Cardio · arrhythmias
Syncope: evaluation, risk stratification and management
Fellowship-level guide to syncope under the 2018 ESC syncope guideline and the 2017 ACC/AHA/HRS syncope guideline, with the newer ESC pacing (2021), ventricular arrhythmia (2022), cardiomyopathy (2023), hypertension (2024) and heart failure (2026) rows where they apply: definitions and classification, pathophysiology, the initial evaluation, emergency department risk stratification and disposition, ECG monitoring, tilt testing, treatment of reflex syncope, orthostatic hypotension and cardiac syncope, special populations and driving.
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Red flags
- Syncope during exertion or when supine, or sudden onset palpitation immediately followed by syncope: major high-risk features in ESC 2018 Table 6
- Unexplained systolic BP in the emergency department below 90 mmHg: a major high-risk feature in ESC 2018 Table 6
- Mobitz II second- or third-degree AV block, sustained or non-sustained VT, or QTc above 460 ms in repeated 12-lead ECGs indicating long QT syndrome: major high-risk ECG features in ESC 2018 Table 6
- ESC 2018 recommends that patients with high-risk features receive an early intensive and prompt evaluation in a syncope unit or an ED observation unit (if available), or are hospitalised (Class I, Level B)
- ACC/AHA/HRS 2017 recommends hospital evaluation and treatment when initial evaluation identifies a serious medical condition potentially relevant to the cause of syncope (COR I, LOE B-NR)
Overview and definitions
ESC 2018 asks first whether the event was TLOC at all, and then whether it was of syncopal or non-syncopal origin.[1] ESC 2018 defines TLOC as a state of real or apparent loss of consciousness (LOC) with loss of awareness, characterised by amnesia for the period of unconsciousness, abnormal motor control, loss of responsiveness and a short duration.[1]
ESC 2018 divides TLOC into TLOC due to head trauma and non-traumatic TLOC.[1] ESC 2018 classifies non-traumatic TLOC into four groupings, in order of how often they occur: syncope, epileptic seizures, psychogenic TLOC and a miscellaneous group of rare causes.[1] ESC 2018 separates the groups by mechanism: cerebral hypoperfusion for syncope, abnormal excessive brain activity for epileptic seizures and the psychological process of conversion for psychogenic TLOC.[1]
ESC 2018 uses the adjective presyncope for symptoms and signs that occur before unconsciousness in syncope, and notes that the noun is often used for a state resembling the prodrome of syncope that is not followed by LOC.[1] ACC/AHA/HRS 2017 defines presyncope (near-syncope) as the symptoms before syncope, which could progress to syncope or abort without it.[2]
Related terms (ACC/AHA/HRS 2017)
| Term | ACC/AHA/HRS 2017 Table 3 definition |
|---|---|
| Transient loss of consciousness | Self-limited loss of consciousness that can be divided into syncope and nonsyncope conditions; nonsyncope conditions include but are not limited to seizures, hypoglycaemia, metabolic conditions, drug or alcohol intoxication, and concussion due to head trauma |
| Unexplained syncope (syncope of undetermined etiology) | Syncope for which a cause is undetermined after an initial evaluation 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 | Symptoms such as frequent, recurrent or persistent lightheadedness, palpitations, tremulousness, generalised weakness, blurred vision, exercise intolerance and fatigue upon standing, with or without orthostatic tachycardia, OH or syncope |
| 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 years of age) |
| Postural (orthostatic) tachycardia syndrome (POTS) | Usually all of: frequent symptoms with standing; a heart rate increase of ≥30 bpm from supine to standing (or ≥40 bpm at 12–19 years of age); and the absence of OH (>20 mm Hg reduction in systolic BP) |
| 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 |
Classification
ESC 2018 states that the efficacy of therapy to prevent recurrence is largely determined by the mechanism of syncope rather than its aetiology.[1] ESC 2018 Table 3 groups the principal causes by common pathophysiology, presentation and risk.[1]
Classification of syncope (ESC 2018 Table 3)
| ESC 2018 group | Causes listed in ESC 2018 Table 3 |
|---|---|
| Reflex (neurally mediated) syncope | Vasovagal (orthostatic: standing, less commonly sitting; emotional: fear, pain, instrumentation, blood phobia); situational (micturition, gastrointestinal stimulation, cough or sneeze, post-exercise, others such as laughing or brass instrument playing); carotid sinus syndrome; non-classical forms (without prodromes and/or without apparent triggers and/or atypical presentation) |
| Syncope due to OH | Drug-induced OH (the most common cause of OH, e.g. vasodilators, diuretics, phenothiazine, antidepressants); volume depletion; primary autonomic failure (pure autonomic failure, multiple system atrophy, Parkinson’s disease, dementia with Lewy bodies); secondary autonomic failure (diabetes, amyloidosis, spinal cord injuries, autoimmune or paraneoplastic autonomic neuropathy, kidney failure) |
| Cardiac syncope | Arrhythmia as primary cause (bradycardia from sinus node dysfunction or atrioventricular conduction system disease; supraventricular or ventricular tachycardia); structural cardiac disease (aortic stenosis, acute myocardial infarction or ischaemia, hypertrophic cardiomyopathy, cardiac masses, pericardial disease or tamponade, congenital anomalies of coronary arteries, prosthetic valve dysfunction); cardiopulmonary and great vessels (pulmonary embolus, acute aortic dissection, pulmonary hypertension) |
ESC 2018 Table 3 adds that hypotension may be exacerbated by venous pooling during exercise, after meals (postprandial hypotension) and after prolonged bed rest.[1] ESC 2018 names two mechanisms in reflex syncope: vasodepression, when insufficient sympathetic vasoconstriction causes hypotension, and cardioinhibition, when bradycardia or asystole predominates.[1]
ACC/AHA/HRS 2017 groups
Table 3
- Reflex (neurally mediated) syncope: syncope due to a reflex that causes vasodilation, bradycardia, or both
- Cardiac (cardiovascular) syncope: caused by bradycardia, tachycardia, or hypotension due to low cardiac index, blood flow obstruction, vasodilatation, or acute vascular dissection
- Noncardiac syncope: due to noncardiac causes, which include reflex syncope, OH, volume depletion, dehydration, and blood loss
- Situational syncope: reflex syncope associated with a specific action, such as coughing, laughing, swallowing, micturition, or defecation
ACC/AHA/HRS 2017 reflex forms
Table 3
- Vasovagal syncope (VVS): the most common form of reflex syncope, mediated by the vasovagal reflex; may occur with upright posture (standing or seated) or with exposure to emotional stress, pain or medical settings; typically characterised by diaphoresis, warmth, nausea and pallor; associated with vasodepressor hypotension and/or inappropriate bradycardia; often followed by fatigue; typical features may be absent in older patients
- Carotid sinus hypersensitivity: a pause ≥3 s and/or a decrease of systolic pressure ≥50 mm Hg on stimulation of the carotid sinus
- Carotid sinus syndrome: syncope in the presence of carotid sinus hypersensitivity
Epidemiology
ACC/AHA/HRS 2017 describes a trimodal distribution in both sexes, with the first episode common around 20, 60 or 80 years of age and the third peak 5 to 7 years earlier in males.[2] In a cross section of 1925 randomly selected Olmsted County residents, all older than 45 years, ACC/AHA/HRS 2017 reports an estimated lifetime syncope prevalence of 19%, with a higher prevalence reported by females (22% versus 15%).[2] ACC/AHA/HRS 2017 reports that older institutionalised patients have a 7% annual incidence of syncope, a 23% overall prevalence and a 30% 2-year recurrence rate.[2]
ESC 2018 gives a composite estimate of outcomes after an ED visit for syncope: in the next 7–30 days, only 0.8% die and 6.9% have a non-fatal severe outcome while in the ED, and another 3.6% have a post-ED serious outcome.[1] ESC 2018 also states that OH is associated with a two-fold higher risk of death, owing to the severity of comorbidities, compared with the general population.[1]
Pathophysiology
ESC 2018 centres the classification on a fall in systemic BP with a decrease in global cerebral blood flow, and shows low BP with global cerebral hypoperfusion as the final common pathway of syncope.[1] ESC 2018 states that a sudden cessation of cerebral blood flow for as short as 6–8 s can cause complete LOC.[1] ESC 2018 states that a systolic BP of 50–60 mmHg at heart level, that is 30–45 mmHg at brain level in the upright position, will cause LOC.[1]
ESC 2018 frames the haemodynamics simply: systemic BP is the product of cardiac output and total peripheral resistance, a fall in either can cause syncope, and in syncope both mechanisms often act together.[1]
Low total peripheral resistance
ESC 2018: three causes
- Decreased reflex activity causing vasodilatation through withdrawal of sympathetic vasoconstriction: the vasodepressive type of reflex syncope
- Functional impairment of the autonomic nervous system
- Structural impairment of the autonomic nervous system
Low cardiac output
ESC 2018: four causes
- Reflex bradycardia: cardioinhibitory reflex syncope
- Cardiovascular causes: arrhythmia, structural disease including pulmonary embolism, and pulmonary hypertension
- Inadequate venous return due to volume depletion or venous pooling
- Chronotropic and inotropic incompetence through autonomic failure, which may impair cardiac output
ESC 2018 Figure 3 places drug-induced, primary and secondary autonomic failure in its outer ring, and ESC 2018 Table 3 lists drug-induced OH, the most common cause of OH, as its own entry, separate from primary autonomic failure and secondary autonomic failure (neurogenic OH).[1]
ESC 2018 notes that these mechanisms may interact: venous pooling can trigger an inappropriate reflex in orthostatic reflex syncope, and a low total peripheral resistance may cause venous pooling below the diaphragm that lowers venous return and cardiac output.[1] ESC 2018 adds that in autonomic failure there is insufficient sympathetic vasoconstriction in response to the upright position, and that reflex syncope and OH both span the two main mechanisms.[1]
ACC/AHA/HRS 2017 describes the pathophysiology of VVS as a reflex causing hypotension and bradycardia, triggered by prolonged standing or exposure to emotional stress, pain or medical procedures.[2] ACC/AHA/HRS 2017 explains that in neurogenic OH the vasoconstrictor mechanisms of vascular tone may be inadequate because of neurodegenerative disorders or autonomic peripheral neuropathies, such as those due to diabetes mellitus and other systemic diseases.[2]
[1]Clinical presentation
ESC 2018 Table 5 lists clinical features that can suggest a diagnosis on initial evaluation.[1]
Clinical features that can suggest a diagnosis on initial evaluation (ESC 2018 Table 5)
| Group | Features that can suggest it (ESC 2018 Table 5) |
|---|---|
| Reflex syncope | Long history of recurrent syncope, in particular occurring before the age of 40 years; after unpleasant sight, sound, smell or pain; prolonged standing; during a meal; being in crowded and/or hot places; autonomic activation before syncope (pallor, sweating and/or nausea or vomiting); with head rotation or pressure on the carotid sinus (as in tumours, shaving, tight collars); absence of heart disease |
| Syncope due to OH | While or after standing; prolonged standing; standing after exertion; post-prandial hypotension; temporal relationship with start or changes of dosage of vasodepressive drugs or diuretics leading to hypotension; presence of autonomic neuropathy or parkinsonism |
| Cardiac syncope | During exertion or when supine; sudden onset palpitation immediately followed by syncope; family history of unexplained sudden death at young age; presence of structural heart disease or coronary artery disease |
| Cardiac syncope: ECG findings suggesting arrhythmic syncope | Bifascicular block (left or right bundle branch block [BBB] with left anterior or left posterior fascicular block); other intraventricular conduction abnormalities (QRS duration ≥0.12 s); Mobitz I second-degree atrioventricular (AV) block and first-degree AV block with markedly prolonged PR interval; asymptomatic mild inappropriate sinus bradycardia (40–50 b.p.m.) or slow atrial fibrillation (40–50 b.p.m.) without negatively chronotropic medications; non-sustained ventricular tachycardia (VT); pre-excited QRS complexes; long or short QT intervals; early repolarisation; type 1 ST-segment elevation in V1–V3 (Brugada pattern); negative T waves in right precordial leads or epsilon waves suggestive of arrhythmogenic right ventricular cardiomyopathy (ARVC); left ventricular hypertrophy suggesting hypertrophic cardiomyopathy |
ACC/AHA/HRS 2017 Table 4 lists historical characteristics associated with, though not diagnostic of, cardiac and noncardiac syncope.[2]
More often cardiac
ACC/AHA/HRS 2017 Table 4
- Older age (>60 years)
- Male sex
- Known ischaemic 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 sudden cardiac death (SCD) (<50 years of age)
- Known congenital heart disease
More often noncardiac
ACC/AHA/HRS 2017 Table 4
- Younger age
- No known cardiac disease
- Syncope only in the standing position
- Positional change from supine or sitting to standing
- Prodrome: nausea, vomiting, feeling warmth
- 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
Differential diagnosis
ESC 2018 Table 4 lists the main features that distinguish syncope from disorders that may be mistaken for it.[1] ESC 2018 states that epilepsy forms in which people remain upright, such as complex partial seizures or absence epilepsy, are not regarded as TLOC but are sometimes misdiagnosed as syncope.[1]
Conditions that may be incorrectly diagnosed as syncope (ESC 2018 Table 4)
| Condition | Features that distinguish it from syncope (ESC 2018 Table 4) |
|---|---|
| Generalised seizures | See ESC 2018 section 8, Table 10 |
| Complex partial seizures, absence epilepsy | No falls, yet unresponsive and later amnesia |
| Psychogenic pseudosyncope (PPS) or “pseudocoma” | Apparent LOC lasting many minutes to hours; high frequency, up to several times a day |
| Falls without TLOC | No unresponsiveness or amnesia |
| Cataplexy | Falls with flaccid paralysis and non-responsive, yet no later amnesia |
| Intracerebral or subarachnoid haemorrhage | Consciousness may be progressively reduced rather than immediately lost; accompanying severe headache, other neurological signs |
| Vertebrobasilar transient ischaemic attack (TIA) | Always focal neurological signs and symptoms, usually without LOC; if consciousness is lost this usually lasts longer than in TLOC |
| Carotid TIA | Consciousness is for all practical purposes not lost, but there are pronounced focal neurological signs and symptoms |
| Subclavian steal syndrome | Associated with focal neurological signs |
| Metabolic disorders including hypoglycaemia, hypoxia, hyperventilation with hypocapnia | Duration much longer than in TLOC; consciousness may be impaired instead of lost |
| Intoxication | Duration much longer than in TLOC; consciousness may be impaired instead of lost |
| Cardiac arrest | LOC yet no spontaneous recovery |
