Introduction
The term ‘syncope’ is derived from the Greek word meaning ‘to cut short’ or ‘interrupt’. Syncope can be described as a transient loss of consciousness due to transient global cerebral hypoperfusion, characterized by rapid onset, short duration, loss of tone and spontaneous complete recovery.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 A literature search performed on definitions of syncope and related disorders found that syncope, neurocardiogenic syncope, neurally mediated syncope, orthostatic intolerance and orthostatic hypotension were defined in only 41, 34, 26, 38 and 48% of papers, respectively, and, when definitions were given, they differed considerably between papers.Reference Thijs, Benditt and Mathias2
It is well recognized that syncope presents in a bimodal age distribution with a 3- to 4-fold rise with advancing age. Younger patients tend to have a reflex mechanism as the most common aetiology, whereas in older patients the aetiology tends to be cardiac in nature, or related to orthostatic hypotension.Reference Galizia, Abete and Mussi3 With the substantial growth in the older population and the corresponding increase in polypharmacy, there is a rising incidence of syncope in this group.
The likelihood of an underlying serious diagnosis (defined as death, myocardial infarction, arrhythmia, pulmonary embolism, stroke, subarachnoid haemorrhage, significant haemorrhage or any condition resulting in a return to the emergency department) as a cause for a syncopal event can be identified primarily thorough history and examination, augmented by the use of stratification algorithms such as the San Francisco Syncope RuleReference Quinn, McDermott, Stiell, Kohn and Wells4 (SFSR) and Ottawa electrocardiographic criteria.Reference Thiruganasambandamoorthy, Hess, Turko, Tran, Wells and Stiell5 Indeed, a study by Mendu et al.Reference Mendu, McAvay, Lampert, Stoehr and Tinetti6 showed that, of commonly performed investigations for suspected syncope (brain imaging, electroencephalogram, carotid Doppler ultrasound and postural blood pressures), the investigation of choice (with the highest yield of results changing management decisions) was postural blood pressure measurement.Reference Mendu, McAvay, Lampert, Stoehr and Tinetti6 Brain and carotid Doppler studies, along with electroencephalogram, rarely provided results that aided diagnosis or changed management when carried out in patients who were deemed a low risk on the SFSR.Reference Quinn, McDermott, Stiell, Kohn and Wells4 Costs per diagnosis of syncope are estimated as £611 in the UK and it has a massive burden on heath economy.Reference Parry and Tan7
Being over 60 is strongly associated with short-term serious events after an emergency department visit for syncope, so this puts even more emphasis on speedy and accurate diagnosis and treatment.Reference Sun, Hoffman, Mangione and Mower8 A study found 7% of older patients with syncope experienced a 30 day serious event. High-risk predictors included age greater than 90, male sex, history of an arrhythmia, systolic blood pressure >160 in triage and abnormal electrocardiogram (ECG) or troponin. A low-risk predictor was near syncope rather than syncope.Reference Sun, Derose and Liang9 Further to the problems associated with increased incidence of cognitive impairment inhibiting an accurate history from certain older patients, up to 60% of episodes are unwitnessed.Reference Sun, Emond and Camargo10 There is evidence that amnesia for loss of consciousness (A-LOC) can be present in up to 50% of patients undergoing head-up tilt-table testing. O'Dwyer et al. demonstrated that older patients in particular were susceptible to A-LOC, and this in turn was associated with a reduced awareness of prodromal symptoms and significantly more fractures compared with those patients without amnesia.Reference O'Dwyer, Bennett, Langan, Fan and Kenny11 This phenomenon has also been demonstrated amongst younger syncopal patients.Reference Lempert, Bauer and Schmidt12
Search methods
A previous review article by Nath and Kenny in 2005Reference Nath and Kenny13 examined the evidence surrounding various aspects of syncope including prevalence, cause, risks, investigations and treatment. This review is based on a search of Medline, PubMed and the Cochrane Collaboration using the terms ‘syncope’, ‘vasovagal syncope’, ‘postural hypotension’ and ‘carotid sinus hypersensitivity’. The term ‘pathophysiology, syncope older people’ was also searched. Search terms were related to ‘older patients’ and ‘elderly patients’. Results were limited to English language articles and we consulted European Society of Cardiology (ESC) guidelines.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1
Epidemiology
Although syncope is common in older people, epidemiological data are limited. A study that looked at syncope in elderly institutionalized individuals revealed a 10-year prevalence of 23% and 1-year incidence of 7%, and a 2-year recurrence rate of 30%.Reference Lipzitz, Wei and Rowe14 A study that looked at the incidence of syncope in a population aged >45 years reported an estimated prevalence of 19%. The age-specific prevalence rates were 45–54 years (20%), 55–64 years (20%), 65–74 years (15%) and 75 years or more (21%), and concluded there was no association of syncope prevalence with age.Reference Chen, Shen and Mahoney15 In contrast, a larger study of 7814 participants with a mean age of 51.1 years (range 20–96) showed the overall incidence rate of a first report of syncope was 6.2 per 1000 person-years.Reference Soteriades, Evans, Larson, Chen, Chen, Benjamin and Levy16 The incidence rates increased with age, with a sharp rise at 70 years.Reference Hainsworth17 This is also supported by many other studies and we can conclude that the overall incidence of syncope increases as one grows older.
