, outcomes would not be expected to be similar for patients with vasovagal syncope (VVS), heart block with preserved ejection fraction, advanced cardiomyopathy and HF, acute gastric bleeding, or aortic dissection. The short-term prognosis of patients presenting with syncope is mainly related to the cause of syncope and the acute reversibility of the underlying condition; long-term prognosis is related to the effectiveness of therapy and the severity and progression of underlying diseases, especially cardiac or terminal illnesses.
Although having precise definitions for high-, intermediate-, and low-risk patient groups after an episode of syncope would be useful for managing these patients, evidence from current clinical studies renders this proposal challenging because of a large number of confounders. Risk markers from history, physical examination, laboratory investigations, study endpoints, adverse event rates, and time intervals between these events are variable from study to study. Current data are best grouped into short-term risk (associated with outcomes in the ED and up to 30 days after syncope) and long-term risk (up to 12 months of follow-up). Risk markers are summarized in Table 5.
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The types of events, event rates, and study durations from investigations that estimated risk scores are summarized in Table 6.64
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Tabled
1Recommendations for Risk Assessment
| COR | LOE | Recommendations |
|---|---|---|
| I | B-NR | Evaluation of the cause and assessment for the short- and long-term morbidity and mortality risk of syncope are recommended (Table 5). 68 , 82 , 83 , 100 |
| See Online Data Supplements 3 and 4. | Syncope may be an acute result of major hemodynamic abnormalities or a manifestation of serious underlying disease. Thus, assessment of the cause of syncope and underlying comorbidities is necessary. Short-term adverse events and deaths are determined largely by the cause of syncope and the effectiveness of the treatment. In patients without a presumptive cause of syncope, risk stratification for potential short-term outcomes is necessary for immediate decision making in the acute setting. Potential predictors of increased short-term risk of death and serious outcomes are listed in Table 5. Long-term adverse events and deaths are more likely determined by the underlying medical comorbidities, many of which are cardiac. The evaluation of patients with syncope should include a full assessment of the long-term risk factors, including those listed in Table 5. 69 , 70 , 72 , 73 , 74 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 95 , 97 | |
| IIb | B-NR | Use of risk stratification scores may be reasonable in the management of patients with syncope. 67 , 68 , 72 , 73 , 75 , 87 , 89 , 100 , 101 |
| See Online Data Supplements 3 and 4. | Investigators have reported numerous risk scores to predict adverse outcomes after syncope (examples in Table 6). This literature has important limitations, including inconsistent definitions of syncope, outcomes, outcome time frames, and predictors; inclusion of patients with serious outcomes already identified in the ED, which biases risk scores toward identifying “obvious” events; the use of composite outcomes that combine events with different pathophysiologies; small samples that limited model reliability; and limited external validation. Risk scores have not performed better than unstructured clinical judgment. 64 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 96 , 98 |
Table 5Short- and Long-Term Risk Factors
∗
Definitions for clinical endpoints or serious outcomes vary by study. The specific endpoints for the individual studies in this table are defined in online Data Supplements 3 and 4 and summarized in Table 6 for selected studies. This table includes individual risk predictors from history, physical examination, and laboratory studies associated with adverse outcomes from selected studies.
| Short-Term Risk Factors (≤30 d) | Long-Term Risk Factors (>30 d) |
|---|---|
| History: Outpatient clinic or ED evaluation | |
| Male sex 74 , 85 , 101 , 102 | Male sex 68 , 90 |
| Older age (>60 y) 88 | Older age 67 , 74 , 75 , 90 |
| No prodrome | |