| Coma | Duration much longer than TLOC |
Initial evaluation
ESC 2018 frames the initial evaluation as four questions: was the event TLOC; if so, is it syncopal or non-syncopal; in suspected syncope, is there a clear aetiological diagnosis; and is there evidence to suggest a high risk of cardiovascular events or death?[1] ESC 2018 states that a detailed clinical history lets physicians differentiate syncope from other forms of TLOC in approximately 60% of cases.[1]
The initial syncope evaluation (ESC 2018)
- 1
History
Careful history of present and previous attacks, with eyewitness accounts in person or by telephone
- 2
Examination
Physical examination, including supine and standing BP measurements
- 3
ECG
Electrocardiogram (ECG)
ACC/AHA/HRS 2017 recommends a detailed history and physical examination in patients with syncope (COR I, LOE B-NR) and calls a resting 12-lead ECG useful in the initial evaluation (COR I, LOE B-NR).[2] ACC/AHA/HRS 2017 supporting text says the examination should include orthostatic BP and heart rate lying, sitting, on immediate standing and after 3 minutes upright.[2] ACC/AHA/HRS 2017 supporting text also asks for a family history, with particular emphasis on syncope or sudden unexplained death (or drowning).[2]
ESC 2018 states that, based on the findings of the initial evaluation, additional examinations may be performed when needed.[1]
- Immediate ECG monitoring when there is a suspicion of arrhythmic syncope.[1]
- Echocardiogram when there is previous known heart disease, data suggestive of structural heart disease, or syncope secondary to cardiovascular cause.[1]
- Carotid sinus massage (CSM) in patients aged >40 years (ESC 2018; the newer ESC 2021 CSM row names no age, see Carotid sinus massage below).[1][4]
- Head-up tilt testing when there is suspicion of syncope due to OH or reflex syncope (ESC 2018; for suspected recurrent reflex syncope, the newer ESC 2021 tilt row applies, see Tilt testing below).[1][4]
- Blood tests when clinically indicated, e.g. haematocrit or haemoglobin for suspected haemorrhage, oxygen saturation and blood gas for suspected hypoxia, troponin for suspected cardiac ischaemia-related syncope, or D-dimer for suspected pulmonary embolism.[1]
When the initial evaluation is diagnostic (ESC 2018)
Diagnostic criteria with initial evaluation (ESC 2018 recommendation table)
| Diagnosis | ESC 2018 criterion | Class, level |
|---|---|---|
| Vasovagal syncope (VVS) | Highly probable if syncope is precipitated by pain, fear or standing, and is associated with typical progressive prodrome (pallor, sweating and/or nausea) | I, C |
| Situational reflex syncope | Highly probable if syncope occurs during or immediately after specific triggers listed in ESC Table 3 | I, C |
| Syncope due to OH | Confirmed when syncope occurs while standing and there is concomitant significant OH | I, C |
| Reflex syncope and OH (no criterion above met) | Should be considered likely when features suggesting reflex syncope or OH are present and features suggesting cardiac syncope are absent (ESC Table 5) | IIa, C |
| Arrhythmic syncope | Highly probable when the ECG shows: persistent sinus bradycardia <40 b.p.m. or sinus pauses >3 s in the awake state and without physical training; Mobitz II second- or third-degree AV block; alternating left and right BBB; VT or rapid paroxysmal supraventricular tachycardia (SVT); non-sustained episodes of polymorphic VT and long or short QT interval; or pacemaker or implantable cardioverter defibrillator (ICD) malfunction with cardiac pauses | I, C |
| Cardiac ischaemia-related syncope | Confirmed when syncope presents with evidence of acute myocardial ischaemia with or without myocardial infarction | I, C |
| Syncope due to structural cardiopulmonary disorders | Highly probable in patients with prolapsing atrial myxoma, left atrial ball thrombus, severe aortic stenosis, pulmonary embolus or acute aortic dissection | I, C |
ESC 2018 states that when a diagnosis is nearly certain or highly likely, no further evaluation is needed and treatment, if any, can be planned.[1] ESC 2018 adds that in young subjects with unexplained syncope, no cardiac history, no family history of sudden death, no supine, sleep or exercise syncope, no unusual triggers and a normal ECG, the chance of cardiac syncope is very low.[1]
Orthostatic BP: active standing
Active standing (ESC 2018 recommendation table)
| ESC 2018 active standing recommendation | Class, level |
|---|---|
| Intermittent sphygmomanometer BP and heart rate (HR) while supine and during active standing for 3 min are indicated at initial syncope evaluation | I, C |
| Continuous beat-to-beat non-invasive BP and HR measurement may be preferred when short-lived BP variations are suspected, such as in initial OH | IIb, C |
| Syncope due to OH is confirmed when there is a fall in systolic BP from baseline ≥20 mmHg or diastolic BP ≥10 mmHg, or a decrease in systolic BP to <90 mmHg, that reproduces spontaneous symptoms | I, C |
| Syncope due to OH should be considered likely when there is an asymptomatic fall in systolic BP from baseline ≥20 mmHg or diastolic BP ≥10 mmHg, or a decrease in systolic BP to <90 mmHg, and symptoms (from history) are consistent with OH | IIa, C |
| Syncope due to OH should be considered likely when there is a symptomatic fall in systolic BP from baseline ≥20 mmHg or diastolic BP ≥10 mmHg, or a decrease in systolic BP to <90 mmHg, and not all of the features (from history) are suggestive of OH | IIa, C |
| Postural orthostatic tachycardia syndrome (POTS) should be considered likely when there is an orthostatic HR increase (>30 b.p.m. or to >120 b.p.m. within 10 min of active standing) in the absence of OH that reproduces spontaneous symptoms | IIa, C |
| Syncope due to OH may be considered possible when there is an asymptomatic fall in systolic BP from baseline ≥20 mmHg or diastolic BP ≥10 mmHg, or a decrease in systolic BP to <90 mmHg, and symptoms (from history) are less consistent with OH | IIb, C |
ESC 2018 notes that its OH definition differs from the 2011 consensus by adding the absolute 90 mmHg systolic threshold, which it considers useful especially when supine BP is below 110 mmHg.[1] ESC 2018 states that the orthostatic HR increase is blunted or absent (usually not >10 b.p.m.) in neurogenic OH, but increases or even exaggerates with anaemia or hypovolaemia.[1]
ACC/AHA/HRS 2017 defines OH as a drop in systolic BP of ≥20 mm Hg or diastolic BP of ≥10 mm Hg with assumption of an upright posture.[2] ACC/AHA/HRS 2017 also defines three subtypes by timing.[2]
- Initial (immediate) OH (ACC/AHA/HRS 2017): a transient BP decrease within 15 s after standing, with presyncope or syncope.[2]
- Classic OH (ACC/AHA/HRS 2017): a sustained reduction of systolic BP of ≥20 mm Hg or diastolic BP of ≥10 mm Hg within 3 min of assuming upright posture.[2]
- Delayed OH (ACC/AHA/HRS 2017): 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.[2]
- Neurogenic OH (ACC/AHA/HRS 2017): a subtype of OH due to dysfunction of the autonomic nervous system and not solely due to environmental triggers such as dehydration or drugs.[2]
Association of orthostatic intolerance and orthostatic hypotension (ESC 2018 Table 8)
| History | Symptomatic abnormal BP fall | Asymptomatic abnormal BP fall | No abnormal BP drop |
|---|---|---|---|
| Highly suggestive of OH | Syncope is due to OH (Class I) | Syncope is likely due to OH (Class IIa) | Unproven |
| Possibly due to OH | Syncope is likely due to OH (Class IIa) | Syncope may be due to OH (Class IIb) | Unproven |
ESC 2018 Table 8 calls a history highly suggestive of OH when syncope and presyncope occur while standing, are absent lying and less severe or absent sitting, with a predilection for the morning.[1] In the same ESC 2018 Table 8 definition, sitting or lying down must help, complaints may get worse immediately after exercise, after meals or in high temperatures, and there is no autonomic activation.[1]
[1] [2]Risk stratification
ESC 2018 gives two reasons for risk stratification: to recognise patients with a likely low-risk condition who can be discharged with adequate patient education, and patients with a likely high-risk cardiovascular condition who need urgent investigation, which may require admission.[1] ESC 2018 states that high-risk patients are more likely to have cardiac syncope, while low-risk patients are more likely to have reflex syncope and have an excellent prognosis.[1]
ESC 2018: Table 6 features at initial evaluation in the ED
High-risk features (that suggest a serious condition) and low-risk features (that suggest a benign condition) at initial evaluation in the ED (ESC 2018 Table 6)
| Domain | Low-risk (suggests a benign condition) | High-risk: major | High-risk: minor |
|---|---|---|---|
| Syncopal event | Prodrome typical of reflex syncope (e.g. light-headedness, feeling of warmth, sweating, nausea, vomiting); after sudden unexpected unpleasant sight, sound, smell or pain; after prolonged standing or crowded, hot places; during a meal or postprandial; triggered by cough, defaecation or micturition; with head rotation or pressure on the carotid sinus (e.g. tumour, shaving, tight collars); standing from supine or sitting position | New onset of chest discomfort, breathlessness, abdominal pain or headache; syncope during exertion or when supine; sudden onset palpitation immediately followed by syncope | High-risk only if associated with structural heart disease or abnormal ECG: no warning symptoms or short (<10 s) prodrome; family history of SCD at young age; syncope in the sitting position |
| Past medical history | Long history (years) of recurrent syncope with low-risk features with the same characteristics of the current episode; absence of structural heart disease | Severe structural or coronary artery disease (heart failure, low left ventricular ejection fraction [LVEF] or previous myocardial infarction) | None listed |
| Physical examination | Normal examination | Unexplained systolic BP in the ED <90 mmHg; suggestion of gastrointestinal bleed on rectal examination; persistent bradycardia (<40 b.p.m.) in the awake state and in the absence of physical training; undiagnosed systolic murmur | None listed |
| ECG | Normal ECG | ECG changes consistent with acute ischaemia; Mobitz II second- and third-degree AV block; slow atrial fibrillation (AF) (<40 b.p.m.); persistent sinus bradycardia (<40 b.p.m.), or repetitive sinoatrial block or sinus pauses >3 s in the awake state and without physical training; BBB, intraventricular conduction disturbance, ventricular hypertrophy, or Q waves consistent with ischaemic heart disease or cardiomyopathy; sustained and non-sustained VT; dysfunction of an implantable cardiac device (pacemaker or ICD); type 1 Brugada pattern; ST-segment elevation with type 1 morphology in V1–V3 (Brugada pattern); QTc >460 ms in repeated 12-lead ECGs indicating long QT syndrome (LQTS) | High-risk only if the history is consistent with arrhythmic syncope: Mobitz I second-degree AV block and first-degree AV block with markedly prolonged PR interval; asymptomatic inappropriate mild sinus bradycardia (40–50 b.p.m.) or slow AF (40–50 b.p.m.); paroxysmal SVT or AF; pre-excited QRS complex; short QTc interval (≤340 ms); atypical Brugada patterns; negative T waves in right precordial leads, epsilon waves suggestive of ARVC |
A footnote to ESC 2018 Table 6 states that some ECG criteria are per se diagnostic of the cause of syncope, and that appropriate therapy is then indicated without further investigations.[1]
ACC/AHA/HRS 2017: short- and long-term risk factors
ACC/AHA/HRS 2017 recommends evaluation of the cause and assessment of the short- and long-term morbidity and mortality risk of syncope (COR I, LOE B-NR).[2] ACC/AHA/HRS 2017 groups current data into short-term risk (outcomes in the ED and up to 30 days after syncope) and long-term risk (up to 12 months of follow-up).[2]
Short- and long-term risk factors (ACC/AHA/HRS 2017 Table 5); history rows first, then examination and laboratory rows
| Short-term risk factors (≤30 days) | Long-term risk factors (>30 days) |
|---|---|
| Male sex | Male sex |
| Older age (>60 years) | Older age |
| No prodrome | Absence of nausea or vomiting preceding the syncopal event |
| Palpitations preceding loss of consciousness | Ventricular arrhythmias |
| Exertional syncope | Cancer |
| Structural heart disease | Structural heart disease |
| Heart failure | Heart failure |
| Cerebrovascular disease | Cerebrovascular disease |
| Family history of SCD | Diabetes mellitus |
| Trauma | High CHADS-2 score (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, and stroke or transient ischaemic attack) |
| Evidence of bleeding | Abnormal ECG |
| Persistent abnormal vital signs | Lower glomerular filtration rate |
| Abnormal ECG | (none in this row) |
| Positive troponin | (none in this row) |
A footnote to ACC/AHA/HRS 2017 Table 5 states that definitions of clinical endpoints or serious outcomes vary by study.[2] A footnote to ACC/AHA/HRS 2017 Table 6 (examples of syncope risk scores) notes that abnormal ECG is defined variably in those studies.[2] The same ACC/AHA/HRS 2017 Table 6 footnote defines an abnormal ECG in syncope evaluation as any rhythm other than normal sinus rhythm, conduction delays (BBB, type 2 second-degree AV block or third-degree AV block), Q waves, ST abnormalities or a prolonged QT interval.[2]
Risk scores
ESC 2018 states that risk stratification scores may be considered for risk stratification in the ED (Class IIb, Level B).[1] ESC 2018 also advises that the scores perform no better than good clinical judgement and should not be used alone to perform risk stratification in the ED.[1] ACC/AHA/HRS 2017 states that use of risk stratification scores may be reasonable in managing patients with syncope (COR IIb, LOE B-NR).[2]
Emergency department management and disposition
ESC 2018 says ED management of suspected syncope should answer three questions: is there a serious underlying cause that can be identified, what is the risk of a serious outcome, and should the patient be admitted?[1] ESC 2018 states that the acute underlying disease, rather than the syncope itself, most frequently determines short-term adverse events.[1] ESC 2018 adds that many (40–45%) non-cardiovascular and some cardiovascular life-threatening underlying conditions are obvious in the ED.[1]
Management of syncope in the emergency department (ESC 2018 recommendation table)
| ESC 2018 recommendation | Class, level |
|---|---|
| Patients with low-risk features, likely to have reflex or situational syncope, or syncope due to OH, are discharged from the ED | I, B |
| Patients with high-risk features receive an early intensive and prompt evaluation in a syncope unit or in an ED observation unit (if available), or are hospitalised | I, B |
| Patients who have neither high- nor low-risk features are observed in the ED or in a syncope unit instead of being hospitalised | I, B |
| Risk stratification scores may be considered for risk stratification in the ED | IIb, B |
- ESC 2018, low-risk patients: they do not need further diagnostic tests in the ED, as they are likely to have reflex, situational or orthostatic syncope.[1]
- ESC 2018, high-risk patients: they need an intensive diagnostic approach and may need urgent treatment and admission; they should be monitored where resuscitation can be performed; ESC 2018 says it is unclear for how long, with most studies suggesting up to 6 hours in the ED and up to 24 hours in hospital.[1]