Pathophysiology
Syncope or near-syncope is not an uncommon effect of gravitational or other stresses and it occurs when cerebral blood flow falls to below about half the normal value. Blood pressure is regulated mainly by baroreceptor reflexes, through their control of vascular resistance and heart rate. Normally, syncope is overcome in a healthy individual by vasoconstriction, whilst heart rate responses are of much less physiological significance. People are more likely to faint when upright, warm, following meals, dehydrated or emotionally stressed and these factors may be involved in some reflex syncope, including micturition and defaecation.Reference Deharo, Mechulan, Giorgi, Franceschi, Prevot and Peyrouse18 Intravascular volume and concurrent use of medications such as anti-hypertensives or diuretics also play a role in these mechanisms.
Due to age-related pathophysiological changes, the older person is more sensitive to syncope due to a variety of reasons, like atherosclerosis and stiffening of arterial vessels, reduced endothelial related nitric oxide release and increased endothelin release, which impair vasodilatory mechanisms in elderly people. Fibrotic ventricular walls leading to diastolic and left ventricular dysfunction and early diastolic filling and reduction in pacemaker cells in the sinus node make the older person more sensitive to reductions in cardiac pre-load and syncope. Older patients have a higher incidence of co-morbidities that predispose to autonomic dysfunction, such as diabetes, Parkinson's disease, congestive cardiac failure and cardiovascular disease and cerebrovascular disease. Medications, including anti-hypertensives, sedatives, vasodilators, diuretics and anti-arrthymics, also contribute to syncope in the older person.
Another proposed pathophysiological mechanism regarding potential causes of syncope (in particular neurally mediated syncope) is the potential correlation of plasma adenosine A2A receptor expression, plasma adenosine levels and a positive head-up tilt test (HUTT). Deharo et al. found that a high plasma adenosine level was associated with a high probability of positive HUTT, while expression of the A2A receptor was lowest in patients with a positive adenosine challenge and negative HUTT, and highest in patients with a negative adenosine challenge and positive HUTT.Reference Deharo, Mechulan, Giorgi, Franceschi, Prevot and Peyrouse18 The relevance of this study to clinical practice remains unclear at present.
Aetiology
It has been established that neurally mediated syncope accounts for around 50% of syncopal events. Cardiac causes account for around 14%, while drug-induced and multifactorial causes can be found in 11 and 17%, respectively.Reference Nath and Kenny13 Neurally mediated syncope includes carotid sinus syndrome, vasovagal syncope and situational syncope. Orthostatic hypotension can be due to autonomic failure or intravascular volume depletion or medications. Cardiac causes include bradycardias, paroxysmal tachycardias and valvular disease. In 2011, Mitro et al. carried out a study examining the aetiology of syncope and the standardized evaluation of patients with syncope.Reference Mitro, Kirsch, Valocik and Murin19 The results were broadly similar to that of previous studies. Reflex syncope, including vasovagal, situational and carotid sinus hypersensitivity were the most frequently occurring cause of syncope, accounting for 46.2% of the study group. Arrhythmogenic syncope accounted for 35.3% with bradyarrhythmia being the most prevalent arrhythmia (this included sick sinus syndrome, atrioventricular (AV) blocks and atrial fibrillation with slow ventricular fibrillation). Tachyarrhythmia accounted for 8.7% of syncope, while cardiac obstructive syncope (aortic stenosis, pulmonary embolism, tricuspid valve obstruction) accounted for 1.2%, and valvular syncope accounted for only 0.4% of patients presenting with syncope. 10.8% of the patients in the study group received a diagnosis of unexplained syncope after investigation.Reference Mitro, Kirsch, Valocik and Murin19
Tan et al. (2008) have described how orthostatic hypotension, vasovagal syncope and carotid sinus hypersensitivity are likely to co-exist in older patients with syncope, unexplained falls and drop attacks. However, the study failed to find a true association between the three conditions, and so does not support a common mechanism.Reference Tan, Newton, Chadwick and Parry20
Carotid sinus syndrome
Carotid sinus syndrome (CSS) is defined as asystole of at least 3 s (cardioinhibitory CSS) and/or systolic blood pressure drop of at least 50 mmHg (vasodepressor CSS) in response to carotid sinus massage (CSM).Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 CSS tends to be an ageing-related autonomic disorder, rarely occurring before the age of 50 years but increasing in incidence thereafter. It is caused by dysfunctional baroreceptor reflex mechanisms. In CSS, mechanical deformation of the carotid sinus (located at the bifurcation of the common carotid artery) leads to an exaggerated response with bradycardia or vasodilatation, resulting in hypotension, presyncope or syncope.
