2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

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.

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.

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^1,2 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

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 manual⁴ and other methodology articles.^5–8

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.

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.

When developing recommendations, the writing committee uses evidence-based methodologies that are based on all available data.^4–7 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”.

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.

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).^4–6

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

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.

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.

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:

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.

For the purpose of this guideline, definitions of syncope and relevant terms are provided in Table 3.

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 1925 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.^49–55

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

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.

The availability of simple and accurate biomarkers might streamline risk stratification and diagnosis of the cause of syncope. This section reviews circulating biomarkers, which are being evaluated as markers either of hypotension or underlying disease processes. None have met with strong success.

Cardiovascular causes of syncope are common. The presence of significant cardiovascular diseases, often associated with the cardiovascular causes of syncope, portends a poor prognosis.^35,132 As such, cardiovascular testing can be a critical element in the evaluation and management of selected patients with syncope. It is important also to recognize that the abnormalities found during cardiovascular testing may not have a causal relationship to syncope itself. Determining the significance of such abnormalities, their causality, and whether subsequent treatment is merited requires clinical judgment and appropriate selection of cardiovascular testing.

Cardiac arrhythmia is a common cause of syncope, and the prompt identification of an arrhythmic etiology has diagnostic and prognostic implications. When bradyarrhythmias and tachyarrhythmias are discovered in patients with syncope, determining their causal relationship to syncope often poses challenges for the practitioner. The baseline presence of an arrhythmia does not necessarily represent the etiology of syncope (eg, marked resting bradycardia in a young patient with syncope). Furthermore, determining the significance of atrial tachyarrhythmias and VT—which are often paroxysmal and occult on initial evaluation—poses additional challenges and may warrant a more extensive evaluation (Section 3.2). Section 4.1 broadly outlines strategies to guide the practitioner when evaluating patients with bradycardia, supraventricular arrhythmias (including AF), and VT.

Syncope occurs not infrequently in patients with underlying heart diseases. Comprehensive guidelines exist for diagnosis and management of many of these diseases, including sections on syncope. In this section, management of syncope is discussed in patients with underlying structural heart disease. The disease-specific ACC/AHA guidelines were assessed first, and then a comprehensive review of literature published since publication of these disease-specific guidelines was performed to ensure that prior recommendations about syncope remained current. If new published data were available, they were incorporated into the present document.

The prevalence of inherited arrhythmic conditions is low, rendering the clinical significance of an abnormal test a challenge. Few syncope-specific studies exist. Most studies of patients with inherited arrhythmias are open label or not randomized and often are uncontrolled. Most of the publications included other cardiac events, such as cardiac arrest and death, either at enrollment or as an outcome. Syncope of suspected arrhythmic cause has been correlated with increased risk of SCD, cardiac arrest, or overall cardiac death. Although ICD is effective in aborting cardiac arrest and presumably reducing risk of death in the patients with inheritable rhythm disorders, its impact on syncope recurrence is unknown.^25,26,220

VVS is the most common cause of syncope and a frequent reason for ED visits.⁶⁶ The underlying pathophysiology of VVS results from a reflex causing hypotension and bradycardia, triggered by prolonged standing or exposure to emotional stress, pain, or medical procedures.^361–365 An episode of VVS is typically associated with a prodrome of diaphoresis, warmth, and pallor, with fatigue after the event. Given the benign nature of VVS and its frequent remissions, medical treatment is usually not required unless conservative measures are unsatisfactory. In some patients, effective treatment is needed, as syncopal events may result in injury and an impaired quality of life (QoL).^366–368 Despite the need and substantial efforts by investigators, there are limited evidence-based therapeutic options.³⁶⁹ Preliminary data from cardiac ganglia plexi ablation in treating selected patients with VVS are encouraging but still insufficient to make recommendations at this time.^370–372 See Figure 4 for the algorithm for treatment of VVS.