- ESC 2018, neither high- nor low-risk: these patients require expert syncope opinion, which can probably be safely managed in an outpatient setting.[1]
- ESC 2018, presyncope: in the ED, presyncope should be managed with the same accuracy as syncope, as it carries the same prognosis.[1]
- ESC 2018, devices: to reduce inappropriate admissions, patients with a cardiac device and syncope should undergo prompt device interrogation.[1]
- ESC 2018, routine tests: diagnostic radiology and laboratory tests such as chest X-ray, brain computed tomography, routine blood haematology, biochemistry, D-dimer and cardiac markers have a low diagnostic yield and impact on risk stratification, and should not routinely be used unless specifically suggested by clinical evaluation.[1]
ESC 2018 Table 7 lists criteria in high-risk patients that favour a stay in an ED observation unit and/or fast-tracking to a syncope unit versus requiring admission to hospital.[1]
High-risk syncope patients: observation unit or fast-track versus admission (ESC 2018 Table 7)
| Favour initial management in ED observation unit and/or fast-track to syncope unit | Favour admission to hospital |
|---|---|
| High-risk features AND: stable, known structural heart disease; severe chronic disease; syncope during exertion; syncope while supine or sitting; syncope without prodrome; palpitations at the time of syncope; inadequate sinus bradycardia or sinoatrial block; suspected device malfunction or inappropriate intervention; pre-excited QRS complex; SVT or paroxysmal AF; ECG suggesting an inheritable arrhythmogenic disorder; ECG suggesting ARVC | High-risk features AND: any potentially severe coexisting disease that requires admission; injury caused by syncope; need of further urgent evaluation and treatment if it cannot be achieved in another way (i.e. observation unit), e.g. ECG monitoring, echocardiography, stress test, electrophysiological study, angiography, device malfunction; need for treatment of syncope |
ESC 2018 warns that unnecessary admission in low-risk patients can be harmful, and that not all patients at high risk need hospitalisation.[1] For patients with neither high- nor low-risk features, ESC 2018 (Figure 6 legend) finds no direct evidence that hospital admission changes outcome, but evidence that management in an ED observation unit and/or fast-track to a syncope outpatient unit is beneficial.[1]
ACC/AHA/HRS 2017: disposition after initial evaluation
Disposition after initial evaluation (ACC/AHA/HRS 2017 recommendation table)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| Hospital evaluation and treatment are recommended for patients presenting with syncope who have a serious medical condition potentially relevant to the cause of syncope identified during initial evaluation | I, B-NR |
| It is reasonable to manage patients with presumptive reflex-mediated syncope in the outpatient setting in the absence of serious medical conditions | IIa, C-LD |
| In intermediate-risk patients with an unclear cause of syncope, use of a structured ED observation protocol can be effective in reducing hospital admission | IIa, B-R |
| It may be reasonable to manage selected patients with suspected cardiac syncope in the outpatient setting in the absence of serious medical conditions | IIb, C-LD |
ACC/AHA/HRS 2017 states that individual risk factors and risk scores are not primary determinants for admission; the presence of at least one serious medical condition in its Table 7 is the key determinant for further in-hospital management.[2]
Examples of serious medical conditions that might warrant consideration of further evaluation and therapy in a hospital setting (ACC/AHA/HRS 2017 Table 7)
| Cardiac arrhythmic conditions | Cardiac or vascular nonarrhythmic conditions | Noncardiac conditions |
|---|---|---|
| Sustained or symptomatic VT; symptomatic conduction system disease or Mobitz II or third-degree heart block; symptomatic bradycardia or sinus pauses not related to neurally mediated syncope; symptomatic SVT; pacemaker or ICD malfunction; inheritable cardiovascular conditions predisposing to arrhythmias | Cardiac ischaemia; severe aortic stenosis; cardiac tamponade; hypertrophic cardiomyopathy (HCM); severe prosthetic valve dysfunction; pulmonary embolism; aortic dissection; acute heart failure; moderate-to-severe left ventricular dysfunction | Severe anaemia or gastrointestinal bleeding; major traumatic injury due to syncope; persistent vital sign abnormalities |
Investigations
ECG monitoring
ESC 2018 states that ECG monitoring is indicated only when there is a high pre-test probability of identifying an arrhythmia associated with syncope, such as those in its Table 5.[1] ESC 2018 calls the correlation between symptoms and an ECG recording the gold standard for diagnosing arrhythmic syncope.[1]
Electrocardiographic monitoring (ESC 2018 recommendation table)
| ESC 2018 recommendation | Class, level |
|---|---|
| Immediate in-hospital monitoring (in bed or by telemetry) is indicated in high-risk patients (defined in Table 6) | I, C |
| Holter monitoring should be considered in patients who have frequent syncope or presyncope (≥1 episode per week) | IIa, B |
| External loop recorders should be considered, early after the index event, in patients who have an inter-symptom interval ≤4 weeks | IIa, B |
| An implantable loop recorder (ILR) is indicated in an early phase of evaluation in patients with recurrent syncope of uncertain origin, absence of high-risk criteria (Table 6), and a high likelihood of recurrence within the battery life of the device | I, A |
| ILR is indicated in patients with high-risk criteria (Table 6) in whom a comprehensive evaluation did not demonstrate a cause of syncope or lead to a specific treatment, and who do not have conventional indications for primary prevention ICD or pacemaker | I, A |
| ILR should be considered in patients with suspected or certain reflex syncope presenting with frequent or severe syncopal episodes | IIa, B |
| ILR may be considered in patients in whom epilepsy was suspected but the treatment has proven ineffective | IIb, B |
| ILR may be considered in patients with unexplained falls | IIb, B |
| Arrhythmic syncope is confirmed when a correlation between syncope and an arrhythmia (bradyarrhythmia or tachyarrhythmia) is detected | I, B |
| In the absence of syncope, arrhythmic syncope should be considered likely when Mobitz II second- or third-degree AV block, a ventricular pause >3 s (with the possible exception of young trained persons, during sleep or rate-controlled AF), or rapid prolonged paroxysmal SVT or VT are detected | IIa, C |
Monitoring when bradycardia is suspected (ESC 2021 pacing guideline)
| ESC 2021 recommendation (pacing guideline) | Class, level |
|---|---|
| Ambulatory ECG monitoring is recommended in the evaluation of patients with suspected bradycardia to correlate rhythm disturbances with symptoms | I, C |
| In patients with infrequent (less than once a month) unexplained syncope or other symptoms suspected to be caused by bradycardia, in whom a comprehensive evaluation did not demonstrate a cause, long-term ambulatory monitoring with an ILR is recommended | I, A |
Where bradycardia is suspected, these ESC 2021 rows are the newer rows; the ESC 2018 rows above cover syncope more generally and are given alongside them.[4][1]
- ESC 2018, presyncope: without a documented arrhythmia, presyncope cannot be considered a surrogate for syncope, whereas a significant arrhythmia documented at the time of presyncope can be considered diagnostic.[1]
- ESC 2018, a normal recording: the absence of arrhythmia during syncope excludes arrhythmic syncope.[1]
- ESC 2018, patience: because syncope recurrence is unpredictable, be prepared to wait up to 4 years or more for a symptom–ECG correlation.[1]
- ESC 2018, limitation: no ECG monitor records BP, so in reflex syncope documented bradycardia or asystole during a syncopal episode does not rule out the possibility that a hidden hypotensive reflex is the principal cause.[1]
Cardiac monitoring and in-hospital telemetry (ACC/AHA/HRS 2017 recommendation tables)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| The choice of a specific cardiac monitor should be determined on the basis of the frequency and nature of syncope events | I, C-EO |
| To evaluate selected ambulatory patients with syncope of suspected arrhythmic etiology, external monitoring can be useful: Holter monitor, transtelephonic monitor, external loop recorder, patch recorder, mobile cardiac outpatient telemetry | IIa, B-NR |
| To evaluate selected ambulatory patients with syncope of suspected arrhythmic etiology, an implantable cardiac monitor (ICM) can be useful | IIa, B-R |
| Continuous ECG monitoring is useful for hospitalised patients admitted for syncope evaluation with suspected cardiac etiology | I, B-NR |
ACC/AHA/HRS 2017 Table 8 fits the Holter monitor to symptoms frequent enough to be detected within 24–72 h of monitoring.[2] ACC/AHA/HRS 2017 Table 8 fits the implantable cardiac monitor to recurrent, infrequent, unexplained syncope (or suspected atypical reflex syncope) of suspected arrhythmic cause after a nondiagnostic initial workup, with or without structural heart disease.[2]
[1] [2]Tilt testing
Tilt testing (ESC 2021 pacing guideline)
| ESC 2021 recommendation (pacing guideline) | Class, level |
|---|---|
| Tilt testing should be considered in patients with suspected recurrent reflex syncope | IIa, B |
Tilt testing (ESC 2018 recommendation table; for suspected recurrent reflex syncope its first row is dated by the ESC 2021 row above)
| ESC 2018 recommendation | Class, level |
|---|---|
| Tilt testing should be considered in patients with suspected reflex syncope, OH, POTS or PPS | IIa, B |
| Tilt testing may be considered to educate patients to recognise symptoms and learn physical manoeuvres | IIb, B |
| Reflex syncope, OH, POTS or PPS should be considered likely if tilt testing reproduces symptoms along with the characteristic circulatory pattern of these conditions | IIa, B |
For suspected recurrent reflex syncope, the current ESC row among the guidelines checked for this topic is the ESC 2021 row (Class IIa, Level B); the ESC 2018 row is history for that group.[4][1] The ESC 2021 row sits in that guideline’s section on evaluating suspected or documented bradycardia or conduction system disease.[4] ESC 2021 text says tilt testing should be considered to confirm a diagnosis of reflex syncope in patients in whom this diagnosis was suspected but not confirmed by initial evaluation.[4] For other suspected reflex syncope, and for OH, POTS and PPS, none of the newer ESC guidelines checked for this topic has a tilt-testing row, so the ESC 2018 row is given as current.[1][4]
- ESC 2018: a negative tilt table response does not exclude a diagnosis of reflex syncope.[1]
- ESC 2018: in syncope of uncertain origin, tilt testing suggests a hypotensive susceptibility, which may exist in reflex syncope and in other causes, including some forms of cardiac syncope.[1]
- ESC 2018: a positive cardioinhibitory response predicts, with high probability, asystolic spontaneous syncope; a vasodepressor, mixed or even negative response does not exclude asystole during spontaneous syncope.[1]
- ESC 2018: tilt testing should not be used to assess the efficacy of a drug treatment.[1]
ESC 2018 cites a systematic literature review: overall tilt positivity in patients with syncope was 66% with the trinitroglycerin protocol and 61% with isoproterenol, against 11–14% in controls, and the test separated patients with syncope from controls with an odds ratio of 12.[1] ESC 2018 also reports positivity of 45–47% in true cardiac arrhythmic syncope, and states that tilt testing should now be considered a means of exposing a hypotensive tendency rather than being diagnostic of VVS.[1]
Tilt-table testing (ACC/AHA/HRS 2017 recommendation table)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| If the diagnosis is unclear after initial evaluation, tilt-table testing can be useful for patients with suspected VVS | IIa, B-R |
| Tilt-table testing can be useful for patients with syncope and suspected delayed OH when initial evaluation is not diagnostic | IIa, B-NR |
| Tilt-table testing is reasonable to distinguish convulsive syncope from epilepsy in selected patients | IIa, B-NR |
| Tilt-table testing is reasonable to establish a diagnosis of pseudosyncope | IIa, B-NR |
| Tilt-table testing is not recommended to predict a response to medical treatments for VVS | III: No Benefit, B-R |
Carotid sinus massage
Carotid sinus massage (ESC 2021 pacing guideline, non-invasive evaluation table)
| ESC 2021 recommendation (pacing guideline) | Class, level |
|---|---|
| Once carotid stenosis is ruled out (footnote below), CSM is recommended in patients with syncope of unknown origin compatible with a reflex mechanism or with symptoms related to pressure/manipulation of the carotid sinus area | I, B |
The ESC 2021 footnote says CSM should not be undertaken after a previous TIA or stroke, or with known carotid stenosis.[4] The same footnote adds that the carotids should be auscultated first, and that a carotid bruit calls for carotid ultrasound to exclude carotid disease.[4] ESC 2018 had indicated CSM in patients >40 years of age with syncope of unknown origin compatible with a reflex mechanism (Class I, Level B).[1] The ESC 2018 CSM row is history here: the ESC 2021 row names no age and adds symptoms related to pressure on or manipulation of the carotid sinus area.[4][1] ESC 2021 text adds that CSM can be helpful in any patient ≥40 years old with symptoms suggestive of carotid sinus syndrome (CSS): syncope or near syncope elicited by tight collars, shaving or turning the head.[4]
Diagnosis of carotid sinus syndrome (ESC 2018 carotid sinus massage recommendation table, selected row)
| ESC 2018 recommendation | Class, level |
|---|---|
| Carotid sinus syndrome (CSS) is confirmed if CSM causes bradycardia (asystole) and/or hypotension that reproduce spontaneous symptoms, and patients have clinical features compatible with a reflex mechanism of syncope | I, B |
ESC 2018 defines carotid sinus hypersensitivity as a ventricular pause lasting >3 s and/or a fall in systolic BP of >50 mmHg, and notes it is common in older men without syncope.[1] ESC 2018 states that a history of syncope reproduced by CSM defines CSS, whereas a positive CSM without a history of syncope defines carotid sinus hypersensitivity.[1] ESC 2018 advises performing CSM supine and upright with continuous beat-to-beat BP monitoring.[1] ESC 2018 had advised only caution after previous TIA or stroke or with known carotid stenosis >70%; the newer ESC 2021 footnote says CSM should not be undertaken after previous TIA or stroke, or with known carotid stenosis.[1][4]
ESC 2018 reports TIAs or strokes in 21 of 8720 patients (0.24%) in pooled data from four studies of CSM.[1]
Echocardiography, exercise testing and electrophysiological study
Cardiac tests after the initial evaluation (selected formal recommendation rows)
| Body | Recommendation | Class or COR, level or LOE |
|---|---|---|
| ESC 2018 | Echocardiography is indicated for diagnosis and risk stratification in patients with suspected structural heart disease | I, B |