A study in 2008 had looked at the accumulation of tau protein in patients with confirmed CSS compared with controls, and found increased tau protein accumulation in the baroreflex associated nuclei compared with other areas, suggesting that medullary degeneration may play a role in CSS.Reference Miller and Kenny21 CSS has been associated with advancing age, male sex, hypertension, coronary artery disease, orthostatic hypotension, vasovagal syncope, Alzheimer's disease, Parkinson's disease, dementia with Lewy bodiesReference McIntosh, Lawson and Kenny22, Reference Ballard, Shaw, McKeith and Kenny23 and medication with digoxin and beta blockers.
CSS can be classified according to the VASIS classification system:Reference Brignole, Menozzi and Del Rosso24
• Type 1 mixed: heart rate falls at the time of syncope, with ventricular rate remaining above 40 beats per minute (b.p.m.), or falls to less than 40 b.p.m. for less than 10 s with or without asystole of less than 3 s. Blood pressure falls before the heart rate falls.
• Type 2A, cardioinhibition without asystole: heart rate falls to a ventricular rate less than 40 b.p.m. for more than 10 s, but asystole of more than 3 s does not occur. Blood pressure falls before the heart rate falls.
• Type 2B, cardioinhibition with asystole: asystole occurs for more than 3 s. Heart rate fall coincides with or precedes blood pressure fall.
• Type 3 vasodepressor: heart rate does not fall more than 10%, from its peak, at the time of syncope.
• Exception 1 – chronotropic incompetence. These patients show no heart rate rise during the tilt (i.e. less 10% from the pre-tilt rate).
• Exception 2 – excessive heart rate rise. These patients show an excessive heart rate rise both at the onset of the upright position and throughout its duration before syncope (i.e. greater than 130 b.p.m.) (postural tachycardia syndrome).
Vasovagal syncope
Vasovagal syncope (VVS) can be defined as a reflex response that when triggered, gives rise to vasodilatation and/or bradycardia, resulting in transient cerebral hypoperfusion.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 Synonyms of VVS include reflex syncope cough, micturition, defaecation, neurocardiogenic syncope, neurocardiovascular syncope and neurogenic syncope. A diagnosis of VVS or situational syncope can usually be obtained from a detailed history, including a collateral history from any witnesses present. This may prevent unnecessary diagnostic procedures being carried out. A recent study, looking at the clinical features of 1060 patients with positive HUTT, also confirmed bimodal age distribution with a larger peak between 70 and 79 years. They also reported that patients over the age of 60 were less likely to report loss of consciousness, near loss of consciousness or palpitations and more likely to present with unexplained falls. The typical provoking factors of prolonged standing, posture change and hot environments were also less common in older patients.Reference Duncan and Tan25
Older people appear to produce a dysautonomic response during tilt-table testing, resulting in sudden loss of consciousness, or a more gradual and asymptomatic response. Furthermore, younger patients tend to have a more bradycardic response, whilst older patients display more hypotensive episodes.Reference Duncan and Tan25 As mentioned above, history and examination are paramount but difficulties arise as older patients do not present with classical features and more tilt tests are being performed to confirm the diagnosis. Another age-related difference that has been demonstrated is that although drug-free HUTT is less sensitive in the older person, glyceryl trinitrate (GTN) induced HUTT seems to have higher sensitivity.Reference Gracie, Newton, Norton, Baker and Freeston26 Finally, a recent study looking at the psychological impact of VVS concluded that patients with VVS have a significant degree of psychological distress, which needs to be considered as part of the management plan.Reference Tinetti, Mendes de Leon, Doucette and Baker27 An older study has also shown that VVS is associated with increased institutionalization in the older person.Reference Gupta and Lipsitz28
Orthostatic hypotension
Orthostatic hypotension (OH) is defined as a drop in systolic/diastolic blood pressure of ≥20/10 mmHg when an individual changes from a supine to a standing position within 3 min of standing.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 It is a common problem in elderly people and associated with significant mortality and morbidity. While acute orthostatic hypotension is usually a result of factors such as medication, fluid or blood loss, or adrenal insufficiency, chronic orthostatic hypotension is frequently due to altered blood pressure regulatory mechanisms and autonomic dysfunction.Reference Gribben, Pickering, Sleight and Peto29 It is also known that hypertension impairs baroreflex sensitivity and also restricts ventricular filling.Reference Immink, van der Born and van Montrans30 This paradoxically can increase periodic hypotension. Hypertension is also known to alter cerebral autoregulation threshold.Reference Baliga and Prabhu31
The reported incidence of OH varies between 4 and 33% amongst community-dwelling elderly.Reference Hiitola and Enlund32 The prevalence of OH was related to the total number of medicines in regular use but there was no specific gender difference. The incidence of OH tends to increase with age, presence of conditions of other diseases such as diabetes, Parkinson's disease and neurodegenerative disorders. Moreover, both increase and pronounced decrease of systolic blood pressure during early orthostasis indicate higher risk of cerebrovascular death.Reference Fedorowski, Hedblad and Melander33
Mussi et al.Reference Mussi, Ungar, Salvioli, Menozzi, Bartoletti, Giada and Lagi34 examined OH as a cause of syncope in patients attending the emergency department for transient loss of consciousness. They found that 12.4% of patients were found to have OH as a cause for their syncope, of which 12.5% were found to have Parkinson's disease and 25% had other neurological diseases. Among drugs commonly associated with OH (diuretics, ACE inhibitors/sartans, calcium channel blockers, beta blockers, digoxin, anti-arrythmic drugs, nitrates and antipsychotics), only diuretics, digoxin and nitrates had a statistically significant association with OH. Parkinson's disease was the only other condition independently associated with syncope due to OH.Reference Mussi, Ungar, Salvioli, Menozzi, Bartoletti, Giada and Lagi34
Falls
The Oxford Handbook of Geriatric Medicine Reference Bowker, Price and Smith35 defines a fall as ‘an event that results in a person non-intentionally coming to rest at a lower level (usually the floor)’. Falls are common in the older population, under-reported and have potentially life-threatening consequences. They affect both confidence and function and account for significant health care costs in terms of hospital admissions and institutionalization, and managing consequences such as fractures.