Pacemakers might seem to be an obvious therapy for VVS, given that bradycardia and asystole are present during some spells. Numerous observational studies and RCTs have assessed whether pacemakers are efficacious in preventing syncope.^404–409 It is becoming clear that strict patient selection on the basis of documented asystole during clinical syncope is important, and that observation combined with a tilt-table test that induces minimal or no vasodepressor response may increase the likelihood of a response to pacing. This is because a positive tilt-table test might identify patients who are likely to also have a vasodepressor response during VVS and therefore not respond as well to permanent pacing. As noted in Section 1.1, the recommendation in this section was 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

Carotid sinus syndrome is associated with mechanical manipulation of the carotid sinus, either spontaneously or with carotid sinus massage. It is diagnosed by the reproduction of clinical syncope during carotid sinus massage, with a cardioinhibitory response if asystole is >3 seconds or if there is AV block, or a significant vasodepressor response if there is ≥50 mm Hg drop in systolic blood pressure, or a mixed cardioinhibitory and vasodepressor response. It occurs more commonly in men >40 years of age^413,414 and is due to an abnormal reflex attributed to baroreceptor and possibly medulla dysfunction.^415,416 Carotid sinus massage should be performed sequentially over the right and left carotid artery sinus in both the supine and upright positions for 5 seconds each, with continuous beat-to-beat heart rate monitoring and blood pressure measurement.⁴¹⁷ Contraindications to performing carotid sinus massage include auscultation of carotid bruit and transient ischemic attack, stroke, or myocardial infarction within the prior 3 months, except if carotid Doppler excludes significant stenosis.⁴¹⁸

Situational syncope is defined as syncope occurring only in certain distinct and usually memorable circumstances, including micturition syncope, defecation syncope, cough syncope, laugh syncope, and swallow syncope.^431–437 Appropriate investigations should be undertaken to determine an underlying etiology, including causes that may be reversible.^{431,433–436} Evidence for treatment is limited mainly to case reports, small case series, and small observational studies.^{431,433–436} Treatment of most types of situational syncope relies heavily on avoidance or elimination of a triggering event. This may not always be possible, so increased fluid and salt consumption and reduction or removal of hypotensive drugs and diuretics are encouraged where appropriate and safe.⁴³⁶

OH involves excessive pooling of blood volume in the splanchnic and leg circulations. With standing, venous return to the heart drops, with a resultant decrease in cardiac output.³¹ Normally, the autonomic nervous system provides compensatory changes in vascular tone, heart rate, and cardiac contractility. In some individuals, this response may be defective or inadequate.³¹ In neurogenic OH, the vasoconstrictor mechanisms of vascular tone may be inadequate because of neurodegenerative disorders, such as multiple system atrophy, pure autonomic failure, Parkinson’s disease, and autonomic peripheral neuropathies, such as those due to diabetes mellitus and other systemic diseases.³¹ Neurogenic OH may present clinically as classic or delayed OH. Most commonly, OH is due to dehydration or medications, such as diuretics and vasodilators. Syncope caused by OH conditions occurs in the upright position. See Figure 5 for the algorithm for treatment of OH.

Syncope related to medication becomes prevalent particularly in older adults, who frequently have multiple comorbidities requiring treatment and are prone to polypharmacy effects.^488–490 Cessation of offending medications is usually key for symptomatic improvement, but often feasibility of cessation of medications is limited by the necessity of the treatments.^491–493 Dehydration may manifest along a spectrum of symptoms, ranging from tachycardia to shock, depending on whether a person has compensated or uncompensated hypovolemia.⁴⁹⁴ Orthostatic tolerance worsens with dehydration and is exacerbated by heat stress, which promotes vasodilation.^495–497 Rehydration, whether by intravenous or oral formulation, should include sodium supplementation for more rapid recovery.^21,498–501