| ACC/AHA/HRS 2017 | Transthoracic echocardiography can be useful in selected patients presenting with syncope if structural heart disease is suspected | IIa, B-NR |
| ACC/AHA/HRS 2017 | Routine cardiac imaging is not useful in the evaluation of patients with syncope unless cardiac etiology is suspected on the basis of an initial evaluation, including history, physical examination or ECG | III: No Benefit, B-NR |
| ESC 2018 | Exercise testing is indicated in patients who experience syncope during or shortly after exertion | I, C |
| ESC 2018 | Syncope due to second- or third-degree AV block is confirmed when the AV block develops during exercise, even without syncope | I, C |
| ESC 2018 | Reflex syncope is confirmed when syncope is reproduced immediately after exercise in the presence of severe hypotension | I, C |
| ESC 2021 (pacing) | Exercise testing is recommended in patients who experience symptoms suspicious of bradycardia during or immediately after exertion | I, C |
| ACC/AHA/HRS 2017 | Exercise stress testing can be useful to establish the cause of syncope in selected patients who experience syncope or presyncope during exertion | IIa, C-LD |
| ESC 2022 (ventricular arrhythmias) | In patients with syncope and previous ST-elevation myocardial infarction (STEMI), programmed electrical stimulation (PES) is indicated when syncope remains unexplained after non-invasive evaluation | I, C |
| ESC 2022 (ventricular arrhythmias) | In patients with dilated cardiomyopathy (DCM) or hypokinetic non-dilated cardiomyopathy (HNDCM), electrophysiological evaluation should be considered when syncope remains unexplained after non-invasive evaluation | IIa, C |
| ESC 2021 (pacing) | In patients with syncope and bifascicular block, an electrophysiology study (EPS) should be considered when syncope remains unexplained after non-invasive evaluation or when an immediate decision about pacing is needed due to severity, unless empirical pacemaker implantation is preferred (especially in elderly and frail patients) | IIa, B |
| ACC/AHA/HRS 2017 | EPS can be useful for evaluation of selected patients with syncope of suspected arrhythmic etiology | IIa, B-NR |
ESC 2021 indicates a pacemaker in unexplained syncope with bifascicular block when EPS shows a baseline His ventricular (HV) interval ≥70 ms, second- or third-degree intra- or infra-Hisian block during incremental atrial pacing, or an abnormal response to pharmacological challenge (Class I, Level B).[4] For bifascicular block, the ESC 2021 row replaces the ESC 2018 row, which said EPS should be considered in patients with syncope and bifascicular BBB when syncope remains unexplained after non-invasive evaluation (Class IIa, Level B).[1][4] For unexplained syncope after previous STEMI, and in DCM or HNDCM, the ESC 2022 rows above replace the ESC 2018 EPS row.[1][5] ESC 2022 also has disease-specific rows on PES or electrophysiological evaluation, which are not limited to unexplained syncope; selected rows follow.[5] In arrhythmogenic right ventricular cardiomyopathy (ARVC) with symptoms highly suspicious for ventricular arrhythmia, PES may be considered for risk stratification (Class IIb, Level C).[5] After repair of tetralogy of Fallot (TOF) with arrhythmia symptoms and non-sustained VT (NSVT), electrophysiologic evaluation including PES should be considered (Class IIa, Level C).[5] These two ESC 2022 rows set their own entry criteria (symptoms highly suspicious for ventricular arrhythmia in ARVC; arrhythmia symptoms and NSVT after TOF repair) rather than unexplained syncope, so they are given beside the ESC 2018 EPS row.[1][5] In myotonic dystrophy with palpitations or syncope suggestive of ventricular arrhythmia, or after surviving a cardiac arrest, invasive electrophysiological evaluation is recommended (Class I, Level C).[5] This row also sets its own entry criteria (palpitations or syncope suggestive of ventricular arrhythmia, or a survived cardiac arrest) rather than syncope that remains unexplained after non-invasive evaluation, so it too is given beside the ESC 2018 EPS row.[5][1] In cardiac sarcoidosis with LVEF 35–50% and minor late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) after resolution of acute inflammation, PES for risk stratification should be considered (Class IIa, Level C).[5] That row names no symptoms, so it is given beside the ESC 2018 EPS row.[5][1] For syncope after other myocardial infarction and in other scar-related conditions, the current row is the ESC 2018 row: EPS is indicated when syncope remains unexplained after non-invasive evaluation (Class I, Level B).[1][5] No newer row indicating EPS for syncope that remains unexplained in these other groups was found in the ESC guidelines checked for this topic.[1] The ESC 2020 adult congenital heart disease guideline has a tetralogy of Fallot section on indications for electrophysiological testing and implantable cardioverter defibrillator.[10] In that section, ESC 2020 supporting text says that patients with unexplained syncope and impaired ventricular function or other risk factors for sudden cardiac death should undergo haemodynamic and electrophysiological evaluation.[10] For congenital heart disease (CHD), this topic gives two ESC 2022 Recommendation Table 38 rows.[5] One is the TOF row above.[5] The other, in the ICD table below, is on ICD implantation in CHD with presumed arrhythmic syncope and either at least moderate ventricular dysfunction or inducible sustained monomorphic VT (SMVT) on PES (Class IIa, Level C).[5] In its section on post-infarct patients with preserved or mildly reduced ejection fraction, ESC 2022 supporting text also recommends PES when syncope remains unexplained after non-invasive evaluation, to guide patient management.[5] ACC/AHA/HRS 2017 notes that EPS has a limited role, especially without known heart disease or with low suspicion of an arrhythmic cause.[2]
Blood tests and neurological tests
Blood and neurological tests (selected formal recommendation rows)
| Body | Recommendation | Class or COR, level or LOE |
|---|---|---|
| ACC/AHA/HRS 2017 | Targeted blood tests are reasonable in the evaluation of selected patients with syncope identified on the basis of clinical assessment from history, physical examination and ECG | IIa, B-NR |
| ACC/AHA/HRS 2017 | Usefulness of brain natriuretic peptide and high-sensitivity troponin measurement is uncertain in patients for whom a cardiac cause of syncope is suspected | IIb, C-LD |
| ACC/AHA/HRS 2017 | Routine and comprehensive laboratory testing is not useful in the evaluation of patients with syncope | III: No Benefit, B-NR |
| ACC/AHA/HRS 2017 | Magnetic resonance imaging (MRI) and computed tomography (CT) of the head are not recommended in the routine evaluation of patients with syncope in the absence of focal neurological findings or head injury that support further evaluation | III: No Benefit, B-NR |
| ACC/AHA/HRS 2017 | Carotid artery imaging is not recommended in the routine evaluation of patients with syncope in the absence of focal neurological findings that support further evaluation | III: No Benefit, B-NR |
| ACC/AHA/HRS 2017 | Routine recording of an electroencephalogram (EEG) is not recommended in the evaluation of patients with syncope in the absence of specific neurological features suggestive of a seizure | III: No Benefit, B-NR |
| ESC 2018 | Brain MRI is recommended if neurological examination indicates Parkinsonism, ataxia, or cognitive impairment | I, C |
| ESC 2018 | EEG, ultrasound of neck arteries, and computed tomography or magnetic resonance imaging of the brain are not indicated in patients with syncope | III, B |
| ACC/AHA/HRS 2017 | Simultaneous monitoring of an EEG and haemodynamic parameters during tilt-table testing can be useful to distinguish among syncope, pseudosyncope and epilepsy | IIa, C-LD |
ACC/AHA/HRS 2017 states that the evidence suggests routine neurological testing is of very limited value in syncope, with a low diagnostic yield and a very high cost per diagnosis.[2]
Management: reflex syncope
ESC 2018 calls non-pharmacological treatment the cornerstone of reflex syncope care, including education, lifestyle modification and reassurance about the benign nature of the condition.[1] ACC/AHA/HRS 2017 states that, given the benign nature of VVS and its frequent remissions, medical treatment is usually not required unless conservative measures are unsatisfactory.[2]
ESC 2018 states that additional treatment may be necessary in severe forms, in particular when very frequent syncope alters quality of life, or when recurrent syncope without or with a very short prodrome exposes the patient to a risk of trauma.[1] ESC 2018 also lists syncope during a high-risk activity (e.g. driving, machine operation, flying or competitive athletics) as a situation in which additional treatment may be necessary.[1] ESC 2018 states that age is the most important discriminant for the choice of therapy, with younger patients aged under 40 years and older patients over 60 years, and an overlap between 40 and 60 years.[1]
Treatment of reflex syncope: non-pacing rows (ESC 2018 recommendation table, selected rows)
| ESC 2018 recommendation | Class, level |
|---|---|
| Explanation of the diagnosis, the provision of reassurance, and explanation of the risk of recurrence and the avoidance of triggers and situations are indicated in all patients | I, B |
| Modification or discontinuation of hypotensive drug regimen should be considered in patients with vasodepressor syncope, if possible | IIa, B |
| Isometric physical counter-pressure manoeuvres (PCM) should be considered in patients with prodromes who are <60 years of age | IIa, B |
| Tilt training may be considered for the education of young patients | IIb, B |
| Fludrocortisone may be considered in young patients with the orthostatic form of VVS, low–normal values of arterial BP, and the absence of contraindication to the drug | IIb, B |
| Midodrine may be considered in patients with the orthostatic form of VVS | IIb, B |
| Beta-adrenergic blocking drugs are not indicated | III, A |
Pacing for reflex syncope (ESC 2021 pacing and cardiac resynchronisation therapy guideline recommendation table)
| ESC 2021 recommendation | Class, level |
|---|---|
| Dual-chamber cardiac pacing is indicated to reduce recurrent syncope in patients aged >40 years, with severe, unpredictable, recurrent syncope who have: spontaneous documented symptomatic asystolic pause(s) >3 s or asymptomatic pause(s) >6 s due to sinus arrest or atrioventricular block (AVB); or cardioinhibitory carotid sinus syndrome; or asystolic syncope during tilt testing | I, A |
| Dual-chamber cardiac pacing may be considered to reduce syncope recurrences in patients with the clinical features of adenosine-sensitive syncope | IIb, B |
| Cardiac pacing is not indicated in the absence of a documented cardioinhibitory reflex | III, B |
The 2021 ESC pacing guideline states that, since the 2018 ESC syncope guideline, trials have added information on tilt-induced asystolic vasovagal syncope.[4] It concludes that sufficient evidence exists to upgrade from IIb to I the indication for pacing in patients aged >40 years with asystolic tilt response >3 s.[4] In patients aged >40 years, the 2018 ESC syncope guideline had graded pacing to reduce syncopal recurrences IIa, B for spontaneous documented symptomatic asystolic pause(s) >3 s or asymptomatic pause(s) >6 s due to sinus arrest, AV block or both.[1] In the same age group with recurrent frequent unpredictable syncope, it had graded pacing to reduce syncope recurrences IIa, B for cardioinhibitory carotid sinus syndrome and IIb, B for tilt-induced asystolic response.[1] The single ESC 2021 row above grades all three Class I, Level A.[4] ESC 2018 text had already limited pacing in reflex syncope to highly selected patients aged ≥40 years (mostly >60 years).[1] It describes them as affected by severe forms of reflex syncope with frequent recurrences associated with a high risk of injury, often due to the lack of prodrome.[1]
ESC 2018 describes the education package as reassurance, awareness and possible avoidance of triggers such as dehydration or hot crowded places, and early recognition of the prodrome so the patient can sit or lie down and start counter-pressure manoeuvres.[1] ESC 2018 explains that isometric muscle contractions increase cardiac output and arterial BP during impending reflex syncope.[1]
ESC 2018 calls careful avoidance of BP-lowering agents (antihypertensives, nitrates, diuretics, neuroleptic antidepressants or dopaminergic drugs) key to preventing recurrence.[1] ESC 2018 states that there is moderate evidence that reducing hypotensive therapy, targeting a systolic BP of 140 mmHg, should reduce recurrences in patients with hypotensive susceptibility.[1]
ESC 2018 states that midodrine (usually 2.5–10 mg, three times daily) has proved effective in small studies, but none satisfied the criteria of a definitive clinical trial.[1] ESC 2018 adds that a systematic review rated confidence in the estimates as moderate because of imprecision and publication bias.[1] In the ESC 2018 account of POST 2, 210 young patients (median age 30 years) with low–normal BP and without comorbidities were randomised to fludrocortisone (titrated at 0.05–0.2 mg once per day) or placebo.[1] In POST 2, as ESC 2018 reports it, the primary endpoint showed only a marginal, non-significant reduction in syncope with fludrocortisone compared with placebo (hazard ratio 0.69, 95% CI 0.46–1.03).[1] ESC 2018 reports that beta-blockers failed to be effective in VVS in two randomised double-blind controlled trials, and may enhance bradycardia in CSS.[1]
Expected syncope recurrence with a permanent pacemaker (ESC 2018 Table 9)
| ESC 2018 clinical setting | Expected 2-year syncope recurrence rate with cardiac pacing |
|---|---|
| Syncope due to established bradycardia and absence of hypotensive mechanism | High efficacy (≤5% recurrence rate) |
| Syncope due to established bradycardia and associated hypotensive mechanism | Moderate efficacy (5–25% recurrence rate) |
| Syncope due to suspected bradycardia and associated hypotensive mechanism | Low efficacy (>25% recurrence rate) |
ESC 2018 explains why: cardiac pacing is the most powerful therapy for bradycardia, but its efficacy is less if hypotension coexists.[1]
ESC 2018 states that syncopal recurrences often decrease spontaneously after medical assessment, even without specific therapy; in general, syncope recurs in fewer than 50% of patients within 1–2 years.[1]
Vasovagal syncope and pacemakers in VVS (ACC/AHA/HRS 2017 recommendation tables)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| Patient education on the diagnosis and prognosis of VVS is recommended | I, C-EO |
| Physical counter-pressure maneuvers can be useful in patients with VVS who have a sufficiently long prodromal period | IIa, B-R |
| Midodrine is reasonable in patients with recurrent VVS with no history of hypertension, heart failure or urinary retention | IIa, B-R |
| The usefulness of orthostatic training is uncertain in patients with frequent VVS | IIb, B-R |
| Fludrocortisone might be reasonable for patients with recurrent VVS and inadequate response to salt and fluid intake, unless contraindicated | IIb, B-R |
| Beta blockers might be reasonable in patients 42 years of age or older with recurrent VVS | IIb, B-NR |