Syncope and falls are often intertwined in their presentation. An initial presentation of syncope may be as a fall and the clinical history can often differentiate the accidental fall from more serious causes such as syncope.Reference Brignole39 Up to 25% of syncopal events initially present as unexplained fallsReference Bien, Wilmanska, Janczak, Wojskowicz, Kasiukiewicz and Klimiuk40 and clinical history surrounding critical aspects of the event may be impeded by factors such as amnesia for loss of consciousnessReference O'Dwyer, Bennett, Langan, Fan and Kenny11 and cognitive impairment. Protective reflexes may be impaired in older patients and gait abnormalities may make this population more vulnerable to minor haemodynamic changes.
Cardiac arrythmias
Cardiac arrhythmia is known to be a cause of syncope in a significant proportion of patients. In their 2011 study, Bien at al. found a cardiac cause for syncope in 17.7% of their study population.Reference Bien, Wilmanska, Janczak, Wojskowicz, Kasiukiewicz and Klimiuk40 Conduction tissue disease is known to cause syncope in the older person. Sick sinus syndrome causing sinus bradycardia, atrial pauses, sinus arrest or atrial fibrillation or tachycardia-bradycardia syndromes may well cause syncope. Atrioventricular node disease can cause variable degrees of AV block and syncope. Around 30% of patients over 65 with bradycardia may have some degree of AV block.Reference Bhat, Watanabe, Rao and Luisada41
Older patients are more likely to have underlying ischaemic heart disease. This predisposes them to ventricular tachycardia along with a background of poor left ventricular systolic function. Torsade des pointes or polymorphic ventricular tachycardia is a subtype of ventricular tachycardia often caused by electrolyte disturbances such as hypocalcaemia, hypokalaemia or hypomagnesaemia. Electrolyte depletion is a widely recognized side-effect of diuretic therapy. Older patients may also be on anti-arrhythmic medication for underlying heart disease and this in turn may predispose to various forms of ventricular tachycardia. Most likely drugs include amiodarone, sotalol, procainamide and flecanide.
A recent Canadian study found that a prediction could be made for adverse cardiac outcomes in patients presenting with syncope to the emergency department if certain ECG findings were detected at presentation. These included second-degree Mobitz type 2 or third-degree AV blocks, bundle branch block with first-degree AV block, right bundle branch with left anterior or posterior fascicular block, new ischaemic changes and left axis deviation. The study proved a sensitivity of 96% (95% CI, 80–100) and a specificity of 76% (95% CI, 75–76) for predicting 30-day adverse cardiac outcomes.Reference Thiruganasambandamoorthy, Hess, Turko, Tran, Wells and Stiell5
Structural heart disease
Syncope in structural heart disease is a common symptom when cardiac output is fixed. The most common structural heart disease associated with syncope, particularly in an elderly population, is aortic stenosis. Left ventricular outflow obstruction brings about syncope on exertion. This carries a poor prognosis in severe aortic stenosis and urgent valve replacement is required.Reference Arthur and Kaye42 Syncope due to aortic stenosis has been recognized for over 40 years.Reference Braunwald43 Symptomatic patients with aortic stenosis have a 25% mortality at 1 year and 50% by 2 years, and around half of deaths are sudden.44 Asymptomatic patients with aortic stenosis have a significant risk of sudden death, as examined by Bhattacharyya et al., with rates per year varying from 0.2 to 13%.Reference Bhattacharyya, Hayward, Pepper and Senior45
Other rarer causes secondary to structural heart disease include cardiomyopathy and atrial myxoma. Pulmonary embolism (PE) and aortic dissection can also present as syncope. The clinical presentation of acute PE was examined in an Italian study in 2012.Reference Miniati, Cenci, Monti and Poli46 It was found that of the study population of 800 patients, between 22 and 26% of patients presented with syncope. PE is usually associated with clinical signs not typically associated with syncope of other aetiology, such as tachycardia, ECG changes, hypoxia, chest pain and abnormal biochemical results such as a raised D-dimer and/or troponin. Aortic dissection may also present as syncope. It has been shown that aortic dissection is misdiagnosed in up to 14% of patients, with syncope being one of the misdiagnoses along with chest pain, acute coronary syndromes or muscular back pain.Reference Quinn, McDermott, Stiell, Kohn and Wells4
Diagnosis and investigations
The various components of the definition of syncope need to be carefully understood and clarified in a clinician's mind starting from history, examination and investigations in order to arrive at an appropriate diagnosis of syncope and then to identify its cause. The numerous articles on this topic emphasize that symptom reproduction is the key to establishing diagnosis. As people are living longer and thus becoming frailer, the ethical issues and the decision-making process becomes even more complicated. The main factor in the assessment and diagnosis is to differentiate syncope from other causes of transient loss of consciousness.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 As mentioned previously, diagnosing syncope remains a difficult challenge in the older person as the history is not always clear. In one study, the diagnosis of the cause of syncope was possible on the basis of the history only in 5% of older patients in comparison with 26% of the young.Reference Del Rosso, Alboni, Brignole, Menozzi and Raviele48