Syncope is common in the pediatric population. By 18 years of age, it is estimated that 30% to 50% of children experience at least 1 fainting episode, and syncope accounts for 3% of all pediatric ED visits.^617–622 The incidence is higher in females and peaks between 15 to 19 years of age.⁶¹⁷ Neurally mediated syncope accounts for 75% of pediatric syncope, followed by psychogenic or unexplained syncope in 8% to 15% of cases.⁶²³ Breath-holding spells are a form of syncope unique to the pediatric population. Cyanotic breath-holding spells typically occur from age 6 months to age 5 years and may be due to desaturation caused by forced expiration during crying. Pallid breath-holding spells are seen in the first 1 to 2 years of age and may be an early form of VVS. The latter episodes are associated with significant bradycardia and prolonged asystole. Pediatric cardiac syncope may result from obstruction to blood flow (HCM, aortic stenosis, pulmonary hypertension), myocardial dysfunction (myocarditis, cardiomyopathy, congenital coronary anomaly, or post–Kawasaki disease) or a primary arrhythmic etiology (LQTS, CPVT, Brugada syndrome, ARVC, or Wolff-Parkinson-White syndrome).

A detailed history with careful attention to the events leading up to the syncope and a complete physical examination can guide practitioners in differentiating the life-threatening causes of syncope (with potential for injury or SCD) from the more common and benign neurally mediated syncope. A detailed family history, with particular attention to premature SCD among first- and second-degree relatives and the manner in which those deaths occurred, is helpful. Given that many of the causes of non-CHD cardiac syncope in children who do not have a form of CHD are similar to those experienced in an adult cohort (LQTS, HCM, Wolff-Parkinson-White, Brugada, and ARVC), interventions recommended for adults with similar conditions presenting with syncope can be applied in children.

Patients with ACHD are at risk for syncope as a result not only of the underlying structural disease, but also as a result of a previous palliative or corrective surgery. These patients may present with syncope of both hemodynamic and either bradycardic or tachycardic origin. Care by a physician with experience in management of CHD can be beneficial. The entire spectrum of arrhythmias may be seen in adults with CHD, including bradyarrhythmias secondary to sinus or AV nodal disease, atrial arrhythmias, and VA. By age 50 years, approximately 38% of patients with ACHD will develop an atrial arrhythmia, and by age 65 years, >50% of patients with severe CHD will develop atrial arrhythmias.⁶⁶⁰ The prevalence of VT after tetralogy of Fallot repair is 3% to 14%.^661,662

The management of syncope in older adults is particularly challenging: The incidence is high; the differential diagnosis is broad; the diagnosis is imprecise because of amnesia, falls, lack of witnesses, and polypharmacy; and secondary morbidity is high because of comorbidities, physical injury, and frailty.^{35,45,666–675} The vulnerability of older adults to syncope increases because of age-associated cardiovascular and autonomic changes, decreased fluid conservation,^{45,671,676–678} and an increased probability of developing multiple concurrent morbidities (with their associated pharmacological treatments) that can overwhelm homeostasis. In many instances, a syncopal event in an older adult is multifactorial, with many predisposing factors present simultaneously.

Older patients (>75 years of age) who present with syncope tend to have poor outcomes, both fatal and nonfatal.^109,679,680 Although some of the risk is attributable to the aspects of syncope described in this guideline, among older adults such risks are usually compounded by multiple morbidities and frailty, which add to age-related vulnerability to syncope,^671,681,682 and by the physical injuries associated with falls, collisions, or trauma, which more commonly result from syncope in old age.⁶⁷⁰ Furthermore, recurrent syncope can lead to nursing home admission and a devastating loss of independence.⁶⁸³ Given the multifactorial etiologies and high risks associated with syncope, a comprehensive and multidisciplinary approach is often necessary to assess for multiple morbidities, frailty, trauma, and other dimensions of health (including cognition and medications) pertinent to diagnosis and management.^{77,188,684,685} A thorough history and physical examination, including orthostatic vital signs, is particularly important in older patients.⁷⁷

The assessment of medical fitness to drive is a common issue for practitioners caring for patients with syncope. The main concern is the risk of causing injury or death to the driver or others as a result of recurrent syncope.⁶⁹¹ Factors to consider in assessing the risk of syncope while driving are summarized in a formula developed by the Canadian Cardiovascular Society 25 years ago⁶⁹² that estimates the risk that a driver will suddenly become incapacitated. The acceptable level of risk then becomes a societal decision.