| Encouraging increased salt and fluid intake may be reasonable in selected patients with VVS, unless contraindicated | IIb, C-LD |
| In selected patients with VVS, it may be reasonable to reduce or withdraw medications that cause hypotension when appropriate | IIb, C-LD |
| In patients with recurrent VVS, a selective serotonin reuptake inhibitor might be considered | IIb, C-LD |
| Dual-chamber pacing might be reasonable in a select population of patients 40 years of age or older with recurrent VVS and prolonged spontaneous pauses | IIb, B-R (systematic review) |
ACC/AHA/HRS 2017 supporting text, for recurrent VVS without a clear contraindication, suggests 2 to 3 L of fluid per day and a total of 6 to 9 g (100 to 150 mmol) of salt per day.[2] ACC/AHA/HRS 2017 supporting text reports that, in a meta-analysis of 5 RCTs in adults and children, midodrine was associated with a 43% reduction in syncope recurrence.[2] The ACC/AHA/HRS 2017 rows on selective serotonin reuptake inhibitors and beta blockers in VVS give no doses.[2]
ACC/AHA/HRS 2017 supporting text reports no statistically significant benefit with active pacing in 2 RCTs.[2] The same ACC/AHA/HRS 2017 text reports that dual-chamber pacing reduced syncope recurrence in a select population of patients >40 years with recurrent syncope and documented spontaneous pauses ≥3 seconds correlated with syncope or an asymptomatic pause ≥6 seconds.[2] ACC/AHA/HRS 2017 supporting text on pacing in VVS reports less benefit from dual-chamber pacing in patients whose positive tilt-table test induced a vasodepressor response.[2]
Carotid sinus syndrome (ACC/AHA/HRS 2017 recommendation table)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| Permanent cardiac pacing is reasonable in patients with carotid sinus syndrome that is cardioinhibitory or mixed | IIa, B-R |
| It may be reasonable to implant a dual-chamber pacemaker in patients with carotid sinus syndrome who require permanent pacing | IIb, B-R |
Management: orthostatic hypotension
Treatment of orthostatic hypotension (ESC 2018 recommendation table)
| ESC 2018 recommendation | Class, level |
|---|---|
| Explanation of the diagnosis, the provision of reassurance, and explanation of the risk of recurrence and the avoidance of triggers and situations are indicated in all patients | I, C |
| Adequate hydration and salt intake are indicated | I, C |
| Modification or discontinuation of hypotensive drug regimens should be considered (ESC 2018 row; for BP-lowering medications in OH with supine hypertension, the ESC 2024 hypertension row in the next table replaces it; for other hypotensive drugs, such as nitrates, neuroleptic antidepressants or dopaminergic drugs, the ESC 2018 row still applies among the ESC guidelines checked for this topic) | IIa, B |
| Isometric PCM should be considered | IIa, C |
| Abdominal binders and/or support stockings to reduce venous pooling should be considered | IIa, B |
| Head-up tilt sleeping (>10 degrees) to increase fluid volume should be considered | IIa, C |
| Midodrine should be considered if symptoms persist | IIa, B |
| Fludrocortisone should be considered if symptoms persist | IIa, C |
ESC 2018 text advises, in the absence of hypertension, 2–3 L of fluids per day and 10 g of sodium chloride.[1] ESC 2018 states that rapid ingestion of cool water is reported to be effective in combating orthostatic intolerance and postprandial hypotension.[1] ESC 2018 explains that head-up sleeping prevents nocturnal polyuria, keeps a more favourable distribution of body fluids and ameliorates nocturnal hypertension.[1]
Managing hypertension in patients with orthostatic hypotension (ESC 2024 hypertension guideline, Recommendation Table 24)
| ESC 2024 recommendation (hypertension guideline) | Class, level |
|---|---|
| Before starting or intensifying BP-lowering medication, it is recommended to test for orthostatic hypotension, by first having the patient sit or lie for 5 min and then measuring BP 1 and/or 3 min after standing | I, B |
| It is recommended to pursue non-pharmacological approaches as the first-line treatment of orthostatic hypotension among persons with supine hypertension. For such patients, it is also recommended to switch BP-lowering medications that worsen orthostatic hypotension to an alternative BP-lowering therapy and not to simply de-intensify therapy | I, A |
ESC 2024 adds in its text that the treatment of orthostatic hypotension among those with supine hypertension is not to automatically down-titrate BP-lowering medications.[8] It adds that reversible causes should be sought and treated (including discontinuation of offending medications), and that patients requiring BP-lowering medication should be switched to BP-lowering medications that are less likely to cause orthostatic hypotension.[8] For BP-lowering medications in OH with supine hypertension, the second ESC 2024 row above replaces the ESC 2018 drug-modification row (Class IIa, Level B).[8][1] ESC 2018 names the vasoactive drugs as any antihypertensive agents, nitrates, diuretics, neuroleptic antidepressants, or dopaminergic drugs.[1] For the other hypotensive drugs, such as nitrates, neuroleptic antidepressants or dopaminergic drugs, the ESC 2018 row is given as current.[1] The same holds for OH without supine hypertension: no newer drug row specific to orthostatic hypotension was found in the ESC guidelines checked for this topic.[1] For very old or frail patients whose BP drops, see also the ESC 2024 deprescription row under Older patients.[8]
BP threshold and target with pre-treatment symptomatic orthostatic hypotension (ESC 2024 hypertension guideline, Recommendation Tables 17 and 18, selected rows)
| ESC 2024 recommendation (hypertension guideline) | Class, level |
|---|---|
| Because the benefit in reducing cardiovascular disease (CVD) outcomes is uncertain in these settings, and noting that close monitoring of treatment tolerance is advised, BP-lowering treatment should only be considered from ≥140/90 mmHg among persons meeting the following criteria: pre-treatment symptomatic orthostatic hypotension, age ≥85 years, clinically significant moderate-to-severe frailty, and/or limited predicted lifespan (<3 years) (Recommendation Table 17) | IIa, B |
| Because the CVD benefit of an on-treatment systolic BP target of 120–129 mmHg may not generalize to the following specific settings, personalized and more lenient BP targets (e.g. <140 mmHg) should be considered among patients meeting the following criteria: pre-treatment symptomatic orthostatic hypotension, and/or age ≥85 years (Recommendation Table 18) | IIa, C |
These two ESC 2024 rows set the BP threshold for starting BP-lowering treatment and the on-treatment BP target in hypertension.[8] They are not rows on the treatment of orthostatic hypotension or syncope.[8]
ESC 2018 states that the principal strategy in drug-induced autonomic failure is eliminating the offending agent.[1]
Neurogenic OH, dehydration and drugs (ACC/AHA/HRS 2017 recommendation tables)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| Acute water ingestion is recommended in patients with syncope caused by neurogenic OH for occasional, temporary relief | I, B-R |
| Physical counter-pressure maneuvers can be beneficial in patients with neurogenic OH with syncope | IIa, C-LD |
| Compression garments can be beneficial in patients with syncope and OH | IIa, C-LD |
| Midodrine can be beneficial in patients with syncope due to neurogenic OH | IIa, B-R |
| Droxidopa can be beneficial in patients with syncope due to neurogenic OH | IIa, B-R |
| Fludrocortisone can be beneficial in patients with syncope due to neurogenic OH | IIa, C-LD |
| Encouraging increased salt and fluid intake may be reasonable in selected patients with neurogenic OH | IIb, C-LD |
| Pyridostigmine may be beneficial in patients with syncope due to neurogenic OH who are refractory to other treatments | IIb, C-LD |
| Octreotide may be beneficial in patients with syncope and refractory recurrent postprandial or neurogenic OH | IIb, C-LD |
| Fluid resuscitation via oral or intravenous bolus is recommended in patients with syncope due to acute dehydration | I, C-LD |
| Reducing or withdrawing medications that may cause hypotension can be beneficial in selected patients with syncope | IIa, B-NR |
| In selected patients with syncope due to dehydration, it is reasonable to encourage increased salt and fluid intake | IIa, C-LD |
ACC/AHA/HRS 2017 adds that syncope in POTS is relatively infrequent, and there is little evidence that the syncope is due to POTS.[2]
Management: cardiac syncope
ESC 2018 states that, even in the absence of specific trials, there is strong consensus that with syncope secondary to structural cardiac disease the goal of treatment is not only to prevent recurrence but to treat the underlying disease and decrease the risk of death.[1] ESC 2018 notes that therapy to prevent recurrence often differs from therapy for the underlying disease.[1]
Pacing for bradycardia and conduction disease (ESC 2021 pacing and cardiac resynchronisation therapy guideline; selected rows from its sinus node dysfunction, atrioventricular block, bundle branch block and suspected-syncope recommendation tables)
| ESC 2021 recommendation | Class, level |
|---|---|
| Pacing is indicated in sinus node dysfunction (SND) when symptoms can clearly be attributed to bradyarrhythmias | I, B |
| In patients with syncope, cardiac pacing may be considered to reduce recurrent syncope when asymptomatic pause(s) >6 s due to sinus arrest is documented | IIb, C |
| Pacing may be considered in SND when symptoms are likely to be due to bradyarrhythmias, when the evidence is not conclusive | IIb, C |
| Pacing is not recommended in patients with bradyarrhythmias related to SND that are asymptomatic or due to transient causes that can be corrected and prevented | III, C |
| Pacing is indicated in patients in sinus rhythm with permanent or paroxysmal third- or second-degree type 2, infranodal 2:1, or high-degree AVB, irrespective of symptoms (footnote below the table) | I, C |
| Pacing is indicated in patients with atrial arrhythmia (mainly AF) and permanent or paroxysmal third- or high-degree AVB irrespective of symptoms | I, C |
| Pacing should be considered in patients with second-degree type 1 AVB that causes symptoms or is found to be located at intra- or infra-His levels at EPS | IIa, C |
| Pacing is not recommended in patients with AVB due to transient causes that can be corrected and prevented | III, C |
| In patients with unexplained syncope and bifascicular block, a pacemaker is indicated in the presence of either a baseline His ventricular (HV) interval of ≥70 ms, second- or third-degree intra- or infra-Hisian block during incremental atrial pacing, or an abnormal response to pharmacological challenge | I, B |
| Pacing is indicated in patients with alternating BBB with or without symptoms | I, C |
| Pacing may be considered in selected patients with unexplained syncope and bifascicular block without EPS (elderly, frail patients, high-risk and/or recurrent syncope) | IIb, B |
| Pacing is not recommended for asymptomatic BBB or bifascicular block | III, B |
| Pacing is not recommended in patients with unexplained syncope without evidence of SND or conduction disturbance | III, C |
A footnote to the ESC 2021 sinus-rhythm AVB row states that, in asymptomatic narrow QRS complex and 2:1 AVB, pacing may be avoided if supra-Hisian block is clinically suspected (concomitant Wenckebach is observed and block disappears with exercise) or demonstrated at EPS.[4] These ESC 2021 rows replace the bradycardia and conduction-disease pacing rows of the ESC 2018 syncope guideline, one of them only in part (below).[1][4] For example, ESC 2018 had graded pacing IIa, C when the relationship between syncope and asymptomatic sinus node dysfunction was less established.[1][4] The row replaced only in part is the ESC 2018 Class I, Level C row indicating pacing in intermittent or paroxysmal intrinsic third- or second-degree AV block, including AF with slow ventricular conduction, although there is no documentation of a correlation between symptoms and ECGs.[1] For second-degree type 1 AV block that is not shown to cause symptoms and is not intra- or infra-Hisian, no newer recommendation row was found in the ESC guidelines checked for this topic.[1][4] The same holds for AF with slow ventricular conduction without third- or high-degree AV block.[1][4] ESC 2021 text, which carries no class or level, states that the indications for pacing are the same for paroxysmal as for permanent AV block.[4] The reasons it gives are the risk of syncope and sudden cardiac death and the potential progression to permanent AV block.[4] For AV block in permanent AF, ESC 2021 text states that, in the absence of a potentially reversible cause, bradycardia or inappropriate chronotropic response associated or reasonably correlated with symptoms is an indication for cardiac pacing.[4] The same text adds that, in the absence of symptoms due to bradycardia and of high-degree or infranodal block, pacing is unlikely to be beneficial and is not indicated.[4] So for these groups the ESC 2018 row is still the newest recommendation row, but the newer ESC 2021 text ties pacing to symptoms or to the type and level of AV block.[1][4]
Treatment of syncope due to tachyarrhythmias (ESC 2018 recommendation table, selected rows)
| ESC 2018 recommendation | Class, level | Status |
|---|---|---|
| Catheter ablation is indicated in patients with syncope due to SVT or VT in order to prevent syncope recurrence | I, B | SVT: current; no newer row specific to syncope due to SVT was found in the ESC guidelines checked for this topic (ESC 2019 SVT examples in the text below this table). VT: dated history; this row cites the 2015 ESC ventricular arrhythmia guideline, which ESC 2022 updates. Newer ESC guidelines grade VT ablation by substrate and setting (ESC 2022 rows in the table below; other tables named in the text after it) |
| Antiarrhythmic drug therapy, including rate-control drugs, should be considered in patients with syncope due to SVT or VT | IIa, C | SVT: current; no newer row specific to syncope due to SVT was found in the ESC guidelines checked for this topic (ESC 2019 SVT examples in the text below this table). VT: dated history; ESC 2018 refers detailed guidance on antiarrhythmic drug use in VT to the 2015 ESC ventricular arrhythmia guideline, which ESC 2022 updates. Newer ESC guidelines grade VT drug therapy by substrate and setting (ESC 2022 rows in the table below; other tables named in the text after it) |
The newer ESC 2019 SVT guideline has no Class/Level recommendation row specific to syncope; its rows include catheter ablation and drug therapy for specific SVTs.[9] For example, catheter ablation is recommended for symptomatic, recurrent atrioventricular nodal re-entrant tachycardia (AVNRT) (Class I, Level B).[9] Catheter ablation of the accessory pathway(s) is recommended in patients with symptomatic, recurrent atrioventricular re-entrant tachycardia (AVRT) (Class I, Level B).[9] For chronic therapy of AVNRT, diltiazem or verapamil (in patients without heart failure with reduced ejection fraction) or beta-blockers should be considered if ablation is not desirable or feasible (Class IIa, Level B).[9] This topic does not reproduce the other ESC 2019 SVT rows.