In the older person, syncope needs to be considered as part of the differential diagnosis of different types of presentations, including falls and collapse. In an Italian studyReference Galizia, Abete, Mussi, Noro, Morrione and Langellotto49 which looked at specific early symptoms to predict cardiac and non-cardiac syncope, 71% of patients experienced symptoms before syncope. The awareness of feeling faint, sweating and blurred vision were more prevalent preceding non-cardiac syncope with good specificity (except for feeling faint). The only symptom predictive of cardiac syncope in the elderly was dyspnoea.Reference Galizia, Abete, Mussi, Noro, Morrione and Langellotto49 Syncopal patients aged 60 and above attending the emergency department are strongly associated with short-term serious events.Reference Sun, Hoffman, Mangione and Mower50
Older patients are less likely to give a typical history and therefore clinicians need to have a high index of suspicion when evaluating the older patient presenting with collapse or syncope, as evidenced in a large study, where about 25% of older patients with syncope presented as unexplained falls. Patients aged ≥60 years were less likely to report total loss of consciousness and more likely to present with unexplained falls.Reference Duncan, Tan, Newton, Reeve and Parry51
Initial assessment
Current ESC guidelines on the evaluation of syncope advocate an initial evaluation strategy of detailed history, clinical examination, orthostatic blood pressure measurement and 12-lead ECG, with subsequent investigations dictated by the likely aetiology based on this initial work-up. This can lead onto a provisional diagnosis and subsequently will enable us through sound clinical judgement to decide on further investigation and ongoing referral processes. An initial thorough assessment is enough to establish the cause in 23–50% of cases.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1
Again the key would be to establish if the event was a syncope or not in the first instance. The particular issues which make the history uncertain are amnesia for the loss of consciousness (LOC), cognitive impairment which makes the history inaccurate, and gait and balance problems with lack of protective reflexes, which can cause some haemodynamic changes that in turn cannot not result in a syncope. Equally important is the differentiation between syncope and non-syncopal conditions. In this case, we need to establish if the LOC was complete or partial, was it transient with quick onset, was there a loss of postural tone and did it result in full spontaneous recovery.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 One of the main tests recommended as part of initial assessment is the active stand test,Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 which involves checking the blood pressure in supine position after 5 min rest and then repeated standing at 1 and 3 min. This test is diagnostic when there is a symptomatic fall in systolic blood pressure (BP) from a baseline value >20 mmHg or diastolic BP >10 mmHg or decrease in systolic BP to <90 mmHg.
For the initial assessment, one solution may be a dedicated and easily accessible syncope clinic run jointly by geriatricians and cardiologists. The use of a structured approach with strict adherence to guidelines and the presence of a dedicated syncope investigation unit reduced unnecessary investigations and improved the diagnostic yield from 36 to 98%.Reference Croci, Brignole, Alboni, Menozzi, Raviele and Del Rosso52 A review of 2016 patients over 65 years assessed the yield of diagnostic testing for syncope based on the San Francisco Syncope Rule (SFSR) and concluded that many unnecessary tests like electrocardiogram, telemetry, cardiac enzyme tests, electroencephalogram and computed tomography scans were obtained. These tests only provided information on diagnosis and management in less than 5% of cases and the aetiology was identified in less than 2% of cases.Reference Ungar, Mussi, Rosso, Noro, Abete and Ghirelli54 Basic tests like postural blood pressure recording, which costs only around £10, identified the aetiology 15–21% of the time and had the highest yield (25–30%). It was done only in 38% of patients.Reference Ungar, Mussi, Rosso, Noro, Abete and Ghirelli54 This would prove cost effective as well. There was a reduction in the frequency of unexplained syncope to about 10% when a standardized diagnostic algorithm for diagnosis of syncope (devised from the ESC guidelines) was used. This was even found to be applicable to the older person up to the age of 90 years.Reference Galizia, Abete, Mussi, Noro, Morrione and Langellotto55
The specific role of geriatricians in rapid access syncope clinics has most recently been described in 2010 in Newcastle in the Falls and Syncope service.Reference Parry and Tan7, Reference Parry, Reeve, Lawson, Shaw, Davison and Norton66 It was a model which was developed with geriatricians running the service at the front end. It provided a high diagnostic yield of 94%. This comprehensive, multidisciplinary syncope service for older people diagnosed 11% of patients to be non-syncopal fallers, highlighting the benefit of such units being run by geriatricians. The diagnostic yield of cardiac causes in the absence of a cardiologist was found to be comparable.