Balancing the need to minimize risk from drivers fainting is the need for patients to drive to meet the demands of family and work. Society recognizes that certain groups, such as younger and older adults, are allowed to drive despite their higher risk of causing harm for reasons other than syncope.⁶⁹³ The societally acceptable risk of injury and death due to motor vehicle accidents has been quantified from an analysis of accident data collected in the United States, United Kingdom, and Canada.⁶⁹⁴ In the general population, the yearly risk of serious injury and death is 0.067%, or 1 in 1500.⁶⁹⁴ The 418 patients in POST I and POST II had a median of 3 vasovagal faints in 1 year but had no serious injuries or deaths and only 2 minor accidents in the subsequent year.⁶⁹⁴ This provides an estimated yearly risk of serious injury and death in the VVS population of <0.0017%, less than the Risk of Harm formula predicted.⁶⁹² However, for patients with other etiologies of syncope or those in whom syncope occurred without prodrome or warning, the risk of causing harm may be higher than for patients with VVS. Public policies, laws, and regulations have not been adapted to these results, and providers caring for patients with syncope should be aware of pertinent local driving laws and restrictions. Although untreated syncope may disqualify patients from driving, effective treatment reduces the risk enough to permit driving after a period of observation has elapsed without recurrent syncope. Regulatory agencies are more likely to disqualify commercial drivers than private drivers because of the amount of driving and the impact of accidents (ie, commercial drivers typically operate vehicles heavier than private automobiles). As the risk of recurrent syncope decreases with treatment or with the natural history of a disease process, the risk of harm may become low enough for private drivers to resuming driving, but not necessarily for commercial drivers because of the higher risk of harm. The suggestions in Table 10 provide general guidance for private drivers. Most suggestions are based on expert opinion and supported by limited data. Commercial driving in the United States is governed by federal law and administered by the US Department of Transportation.⁶⁹⁵

Syncope occurring in the athlete is predominantly of vasovagal origin, but underlying cardiac conditions may place athletes at undue risk for adverse events.⁷⁰³ Syncope during exercise is associated with increased probability of cardiac causes of syncope (Table 4). A thorough history, differentiating syncope occurring during exercise from syncope occurring after exercise or at other times, with typical characteristics of dehydration or VVS, is critically important during initial evaluation. The definition of an athlete is imprecise, but athlete can be defined as someone who engages in routine vigorous training (eg, >150 minutes per week) and is skilled in exercises, sports, or games requiring physical strength, agility, or stamina.⁷⁰⁴ More importantly, cardiac adaptations to high levels of exercise may lead to the “athlete’s heart” and thus alter the myocardial substrate.⁷⁰⁵ Primary or secondary prevention of syncope, morbidity, and mortality in at-risk athletes is a major consideration, but current strategies are largely inadequate.⁷⁰⁶ The current evidence base is insufficient to support general screening with ECG or echocardiography at baseline.^706,707

Several approved therapeutics, especially macrolide antibiotics and antihistamines/decongestants, have been associated with syncopal episodes.⁷⁰⁸ Performance-enhancing agents, such as somatotrophic compounds and amphetamine-like stimulants, are associated with precipitous collapse. A careful history is required in the athlete with syncope to rule out exposure to any of these agents.⁷⁰⁹ Similarly, before drugs are prescribed to highly competitive athletes, it is prudent to determine whether the drug or its metabolites are on lists of banned substances.

QoL is reduced with recurrent syncope,^725–733 as demonstrated in studies that compared patients with and without syncope.^727,731 QoL associated with recurrent syncope was equivalent to severe rheumatoid arthritis and chronic low-back pain in an adult population.⁷²⁸ Similarly, pediatric patients with recurrent syncope reported worse QoL than individuals with diabetes mellitus and equivalent QoL to individuals with asthma, end-stage renal disease, and structural heart disease.⁷²⁵ In a hospital-based cohort of patients with a prior episode of syncope, 33% reported syncope-related functional impairments with daily activities, such as driving or working.⁷³² Those with more frequent syncope have reported poorer QoL.^{726,729,730,732} There is consistent evidence that syncope is associated with worse function on multiple domains of QoL, such as perceptions of low overall physical health^725,730,734; perception of mental health, including increased fear, somatization, depression, and anxiety^{725,727,728,731,734}; and impairment in activities of daily living, such as driving, working, and attending school.