ESC 2022 grades catheter ablation and antiarrhythmic drugs (AADs) for VT within its substrate-specific recommendation tables, for example chronic coronary artery disease (CAD) in Recommendation Table 24 and DCM/HNDCM in Recommendation Table 28.[5] In chronic CAD, the ESC 2022 Class I, Level B ablation row applies to recurrent, symptomatic sustained monomorphic VT (SMVT), or ICD shocks for SMVT, despite chronic amiodarone therapy.[5] In that setting, ablation is recommended in preference to escalating AAD therapy; the other catheter ablation rows in Recommendation Table 24 are Class IIa or IIb.[5]
Catheter ablation and antiarrhythmic drugs for VT by substrate (ESC 2022 ventricular arrhythmia guideline, selected rows from its chronic CAD and DCM/HNDCM recommendation tables)
| Guideline and setting | Recommendation | Class, level |
|---|---|---|
| ESC 2022, chronic CAD (Recommendation Table 24) | In patients with CAD and recurrent, symptomatic SMVT, or ICD shocks for SMVT despite chronic amiodarone therapy, catheter ablation is recommended in preference to escalating AAD therapy | I, B |
| ESC 2022, chronic CAD (Recommendation Table 24) | The addition of oral amiodarone or beta-blocker replacement by sotalol should be considered in patients with CAD with recurrent, symptomatic SMVT, or ICD shocks for SMVT while on beta-blocker treatment | IIa, B |
| ESC 2022, chronic CAD (Recommendation Table 24) | Catheter ablation should be considered in patients with CAD and recurrent, symptomatic SMVT, or ICD shocks for SMVT despite beta-blockers or sotalol treatment | IIa, C |
| ESC 2022, chronic CAD (Recommendation Table 24) | In patients with CAD eligible for ICD implantation, catheter ablation may be considered just before (or immediately after) ICD implantation to decrease subsequent VT burden and ICD shocks | IIb, B |
| ESC 2022, DCM/HNDCM (Recommendation Table 28) | Catheter ablation in specialized centres should be considered in patients with DCM/HNDCM and recurrent, symptomatic SMVT or ICD shocks for SMVT, in whom AADs are ineffective, contraindicated, or not tolerated | IIa, C |
| ESC 2022, DCM/HNDCM (Recommendation Table 28) | The addition of oral amiodarone or replacement of beta-blockers by sotalol should be considered in patients with DCM/HNDCM and an ICD who experience recurrent, symptomatic ventricular arrhythmia (VA) despite optimal device programming and beta-blocker treatment | IIa, B |
The ESC 2022 chronic CAD row on catheter ablation as an alternative to an ICD in haemodynamically well-tolerated SMVT with LVEF ≥40% is given in the ICD table below.[5] So are the ESC 2022 Recommendation Table 12 rows on amiodarone or catheter ablation for patients with an ICD indication when an ICD is not available, contraindicated for concurrent medical reasons, or declined by the patient.[5] ESC 2022 has further rows on treating ventricular arrhythmias in its other substrate tables, for example idiopathic premature ventricular complexes/VT (Recommendation Table 26), hypertrophic cardiomyopathy (Table 30), cardiac sarcoidosis (Table 35) and congenital heart disease (Table 39).[5] For arrhythmogenic right ventricular cardiomyopathy, the newer ESC 2023 cardiomyopathy guideline has its own antiarrhythmic table (Recommendation Table 28).[7] Rows on the acute management of sustained VT and electrical storm are in ESC 2022 Recommendation Table 9.[5] This topic does not reproduce the rows in the tables named in the last three sentences.
ICD after a documented ventricular arrhythmia (ESC 2022, 2023 and 2026 recommendation tables, selected rows)
| Guideline and setting | Recommendation | Class, level |
|---|---|---|
| ESC 2022, all patients (Recommendation Table 11) | Implantation of a cardioverter defibrillator is only recommended in patients who have an expectation of good quality survival >1 year | I, C |
| ESC 2022, all patients (Recommendation Table 12) | ICD implantation is recommended in patients with documented ventricular fibrillation (VF) or haemodynamically not-tolerated VT in the absence of reversible causes | I, A |
| ESC 2022, all patients (Recommendation Table 12) | In patients with VT/VF, an indication for ICD, and no contraindication for amiodarone, amiodarone may be considered when an ICD is not available, contraindicated for concurrent medical reasons, or declined by the patient | IIb, C |
| ESC 2022, all patients (Recommendation Table 12) | In patients with sustained monomorphic VT (SMVT) or sustained polymorphic VT (SPVT)/VF triggered by a premature ventricular complex (PVC) with similar morphology and an indication for ICD, catheter ablation may be considered when an ICD is not available, contraindicated for concurrent medical reasons, or declined by the patient | IIb, C |
| ESC 2022, chronic coronary artery disease (CAD) (Recommendation Table 24) | ICD implantation is recommended in patients without ongoing ischaemia with documented VF or haemodynamically not-tolerated VT occurring later than 48 h after myocardial infarction | I, A |
| ESC 2022, chronic CAD (Recommendation Table 24) | In patients with CAD and haemodynamically well-tolerated SMVT and LVEF ≥40%, catheter ablation in experienced centres should be considered as an alternative to ICD therapy, provided that established endpoints have been reached (footnote: VT non-inducibility and elimination of electrograms consistent with conduction delay) | IIa, C |
| ESC 2022, chronic CAD (Recommendation Table 24) | ICD implantation should be considered in patients with a haemodynamically tolerated SMVT and an LVEF ≥40% if VT ablation fails, is not available, or is not desired | IIa, C |
| ESC 2023, cardiomyopathy (Recommendation Table 12) | Implantation of an ICD is recommended in patients with hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC) who have survived a cardiac arrest due to VT or VF, or who have spontaneous sustained ventricular arrhythmia causing syncope or haemodynamic compromise in the absence of reversible causes | I, B |
| ESC 2023, cardiomyopathy (Recommendation Table 12) | Implantation of an ICD is recommended in patients with non-dilated left ventricular cardiomyopathy (NDLVC) and restrictive cardiomyopathy (RCM) who have survived a cardiac arrest due to VT or VF, or who have spontaneous sustained ventricular arrhythmia causing syncope or haemodynamic compromise in the absence of reversible causes | I, C |
| ESC 2023, cardiomyopathy (Recommendation Table 12) | ICD implantation should be considered in patients with cardiomyopathy presenting with haemodynamically tolerated VT, in the absence of reversible causes | IIa, C |
| ESC 2023, DCM (Recommendation Table 24) | An ICD is recommended to reduce the risk of sudden death and all-cause mortality in patients with DCM who have survived a cardiac arrest or have recovered from a ventricular arrhythmia causing haemodynamic instability | I, B |
| ESC 2023, non-dilated left ventricular cardiomyopathy (NDLVC) (Recommendation Table 26) | An ICD is recommended to reduce the risk of sudden death and all-cause mortality in patients with NDLVC who have survived a cardiac arrest or have recovered from a ventricular arrhythmia causing haemodynamic instability | I, C |
| ESC 2026, heart failure | An ICD is recommended in patients who have recovered from a ventricular arrhythmia causing haemodynamic instability (secondary prevention), and who are expected to survive for >1 year with good functional status, in the absence of reversible causes, or unless the ventricular arrhythmia has occurred <48 h after a myocardial infarction, to reduce the risk of sudden death and all-cause death | I, A |
ESC 2026 heart failure refers secondary-prevention ICD to the 2022 ventricular arrhythmia guideline, and cardiomyopathy-specific recommendations for secondary-prevention ICD to the 2023 cardiomyopathy guideline.[6]
ESC 2018 defines unexplained syncope, for patients at high risk of sudden cardiac death, as syncope that does not meet any Class I diagnostic criterion in its section 4 recommendation tables.[1] ESC 2018 states that patients with unexplained syncope and an established ICD indication must receive an ICD before, and independently of, evaluation of the mechanism of syncope.[1]
Primary-prevention ICD rows in CAD, DCM, NDLVC and CHD (ESC 2022 and ESC 2023, selected rows)
| Guideline and setting | Recommendation | Class, level |
|---|---|---|
| ESC 2022, chronic CAD (Recommendation Table 24) | ICD implantation should be considered in patients with CAD, LVEF ≤40% despite ≥3 months of optimal medical treatment (OMT), and non-sustained VT (NSVT), if they are inducible for SMVT by programmed electrical stimulation (PES) | IIa, B |
| ESC 2022, chronic CAD (Recommendation Table 24) | ICD therapy should be considered in patients with CAD, New York Heart Association (NYHA) class I, and LVEF ≤30% despite ≥3 months of OMT | IIa, B |
| ESC 2023, DCM (Recommendation Table 24) | An ICD should be considered in patients with DCM with a genotype associated with high sudden cardiac death (SCD) risk and LVEF >35% in the presence of additional risk factors (see ESC 2023 Table 21, high-risk genotypes and associated predictors of sudden cardiac death) | IIa, C |
| ESC 2023, DCM (Recommendation Table 24) | An ICD may be considered in patients with DCM without a genotype associated with high SCD risk and LVEF >35% in the presence of additional risk factors (footnote: additional risk factors include syncope and the presence of late gadolinium enhancement [LGE] on cardiac magnetic resonance [CMR]) | IIb, C |
| ESC 2023, NDLVC (Recommendation Table 26) | An ICD should be considered in patients with NDLVC with a genotype associated with high SCD risk and LVEF >35% in the presence of additional risk factors (see ESC 2023 Table 21) | IIa, C |
| ESC 2023, NDLVC (Recommendation Table 26) | An ICD may be considered in patients with NDLVC without a genotype associated with high SCD risk and LVEF >35% in the presence of additional risk factors (footnote: additional risk factors include syncope, LGE presence on CMR) | IIb, C |
| ESC 2022, congenital heart disease (CHD) (Recommendation Table 38) | In patients with CHD with presumed arrhythmic syncope and with either at least moderate ventricular dysfunction or inducible SMVT on PES, ICD implantation should be considered | IIa, C |
ESC 2023 defines the non-dilated LV cardiomyopathy phenotype as non-ischaemic LV scarring or fatty replacement without LV dilatation, with or without wall motion abnormalities.[7] The same definition includes isolated global LV hypokinesia without scarring, unexplained solely by abnormal loading conditions (hypertension, valve disease) or CAD.[7] ESC 2022 notes that a new category of hypokinetic non-dilated cardiomyopathy (HNDCM) has been proposed, and its recommendation table covers DCM and HNDCM together.[5] ESC 2023 proposes replacing the term hypokinetic non-dilated cardiomyopathy with non-dilated left ventricular cardiomyopathy (NDLVC), so the NDLVC rows above are the ESC 2023 rows for non-dilated hypokinetic disease.[7] ESC 2023 adds that its recommendations for ICD implantation in DCM with LVEF <35% also apply to patients with NDLVC and LVEF <35%.[7]
Earlier ESC ICD and ILR rows that newer ESC rows cover only in part (current for patients outside the newer rows)
| Earlier row (guideline) | Class, level | Newer ESC rows, and where the earlier row is the newest |
|---|---|---|
| An ICD is indicated in patients with syncope and previous myocardial infarction who have VT induced during EPS (ESC 2018) | I, C | Newer rows cover part of this group: in CAD, the ESC 2022 rows above (LVEF ≤40% despite ≥3 months of OMT with NSVT, if SMVT is inducible at PES, Class IIa, Level B; NYHA class I with LVEF ≤30% despite ≥3 months of OMT, Class IIa, Level B); the ESC 2026 ischaemic heart failure row below; and the two ESC 2026 Class III rows and the disease-specific ESC 2022 and ESC 2023 tables named below this table. For other patients after myocardial infarction, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2018 row is the newest |
| An ICD should be considered in patients with unexplained syncope with systolic impairment, but without a current indication for ICD, to reduce the risk of sudden death (ESC 2018) | IIa, C | Newer rows cover part of this group: in CAD, the ESC 2022 rows above (LVEF ≤40% despite ≥3 months of OMT with NSVT and SMVT inducible at PES; NYHA class I with LVEF ≤30% despite ≥3 months of OMT); in CHD, the ESC 2022 CHD row above; in DCM and NDLVC with LVEF >35%, the ESC 2023 primary-prevention rows above; in DCM and NDLVC with symptomatic heart failure and LVEF ≤35% despite >3 months of OMT, the ESC 2023 rows below; in DCM/HNDCM with LVEF ≤35% and ≥2 risk factors outside those ESC 2023 rows and the ESC 2026 heart failure rows, the ESC 2022 row below; and the two ESC 2026 Class III rows and the disease-specific ESC 2022 and ESC 2023 tables named below this table. Symptomatic heart failure (NYHA class II/III) with LVEF ≤35% despite ≥3 months of optimal therapy, with expected survival longer than 1 year with good functional status, has its own ICD rows (ESC 2026 heart failure table below), and this ESC 2018 row is for patients without a current indication for ICD. For patients outside these newer rows and tables, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2018 row is the newest |
| Instead of an ICD, an ILR may be considered in patients with recurrent episodes of unexplained syncope with systolic impairment, but without a current indication for ICD (ESC 2018) | IIb, C | For unexplained syncope after previous STEMI and in DCM or HNDCM, ESC 2022 has newer rows on PES and on electrophysiological evaluation (cardiac tests table); its algorithms for chronic CAD with reduced ejection fraction (Figure 15) and for DCM/HNDCM (Figure 19) include PES and an ILR step, and cite the ESC 2018 syncope guideline for the ILR step. For patients outside these newer rows and the disease-specific tables named below this table, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2018 row is the newest |