Various risk scores have recently been developed to identify high-risk syncope patients. These include the previously mentioned SFSR, the OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio) score and EGSYS (European Guidelines in Syncope Study) score.Reference Parry and Tan7 SFSR (the simplest), uses the presence of an abnormal electrocardiogram, heart failure, anaemia (haematocrit <30%), or systolic hypotension (<90 mmHg) to identify patients who require urgent action. SFSR has been validated to have 96% (92–100%) sensitivity and 62% (58–66%) specificity in identifying patients with short-term adverse outcomes. Similar results were seen in a prospective study done in 2010 by Mitro et al.,Reference Mitro, Kirsch, Valočik and Murín56 where standardized diagnostic evaluation determined the cause of syncope in 89% of patients. Specific diagnostic yield was as follows: tilt test 52%, implantable loop recorder 51%, electrophysiological studies 33%, initial evaluation 31%, ECG Holter 12%, orthostatic test 10%, transoesophageal stimulation 9%, carotid sinus massage 4% and echocardiography 2%.
Electrocardiogram and ambulatory cardiac monitoring
Further evaluation of patients after the initial assessment and the likelihood of a cardiac cause of the syncope would depend to a great extent on the ECG abnormalities. The Framingham study cohort's age- and sex-adjusted hazard ratios for death over a mean follow-up of 8.6 years was 2.4 for cardiac syncope compared with 1.17 in the vasovagal group.Reference Parry and Tan7, Reference Soteriades, Evans, Larson, Chen, Chen, Benjamin and Levy57 The ESC guidelines 2009Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 suggest that ECG changes of bradycardia, AV block, intraventricular conduction abnormality and tachydysrhythmia in the appropriate clinical setting will provide an answer to the clinician for the syncopal event. Other findings that are thought to be significant include the various ST segment and T-wave abnormalities of acute coronary syndrome, ventricular pre-excitation as seen in the Wolff–Parkinson–White syndrome, Brugada syndrome with the associated tendency for sudden death, prolonged QT interval common in the diverse long QT interval presentations, and right ventricular hypertrophy suggestive of hypertrophic cardiomyopathy. However, the decision on prolonged cardiac monitoring would largely depend on the baseline ECG abnormalities along with frequency and nature of the syncopal events.
In a case-control study of a prospective versus historical cohort of patients presenting to emergency services with syncope, 24-hour Holter monitoring revealed only a single diagnosis in 155 tests in patients with previously normal heart disease, in comparison with 18 diagnoses in 195 tests in those with established cardiac syncope.Reference Farwell and Sulke58 However, in selected patients with frequent syncopal symptoms, external retrospective loop recorders had a relatively high diagnostic yield of 25%.Reference Gula, Krahn, Massel, Skanes, Yee and Klein59 Another recent study that compared external loop recorders with conventional Holter monitoring reported a symptom rhythm correlation of 56% (44/78) for loop recorders versus 22% for Holter monitors.Reference Sivakumaran, Krahn, Klein, Finan, Yee, Renner and Skanes60 On the other hand it was noted that 23% of symptomatic patients fail to activate their loop recorder. Older patients who live alone and are unfamiliar with technology or lack motivation will have a lower diagnostic yield from external loop recorders.
Carotid sinus massage
Carotid sinus hypersensitivity (CSH) is increasingly being recognized as the most common cause of syncope in the older person since the number of carotid sinus massages being done has increased. ESC suggests that CSM should be done on all patients greater than 40 years who present with syncope of uncertain etiology.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 It is contraindicated in patients with previous stroke or transient ischaemic attack (TIA) in the previous 3 months and if carotid bruit is present (which should be investigated further to exclude significant carotid stenosis). The test is usually done in conjunction with a HUTT in the elective setting and on its own in the emergent setting. The carotid sinus is massaged both on the right and the left in firm longitudinal fashion for about 5 min after a supine rest, in both supine and upright positions. In about a third of patients the test is positive in the upright position. Positive response to the test would be cardioinhibitory if there is asystole of more than 3 s, vasodepressor if the systolic BP falls by 50 mmHg without significant bradycardia, and a mixed response if both.