QoL impairments associated with syncope improve over time.⁷³³ In the Fainting Assessment Study,⁷³³ general and syncope-specific QoL improved over a 1-year period. Predictors of worse QoL over time include advanced age, recurrent syncope, neurological or psychogenic reason for syncope, and greater comorbidity at baseline.⁷³³ Syncope-related QoL can be improved through effective diagnosis and treatment. In 1 study, use of an implantable loop recorder increased diagnostic rate, reduced syncope recurrence, and improved QoL as compared with patients who received a conventional diagnostic workup.¹⁶⁴ In a second study, nonpharmacological treatment of recurrent syncope was associated with reductions in recurrent syncope and improvements in QoL.⁷²⁹

High healthcare costs are associated with the evaluation and management of syncope. Costs are defined as the resources needed to produce a set of services and are distinct from charges billed by facilities and healthcare providers.⁷³⁵ Most studies have focused on facility costs and excluded professional fees and patient copays. These high costs have been estimated both in the United States and abroad. In the US Healthcare Utilization Project, total annual hospital costs exceeded $4.1 billion in 2014 dollars, with a mean cost of $9400 per admission.⁷³⁶ Total costs and costs per admission for presumptive undiagnosed syncope were $1.6 billion and $7200, respectively.⁷³⁶ Single-center studies from multiple countries, including Austria, the United Kingdom, Israel, and Spain, confirm similarly high costs associated with the hospital evaluation of syncope.^122,737,738

Several investigators have estimated the costs per clinically meaningful test result. Physician reviewers determined whether the results of a diagnostic test affected clinical management at a US tertiary referral hospital after an episode of syncope.⁷⁷ The cost per informative diagnosis (as ordered in routine practice) affecting clinical management varied widely by specific diagnostic test, from postural blood pressure ($50) through telemetry ($1100) to EEG ($32 973).⁷⁷ Similar high costs per actionable diagnosis occur in children admitted for new-onset syncope. Finally, mean costs per diagnostic result were also high in an outpatient ($19 900) specialty clinic for unexplained recurrent syncope.¹⁶³

Reported incidence and prevalence of syncope vary significantly because of several confounders: variable definitions for syncope versus transient loss of consciousness, different populations, different clinical settings, and different study methodologies. Definition and classification of syncope provided in this document will set the standard for future research. Standardized national registries and large sample databases are needed to gather data on a continuous basis to understand the true incidence and prevalence of syncope, understand patient risk, inform driving policies, improve patient outcomes, and improve and streamline health service delivery.

At a patient’s presentation, several key questions follow: What is the likely cause of syncope? Does the patient have significant underlying heart disease and/or comorbid medical illnesses? If the cause of syncope is determined, is there an effective therapy to prevent recurrent syncope, prevent syncope-related nonfatal outcomes (injury, diminished healthcare–related QoL, lost workdays), or improve survival? What are the predictors of short- and long-term clinical outcomes? What are the key outcomes relevant to patients with syncope, including recurrent syncope? When the cause of syncope is unknown, what is the standard of care for this group of patients?

Because of the concerns that patients presenting with syncope are at higher risk for an impending catastrophic event, overuse and inappropriate use of testing and hospital admission are common. Answers to the following question will improve the effectiveness of patient evaluation: How should the initial evaluation and subsequent follow-up vary by risk (low, intermediate, or high) to assess clinical outcomes?

Richard A. Chazal, MD, FACC, President

Shalom Jacobovitz, Chief Executive Officer

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

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

Katherine Sheehan, PhD, Director, Guideline Strategy and Operations

Lisa Bradfield, CAE, Director, Guideline Methodology and Policy

Abdul R. Abdullah, MD, Science and Medicine Advisor

Clara Fitzgerald, Project Manager, Science and Clinical Policy

Allison Rabinowitz, MPH, Project Manager, Science and Clinical Policy

Steven R. Houser, PhD, FAHA, President

Nancy Brown, Chief Executive Officer

Rose Marie Robertson, MD, FAHA, Chief Science and Medicine Officer

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

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