| ICD implantation should be considered in DCM/HNDCM patients with an LVEF <50% and ≥2 risk factors (syncope, LGE on CMR, inducible SMVT at PES, pathogenic mutations in LMNA [footnote: see the specific recommendations for LMNA], PLN, FLNC and RBM20 genes) (ESC 2022) | IIa, C | For LVEF >35%, the ESC 2023 DCM rows above and, for non-dilated (hypokinetic) disease, the ESC 2023 NDLVC rows (Recommendation Table 26) replace it. For LVEF ≤35%, newer rows cover part of this group: with symptomatic heart failure despite >3 months of OMT, the ESC 2023 DCM and NDLVC rows below; with symptomatic heart failure (NYHA class II/III) despite ≥3 months of optimal therapy, in patients expected to survive longer than 1 year with good functional status, the ESC 2026 heart failure rows below; and the ESC 2026 Class III row on NYHA class IV named below this table. For other patients with LVEF ≤35%, such as those without symptomatic heart failure, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2022 row is the newest |
| An ICD should be considered to reduce the risk of sudden death and all-cause mortality in patients with DCM, symptomatic heart failure, and LVEF ≤35% despite >3 months of OMT (ESC 2023) | IIa, A | Newer rows cover part of this group: for symptomatic HFrEF (NYHA class II/III) of a non-ischaemic aetiology with LVEF ≤35% despite ≥3 months of optimal foundational medical therapy, in patients expected to survive longer than 1 year with good functional status, the ESC 2026 non-ischaemic heart failure row below (Class IIa, Level B1); and the ESC 2026 Class III row on NYHA class IV named below this table. For other patients in this group, such as NYHA class IV patients who are not refractory to pharmacological therapy or who are candidates for cardiac resynchronisation therapy, a ventricular assist device or heart transplantation, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2023 row is the newest |
| An ICD should be considered to reduce the risk of sudden death and all-cause mortality in patients with NDLVC, heart failure symptoms, and LVEF ≤35% despite >3 months of OMT (ESC 2023) | IIa, A | The same newer rows as for the ESC 2023 DCM row above cover part of this group. For other patients in this group, no newer row was found in the ESC guidelines checked for this topic, and this ESC 2023 row is the newest |
ESC 2022 and ESC 2023 also have disease-specific tables on sudden cardiac death prevention.[5][7] Examples are ARVC (ESC 2022 Recommendation Table 29; ESC 2023 Recommendation Table 29), hypertrophic cardiomyopathy (ESC 2022 Table 30; ESC 2023 Table 23), neuromuscular diseases (ESC 2022 Table 33) and cardiac sarcoidosis (ESC 2022 Table 35).[5][7] Some of their rows on ICD implantation apply to patients in the groups above; for ARVC and hypertrophic cardiomyopathy, the ESC 2023 tables are the newer source of sudden cardiac death prevention rows.[7][5] For example, for primary prevention in patients with ARVC, ESC 2023 says high-risk features should be considered to aid individualised decision-making for ICD implantation (Class IIa, Level B).[7] A footnote to that ESC 2023 row lists the high-risk features as arrhythmic syncope, NSVT, right ventricular ejection fraction (RVEF) <40%, LVEF <45% and SMVT at PES.[7] ESC 2022 says ICD implantation is recommended in cardiac sarcoidosis with LVEF ≤35% (Class I, Level B).[5] This topic names these tables but does not reproduce them.[5][7]
Two ESC 2026 heart failure Class III rows also cover part of these groups.[6] ICD implantation for primary prevention is not recommended within 40 days of a myocardial infarction, as implantation during this period does not improve prognosis (Class III, Level B1).[6] ICD implantation is not recommended in NYHA class IV with severe symptoms refractory to pharmacological therapy, unless the patient is a candidate for cardiac resynchronisation therapy, a ventricular assist device or heart transplantation (Class III, Level C).[6]
ESC 2022 Figure 15, its algorithm for chronic CAD with reduced ejection fraction, contains boxes for NSVT or unexplained syncope, PES, inducible SMVT and ICD implantation (Class IIa).[5] The figure is an algorithm, not a recommendation-table row, so the table above does not count it as a newer row.[5] For post-infarct patients with preserved or mildly reduced LVEF, ESC 2022 supporting text states that there are no data supporting primary prophylactic ICD implantation.[5]
Earlier ESC ICD rows (selected), given here only as dated history
| Earlier row (guideline) | Class, level | Now given by |
|---|---|---|
| An ICD is indicated in patients with syncope due to VT and an ejection fraction ≤35% (ESC 2018) | I, A | The ESC 2022, 2023 and 2026 rows above on ICD after a documented ventricular arrhythmia |
| An ICD should be considered in patients with an ejection fraction >35% with recurrent syncope due to VT when catheter ablation and pharmacological therapy have failed or could not be performed (ESC 2018) | IIa, C | The same ESC 2022, 2023 and 2026 rows above, including the ESC 2022 CAD rows for haemodynamically tolerated SMVT with LVEF ≥40% |
| ICD implantation is recommended in patients with DCM/HNDCM, who survive sudden cardiac arrest due to VT/VF or experience haemodynamically not-tolerated SMVT (ESC 2022) | I, B | The ESC 2023 cardiomyopathy, DCM and NDLVC secondary-prevention rows |
| ICD implantation should be considered in patients with DCM/HNDCM and haemodynamically tolerated SMVT (ESC 2022) | IIa, C | The ESC 2023 row for cardiomyopathy with haemodynamically tolerated VT |
Primary-prevention ICD in heart failure (ESC 2026 heart failure guideline recommendation table, selected rows; levels as printed)
| ESC 2026 recommendation | Class, level |
|---|---|
| An ICD is recommended in patients with symptomatic heart failure with reduced ejection fraction (HFrEF) (NYHA class II/III) of an ischaemic aetiology (unless they have had a myocardial infarction in the prior 40 days), and an LVEF ≤35% despite ≥3 months of optimal foundational medical therapy, provided they are expected to survive longer than 1 year with good functional status, to reduce the risk of sudden death and all-cause death | I, B1 |
| An ICD should be considered in patients with symptomatic HFrEF (NYHA class II/III) of a non-ischaemic aetiology, and an LVEF ≤35% despite ≥3 months of optimal foundational medical therapy, provided they are expected to survive longer than 1 year with good functional status, to reduce the risk of sudden death and all-cause death | IIa, B1 |
| ICD implantation for primary prevention is not recommended within 40 days of a myocardial infarction as implantation during this period does not improve prognosis | III, B1 |
The ESC 2026 rows above separate ischaemic from non-ischaemic aetiology.[6] The ESC 2018 syncope guideline row they replace recommended ICD therapy to reduce SCD in symptomatic heart failure (NYHA class II–III) with LVEF ≤35% after ≥3 months of optimal medical therapy.[1] That row was limited to patients expected to survive ≥1 year with good functional status and was Class I, Level A without separating aetiology.[1] Before ESC 2026, the 2022 ESC ventricular arrhythmia guideline had graded ICD therapy in symptomatic heart failure (NYHA class II–III) with LVEF ≤35% after ≥3 months of OMT Class I, Level A in CAD and Class IIa, Level A in dilated or hypokinetic non-dilated cardiomyopathy.[5] ESC 2023 graded an ICD Class IIa, Level A in DCM or NDLVC with symptomatic heart failure and LVEF ≤35% despite >3 months of OMT.[7] Those rows have no NYHA class or survival limit and are given in the partly-covered table above.[7] The first two ESC 2026 rows above are for symptomatic HFrEF in NYHA class II/III.[6] They do not cover the ESC 2022 CAD row for NYHA class I with LVEF ≤30% despite ≥3 months of OMT (Class IIa, Level B) in the primary-prevention table above.[5][6] That row is given as current among the ESC guidelines checked for this topic.[5]
Cardiac and inheritable conditions (selected rows from the ACC/AHA/HRS 2017 recommendation tables)
| ACC/AHA/HRS 2017 recommendation | COR, LOE |
|---|---|
| In patients with syncope associated with bradycardia, guideline-directed management and therapy (GDMT) is recommended | I, C-EO |
| In patients with syncope and SVT, GDMT is recommended | I, C-EO |
| In patients with syncope and ventricular arrhythmia (VA), GDMT is recommended | I, C-EO |
| In patients with syncope associated with ischaemic and nonischaemic cardiomyopathy, GDMT is recommended | I, C-EO |
| In patients with syncope associated with valvular heart disease, GDMT is recommended | I, C-EO |
| In patients with syncope associated with HCM, GDMT is recommended | I, C-EO |
| ICD implantation is recommended in patients with ARVC who present with syncope and have a documented sustained VA | I, B-NR |
| ICD implantation is reasonable in patients with Brugada ECG pattern and syncope of suspected arrhythmic etiology | IIa, B-NR |
| ICD implantation is not recommended in patients with Brugada ECG pattern and reflex-mediated syncope in the absence of other risk factors | III: No Benefit, B-NR |
| Beta-blocker therapy, in the absence of contraindications, is indicated as a first-line therapy in patients with LQTS and suspected arrhythmic syncope | I, B-NR |
ACC/AHA/HRS 2017 cautions that the baseline presence of an arrhythmia does not necessarily represent the cause of syncope, giving marked resting bradycardia in a young patient as an example.[2] ACC/AHA/HRS 2017 supporting text notes that patients with aortic stenosis may experience syncope during exertion, often by a haemodynamic rather than arrhythmic mechanism.[2]
Special populations
Older patients
Older patients (formal recommendation rows)
| Body | Recommendation | Class or COR, level or LOE |
|---|---|---|
| ESC 2018 | Multifactorial evaluation and intervention is recommended in older patients because more than one possible cause for syncope and unexplained fall may be present | I, B |
| ESC 2018 | Cognitive assessment and physical performance tests are indicated in older patients with syncope or unexplained fall | I, C |
| ESC 2018 | Modification or discontinuation of possible culprit medications, particularly hypotensive drugs and psychotropic drugs, should be considered in older patients with syncope or unexplained fall (for BP-lowering medications in older patients with OH and supine hypertension, the ESC 2024 hypertension row in the orthostatic hypotension section applies instead: it recommends switching BP-lowering medications that worsen OH to an alternative BP-lowering therapy rather than simply de-intensifying therapy, Class I, Level A; for frail patients whose BP drops, the ESC 2024 deprescription row below is given beside this row) | IIa, B |
| ESC 2024 (hypertension, very old or frail) | If BP drops with progressing frailty, deprescription of BP-lowering medications (and other drugs that can reduce BP, such as sedatives and prostate-specific alpha-blockers) may be considered | IIb, C |
| ESC 2021 (pacing) | In patients with recurrent unexplained falls, the same assessment as for unexplained syncope should be considered | IIa, C |
| ESC 2021 (pacing) | Pacing is not recommended in patients with unexplained falls in the absence of any other documented indication | III, B |
| ACC/AHA/HRS 2017 | For the assessment and management of older adults with syncope, a comprehensive approach in collaboration with an expert in geriatric care can be beneficial | IIa, C-EO |
| ACC/AHA/HRS 2017 | It is reasonable to consider syncope as a cause of nonaccidental falls in older adults | IIa, B-NR |
ESC 2018 applies the same assessment as for unexplained syncope to any unexplained fall (Class IIa, Level C).[1] For recurrent unexplained falls, the ESC 2021 row above replaces it.[1][4] For an unexplained fall that is not recurrent, no newer row was found in the ESC guidelines checked for this topic, so the ESC 2018 row is the newest.[1][4]
ESC 2018 states that syncope may be unwitnessed in over half of older patients, which makes falls and syncope hard to tell apart.[1] ESC 2018 adds that coincidental cardiovascular findings, such as aortic stenosis or AF, may not be the cause of events.[1] ACC/AHA/HRS 2017 reports a 1-year fall rate of 38% among older fainters versus 18.3% among nonfainters.[2]
Children and adolescents
ESC 2018 states that diagnostic evaluation in paediatric patients is similar to that in adults.[1] ESC 2018 states that careful taking of personal and family history and a standard ECG are the most important methods of distinguishing benign reflex syncope (including reflex anoxic seizures or breath-holding spells) from other causes.[1] ESC 2018 states that children with a history suggesting VVS, a normal ECG and no family history of arrhythmia should not undergo further cardiac investigations.[1]
- ESC 2018, history that should prompt cardiac evaluation: family history of premature SCD at age <40 years and/or familial heart disease; known or suspected heart disease; triggers of loud noise, fright or extreme emotional stress; syncope during exercise, including swimming; syncope without prodromes, while supine or sleeping, or preceded by chest pain or palpitations.[1]
- ESC 2018, pacing: even in VVS with prolonged asystole, pacemakers should be avoided in children because of the relatively transient and benign nature of the syndrome.[1]
Paediatric syncope (selected rows from the ACC/AHA/HRS 2017 recommendation table)
| ACC/AHA/HRS 2017 recommendation (paediatric) | COR, LOE |
|---|---|
| VVS evaluation, including a detailed medical history, physical examination, family history and a 12-lead ECG, should be performed in all paediatric patients presenting with syncope | I, C-LD |
| Noninvasive diagnostic testing should be performed in paediatric patients presenting with syncope and suspected congenital heart disease, cardiomyopathy or primary rhythm disorder | I, C-LD |
| In paediatric patients with VVS not responding to lifestyle measures, it is reasonable to prescribe midodrine | IIa, B-R |
| Beta blockers are not beneficial in paediatric patients with VVS | III: No Benefit, B-R |
| Cardiac pacing may be considered in paediatric patients with severe neurally mediated syncope secondary to pallid breath-holding spells | IIb, B-NR |
Psychogenic pseudosyncope
Psychogenic pseudosyncope (formal recommendation rows)
| Body | Recommendation | Class or COR, level or LOE |
|---|---|---|
| ESC 2018 | The recording of spontaneous attacks with a video by an eyewitness should be considered for diagnosis of PPS | IIa, C |
| ESC 2018 | Tilt testing, preferably with concurrent EEG recording and video monitoring, may be considered for diagnosis of PPS | IIb, C |
| ESC 2018 | Doctors who diagnose PPS should present the diagnosis of PPS to the patient | IIa, C |
| ESC 2018 | Cognitive behavioural therapy may be considered in the treatment of PPS if attacks persist after explanation | IIb, C |
| ACC/AHA/HRS 2017 | In patients with suspected pseudosyncope, a candid discussion with the patient about the diagnosis may be reasonable | IIb, C-LD |