An abnormal response to CSM may not indicate syncope caused by CSH and needs to be considered in the light of the patient's age, duration of syncopal episodes and detailed history of provocative stimuli. Identifying VVS with an abnormal response to CSM from CSH has implications in practice from advice on driving to treatment strategies.Reference Humm and Mathias61 In a study carried out to determine positive response to carotid sinus massage and tilt-table testing, male sex, increasing age and being referred with syncope were all associated with an increased likelihood of receiving a diagnosis of either OH or CSH.Reference Milton, Lee and Jackson62
Tilt-table test
HUTT is the investigation of choice for the diagnosis of neurally mediated syncope. It has been diagnosed with increasing frequency in older patients since HUTT was described about two and a half decades ago by Kenny et al., who found that 67% of patients with unexplained syncope had neurocardiogenic cause of the syncope identified by the test.Reference Kenny, Ingram, Bayliss and Sutton63 The test is also a useful diagnostic tool in people with unexplained syncope, dizziness and falls. The basic principle of tilt testing is the ability to replicate the patient's symptoms whilst there is continuous beat-to-beat monitoring of the patient's blood pressure and the heart rate.
The exact timing of the test in the investigative pathway for syncope needs still to be defined. The consensus would be that once a cardiac syncope is ruled out in the initial assessment, and if further history and assessment fails to conclusively rule out a neurally mediated syncope, then a tilt-table test needs to be requested, either to establish the diagnosis or reinforce a suspicion. In the older person, pre-existing co-morbidities and medications affecting haemodynamic response might affect HUTT outcome.Reference Vetta, Ronzoni, Costarella, Donadio, Battista, Renzulli, Gentile and Zuccaro64 In one study, HUTT was a reliable diagnostic tool in a population characterized by significant co-morbidities and polypharmacy.Reference Paul, Gieroba and Mangoni65
Different tilt-table protocols are being used with variations in the initial stabilization phase, duration of tilting (20–45 min) and application of pharmacological agents. The most favoured protocol is the Italian protocol (details of which are described earlier in this paper) in which the patient is passively tilted for 20 min at 70 deg, following which 400 μg of sublingual glyceryl trinitrate is administered and the patient is further passively tilted for 15 min.Reference Nath and Kenny13, Reference Parry, Reeve, Lawson, Shaw, Davison and Norton66 In a study carried out to assess appropriate duration for HUTT, it was found that at least 25 min during the passive basic phase and 15 min during the nitroglycerin provocation phase was required for a positive test.Reference Liu, Fang, Liu, Lu, Li, Li and Wang67 If isoproterenol is used, an incremental infusion rate from 1 up to 3 μg min−Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 is used to obtain a target heart rate of 20–25% above baseline. In a recent analysis of pooled data published by Brignole, a positive HUTT was found in 62–69% of patients with unexplained syncope, with a sensitivity of 94%.Reference Brignole, Alboni, Benditt, Bergfeldt, Blanc and Thomsen68 Another study used a shortened ‘front-loaded’ 20-min glyceryl trinitrate-provoked head-up tilt (FLGTN-HUT) with the standard 40-min passive tilt as first-line investigation in patients with unexplained syncope and asymptomatic controls. It resulted in the front-loaded GTN protocol providing a higher diagnostic rate than passive tilt testing, and provides a rapid alternative to conventional methods, though false positivity rates are higher.Reference Parry, Gray, Newton, Reeve, O'Shea and Kenny69
In an elderly population with syncope of unknown origin submitted to HUTT, the response to glyceryl trinitrate is not dose dependent, and no difference was found in the rate of exaggerated responses to nitrates with different GTN dosages.Reference Timoteo, Oliveira, Feliciano, Antunes, Nogueira da Silva and Silva70 Autonomic dysfunction, which can be found during tilt test, is probably an important cause of syncope in the elderly, regardless of the occurrence of symptoms during the tilt test.Reference De Castro and Nobrega71 A fall in systolic blood pressure 2 min after 70 deg head-up tilt and a postural decrease in SBP of 15 mmHg in comparison with 20 mmHg is associated with a positive test result and this may allow the early prediction of HUTT outcomes.Reference Yiu, Gieroba, Hall, Mackintosh, Russell and Mangoni72 Supine haemodynamic measures derived from transthoracic impedence cardiography can simply, non-invasively and sensitively differentiate HUTT positive patients from those with negative tilt tests, but this needs to be fully evaluated before routine use.Reference Parry, Norton, Pairman, Baptist, Wilton and Reeve73
The HUTT is a very useful test in the diagnosis of syncope in the elderly, but it is limited in that it is time-consuming and requires experienced medical staff and sophisticated equipment. Also, the reproducibility of a positive head-up tilt-table test varies hugely and it has been shown in several studies that the mechanism of syncope during a tilt-table test is the same as that of a spontaneous syncope. Hence, the HUTT is not a useful test to determine therapeutic strategies for patients with neurally mediated syncope. However, since its inception, it still remains one of the main non-invasive diagnostic tools for syncope in the older person.