| ACC/AHA/HRS 2017 | Cognitive behavioural therapy may be beneficial in patients with pseudosyncope | IIb, C-LD |
ESC 2018 advises that, in suspected PPS, tilt testing should preferably be done with EEG monitoring, where a normal EEG helps to confirm the diagnosis.[1]
Driving
ACC/AHA/HRS 2017 states that it can be beneficial for healthcare providers to know the driving laws and restrictions in their regions and to discuss the implications with the patient (COR IIa, LOE C-EO).[2] The ESC 2018 Web Practical Instructions advise first stratifying the clinical risk of the patient and the likely chance of a syncope recurrence.[3]
Avoidance of private driving after an episode of syncope: suggested symptom-free waiting times (ACC/AHA/HRS 2017 Table 10)
| Condition | Suggested symptom-free waiting time |
|---|---|
| OH | 1 month |
| VVS, no syncope in prior year | No restriction |
| VVS, 1–6 syncope per year | 1 month |
| VVS, >6 syncope per year | Not fit to drive until symptoms resolved |
| Situational syncope other than cough syncope | 1 month |
| Cough syncope, untreated | Not fit to drive |
| Cough syncope, treated with cough suppression | 1 month |
| Carotid sinus syncope, untreated | Not fit to drive |
| Carotid sinus syncope, treated with permanent pacemaker | 1 week |
| Syncope due to nonreflex bradycardia, untreated | Not fit to drive |
| Syncope due to nonreflex bradycardia, treated with permanent pacemaker | 1 week |
| Syncope due to SVT, untreated | Not fit to drive |
| Syncope due to SVT, pharmacologically suppressed | 1 month |
| Syncope due to SVT, treated with ablation | 1 week |
| Syncope with LVEF <35% and a presumed arrhythmic etiology without an ICD | Not fit to drive |
| Syncope with LVEF <35% and presumed arrhythmic etiology with an ICD | 3 months |
| Syncope presumed due to VT/VF, structural heart disease, and LVEF ≥35%, untreated | Not fit to drive |
| Syncope presumed due to VT/VF, structural heart disease, and LVEF ≥35%, treated with an ICD and guideline-directed drug therapy | 3 months |
| Syncope presumed due to VT with a genetic cause, untreated | Not fit to drive |
| Syncope presumed due to VT with a genetic cause, treated with an ICD or guideline-directed drug therapy | 3 months |
| Syncope presumed due to a nonstructural heart disease VT, such as RVOT or LVOT, untreated | Not fit to drive |
| Syncope presumed due to a nonstructural heart disease VT, such as RVOT or LVOT, treated successfully with ablation or suppressed pharmacologically | 3 months |
| Syncope of undetermined etiology | 1 month |
A footnote to the symptom-free waiting-time column of ACC/AHA/HRS 2017 Table 10 states that it may be prudent to wait and observe for the listed waiting time without a syncope spell before resuming driving.[2] In ACC/AHA/HRS 2017 Table 10, RVOT and LVOT mean right and left ventricular outflow tract, and VF means ventricular fibrillation.[2]
Advice for driving in patients with syncope (ESC 2018 Web Practical Instructions, Web Table 3)
| Disorder causing syncope | Group 1 (private drivers) | Group 2 (professional drivers) |
|---|---|---|
| Untreated arrhythmias | Unfit to drive | Unfit to drive |
| Cardiac arrhythmia, not life-threatening, medical treatment | After successful treatment is established | After successful treatment is established |
| Cardiac arrhythmia, life-threatening (e.g. inheritable disorders), medical treatment | After successful treatment is established | Permanent restriction |
| Pacemaker implant | After 1 week | After appropriate function is established (first post-implant visit) |
| Catheter ablation | After successful treatment is established | After successful treatment is established |
| ICD implant | After 1 month; the risk may increase in the few months following an ICD shock (3 months) | Permanent restriction |
| Structural cardiac or cardiopulmonary | After appropriate function is established | After appropriate function is established |
| OH (neurogenic): syncope while sitting | After successful treatment is established | After successful treatment is established |
| Reflex syncope: single or mild | No restrictions unless it occurred during driving | No restriction unless it occurred during driving or without prodromes |
| Reflex syncope: recurrent and severe | After successful treatment is established | After successful treatment is established; particular caution if it occurred during driving or without prodromes |
| Unexplained syncope | No restrictions unless absence of prodrome, occurrence during driving, or presence of severe structural heart disease; if yes, after diagnosis and appropriate therapy is established | After diagnosis and appropriate therapy is established |
The ESC Web Practical Instructions define group 1 as private drivers of motorcycles, cars and other small vehicles with and without a trailer, and group 2 as professional drivers of vehicles over 3.5 tons or passenger vehicles with more than eight seats excluding the driver.[3] The same document says taxicabs, small ambulances and other vehicles form an intermediate category that should follow local legislation, and that observation of therapy efficacy should generally be longer in group 2.[3] The Web Practical Instructions report that recurrence of syncope during driving spans 3–9.8% among patients with a history of syncope, and that syncope-mediated car accidents occur at less than 1% per year.[3]
Evidence, guidelines and regional differences
This topic follows the 2018 ESC syncope guideline, its Web Practical Instructions and the 2017 ACC/AHA/HRS syncope guideline; ESC grades rows by Class and Level, and ACC/AHA/HRS by COR and LOE.[1][2] Where a newer ESC guideline checked for this topic (listed below) has a row on the same question, the topic gives the newest such row.[4][5][7][6][8] Superseded ESC rows then appear only as dated history.[4][5][7][6] For VT, catheter ablation and antiarrhythmic drugs follow a different rule.[1] ESC 2018 cites, and refers detailed drug guidance in VT to, the 2015 ESC ventricular arrhythmia guideline, which ESC 2022 updates; the topic therefore gives the VT half of the ESC 2018 rows only as dated history.[1][5] The topic gives selected ESC 2022 catheter ablation and AAD rows for treating VT in chronic CAD and in DCM/HNDCM, and the rows for patients with an ICD indication when an ICD is not available, contraindicated for concurrent medical reasons, or declined by the patient.[5] For other VT substrates and settings (for example idiopathic VT, or the acute management of sustained VT), it names examples of the ESC tables that hold those rows but does not reproduce them.[5][7] For SVT, no newer row on catheter ablation or drug therapy specific to syncope was found in the ESC guidelines checked for this topic.[9] The topic therefore keeps the ESC 2018 rows for syncope due to SVT and gives examples of ESC 2019 rows for specific SVTs.[1][9] Outside these ablation and drug rows, an older ESC row that a newer row covers only in part is still given, alongside the newer row or for the rest.[4][1][8] Examples are suspected bradycardia, and BP-lowering medications in orthostatic hypotension with supine hypertension (including in older patients).[4][1][8] Another is EPS after myocardial infarction or in other scar-related conditions.[1][5] Others are the ESC 2018 ICD row for syncope with VT induced during EPS after myocardial infarction, and the ESC 2018 row on an ICD to reduce the risk of sudden death in unexplained syncope with systolic impairment.[1][5][7] The same holds for the ESC 2018 ILR alternative to that ICD, and for the ESC 2022 DCM/HNDCM ICD row for LVEF <50% with ≥2 risk factors.[1][5][7][6] So are the ESC 2023 DCM and NDLVC ICD rows for symptomatic heart failure with LVEF ≤35%.[7][6] Another is the assessment of an unexplained fall that is not recurrent.[1][4] The two bodies agree on the core: history, examination with orthostatic BP, and an ECG.[1][2]
The 2021 ESC pacing guideline covers pacing and EPS in bradycardia, conduction disease and reflex syncope.[4] The 2021 ESC pacing guideline also has rows on carotid sinus massage, ambulatory ECG monitoring, exercise testing, tilt testing, ILR and unexplained falls.[4] The 2022 ESC ventricular arrhythmia guideline covers secondary-prevention ICD, PES and ICD in chronic CAD, and electrophysiological evaluation in DCM or HNDCM.[5] It also covers catheter ablation and antiarrhythmic drugs for VT in chronic CAD and in DCM or HNDCM.[5] The 2019 ESC SVT guideline has rows on catheter ablation and drug therapy for specific SVTs; the topic gives examples of them.[9] The 2023 ESC cardiomyopathy guideline supplies the cardiomyopathy, DCM and NDLVC ICD rows given here.[7] The 2026 ESC heart failure guideline supplies the primary- and secondary-prevention ICD rows in heart failure, including the row against primary-prevention ICD within 40 days of a myocardial infarction.[6]
The 2024 ESC hypertension guideline supplies the rows on testing for orthostatic hypotension before starting or intensifying BP-lowering medication, and on BP-lowering drugs in orthostatic hypotension with supine hypertension.[8] It also supplies the BP threshold and target rows for pre-treatment symptomatic orthostatic hypotension.[8] The newer ESC guidelines checked for this topic are those on supraventricular tachycardia (2019), pulmonary embolism (2019), dyslipidaemias (2019 and 2025), adult congenital heart disease (2020), pacing (2021), ventricular arrhythmias (2022) and non-cardiac surgery (2022). The others checked are those on acute coronary syndromes, endocarditis and cardiomyopathies (2023), and on atrial fibrillation, chronic coronary syndromes, hypertension, and peripheral arterial and aortic diseases (2024). The last are those on valvular heart disease and pregnancy (2025), and on heart failure and cardiac rehabilitation (2026). For the 2020 sports cardiology guideline only the narrative text was checked, because its recommendation tables were not available as text. For the 2019 and 2025 dyslipidaemia documents, only the recommendation tables available as text were checked. The ESC guidelines on myocardial revascularisation (2018), cardiovascular disease prevention (2021), cardio-oncology (2022) and pulmonary hypertension (2022) were not checked. Nor were those on cardiovascular disease in diabetes (2023), myocarditis and pericarditis (2025), and cardiovascular disease in chronic kidney disease (2026). Statements in this topic that no newer ESC row was found refer to the checked guidelines only.
ESC (2018 syncope; 2021 pacing)
where the guidelines differ
- ESC 2018: beta-adrenergic blocking drugs are not indicated in reflex syncope (Class III, Level A)
- ESC 2021: dual-chamber pacing is indicated to reduce recurrent syncope in patients aged >40 years with severe, unpredictable, recurrent syncope who have spontaneous documented asystolic pauses (>3 s symptomatic or >6 s asymptomatic) due to sinus arrest or AVB; or cardioinhibitory carotid sinus syndrome; or asystolic syncope during tilt testing (Class I, Level A)
- ESC 2018: midodrine may be considered in the orthostatic form of VVS (Class IIb, Level B)
- ESC 2018: ED disposition is driven by Table 6 high- and low-risk features
ACC/AHA/HRS 2017
where the guidelines differ
- Beta blockers might be reasonable at 42 years or older with recurrent VVS (COR IIb, LOE B-NR)
- Dual-chamber pacing might be reasonable in a select population of patients 40 years or older with recurrent VVS and prolonged spontaneous pauses (COR IIb, LOE B-R, systematic review)
- Midodrine is reasonable in recurrent VVS with no history of hypertension, heart failure or urinary retention (COR IIa, LOE B-R)
- A serious medical condition (Table 7) is the key determinant for in-hospital management
ACC/AHA/HRS 2017 notes that the logistical and financial feasibility of specialised syncope units in North American settings is unknown.[2] ESC 2018 states that tilt training has little efficacy in reducing recurrence of syncope in young patients with long-lasting recognisable prodromes, and ACC/AHA/HRS 2017 calls the usefulness of orthostatic training uncertain in patients with frequent VVS (COR IIb, LOE B-R).[1][2]
Exam pearls
- ESC 2018 lists four features of TLOC: short duration, abnormal motor control, loss of responsiveness, and amnesia for the period of LOC.[1]
- ESC 2018 Table 6 counts syncope during exertion or when supine as a major high-risk feature, but syncope in the sitting position as minor (high-risk only with structural heart disease or an abnormal ECG).[1]
- ESC 2018 Table 7 lists injury caused by syncope among the features that favour admission in a patient with high-risk features.[1]
- ESC 2018 states that the absence of arrhythmia during syncope excludes arrhythmic syncope.[1]
- ESC 2018 states that CSM in carotid sinus syndrome usually shows a period of asystole >6 s.[1]
- ESC 2018 states that EEG, neck artery ultrasound and brain CT or MRI are not indicated in patients with syncope (Class III, Level B), but in the same table recommends brain MRI if neurological examination indicates Parkinsonism, ataxia or cognitive impairment (Class I, Level C); ACC/AHA/HRS 2017 does not recommend routine EEG without specific neurological features suggestive of a seizure, or routine carotid imaging or head MRI and CT without focal neurological findings (or, for head imaging, head injury) that support further evaluation (each COR III: No Benefit).[1][2]
References10ShowHide
- [1]Brignole M, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J, 2018.PMID 29562304
- [2]Shen WK, et al. 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. Circulation, 2017.PMID 28280231
- [3]Brignole M, et al. Practical Instructions for the 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J, 2018.PMID 29562291
- [4]Glikson M, et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J, 2021.PMID 34455430
- [5]Zeppenfeld K, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J, 2022.PMID 36017572
- [6]Køber L, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
- [7]Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies. Eur Heart J, 2023.PMID 37622657
- [8]McEvoy JW, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J, 2024.PMID 39210715
- [9]Brugada J, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardiaThe Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J, 2020.PMID 31504425
- [10]Baumgartner H, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J, 2021.PMID 32860028