Implantable loop recorder
The implantable loop recorder (ILR) is an investigation when the suspected aetiology is arrhythmic, either primary cardiac rhythm disturbance or as part of neurally mediated syncope. It is currently considered after a series of investigations, which may include ambulatory or external loop recorder monitoring, tilt testing, carotid sinus massage, echocardiography and exercise testing. This guidance is based on very few randomized controlled clinical trials and modestly sized observational studies. The strength of ILR lies in the ECG monitoring of infrequent episodes and the ability to retrospectively assess heart rate and rhythm during a syncopal episode, both of which allow symptom rhythm correlation, the gold standard of syncope diagnosis.Reference Parry and Matthews74 In older people, the main issue with ILR is activation of the device, mainly due to cognitive impairment and dexterity problems. These problems will have been nullified with recent advances in remote monitoring and auto-activation of these devices.
There is a supportive but limited evidence base for the routine use of ILRs in syncope, particularly where arrhythmia is suspected, and although the mean age of participants in the only two randomized trials [Eastbourne Syncope Assessment Study (EaSyAS) and Randomised Assessment of Syncope Trial (RAST)] to date was >65 there is still a lack of conclusive evidence for its use, and the decision needs to be made on an individual basis, also taking into account the cost effectiveness, the cost of a single device being £1200. ISSUE 2, an observational study, supports the role of early diagnostic ILR application in suspected recurrent neurally mediated syncope due to the high rate of ‘hard’ arrhythmic diagnoses.Reference Moya, Sutton and Ammirati75 ISSUE 2 suggests that early application of an implantable loop recorder allows effective specific therapy in patients with recurrent suspected neurally mediated syncope, with therapy delayed until documentation of syncope, which in turn allows a safe, specific and effective therapy in such patients.Reference Brignole, Menozzi and Moya76
In a multicentre observational study carried out to collect information on the use of the ILR and to investigate its effectiveness in the diagnosis of unexplained recurrent syncope, the ILR contributed to establishing the mechanism of unexplained syncope/presyncope in 78% of patients. Significant physical trauma had been experienced in association with a syncopal episode by 36% of patients. The findings support the recommendation in current guidelines that an ILR should be implanted early rather than late in the evaluation of unexplained syncope.Reference Brignole, Sutton, Menozzi, Garcia-Civera, Moya and Wieling77 The Reveal in the Investigation of Syncope and Epilepsy study was the first prospective study to show, by means of ILR, a high incidence of asystole in patients misdiagnosed with epilepsy (normally one in four) or where the diagnosis of epilepsy was in doubt. Convulsive syncope is the most likely diagnosis in such instances.Reference Edvardsson, Frykman, Mechelen, Mitro, Mohii-Oskarsson and Pasquie78 Remote monitoring is a rapidly expanding field. Continuous wireless transmission of real-time ECG signals to a home hub and then though a telephone to a remote monitoring station can ensure that all arrhythmias are captured. Patients with cognitive impairment or manual dexterity and mobility issues who have difficulty with self-activation devices will particularly benefit from such advances in technology. Taking into account the high proportion of arrhythmic causes of syncope and its impact in older patients, these advances are vital in informing new technologies and studies examining the clinical and cost effectiveness. Future research will also need to focus on establishing the optimal timing of ILR in the diagnostic pathway. In the meantime, the ILR offers a useful adjunct in the investigation of unexplained syncope, especially where an arrhythmic cause is suspected.
Echocardiogram
According to the ESC guidelines, an echocardiogram is required if a patient with syncope is suspected to have structural heart disease, previously known heart disease, an abnormality on the electrocardiogram, or the initial assessment suggests a cardiac cause. Severe aortic stenosis, obstructive cardiomyopathy, cardiac tumours, large obstructive thrombi, aortic dissection, pericardial tamponade and congential anomalies of coronary arteries are the main echocardiographic findings attributed to a cardiac syncope.Reference Petkar, Iddon, Bell, Rice, Mckee, Curtis, Cooper and Fitzpatrick79 Cases have been reported of an atrial myxoma presenting with syncope.Reference Gupta, Molina, Palma and Macha80 A study addressing the association between echocardiographic abnormalities and falls in older people found that the presence of pulmonary hypertension or regurgitation of mitral, tricuspid or pulmonary valves was associated with a higher fall risk.Reference Van der Velde, Stricker, Roelandt, Ten Cate and van der Cammen81 The use of echocardiogram in the investigation of syncope should be mainly directed to cardiac causes and should not be a routine diagnostic tool.
Other investigations
An electrophysiological study (EPS) is an invasive test and it should be requested with a more pragmatic approach in the older person. The usefulness of EPS is, as a result, highly dependent on the pre-test probability, which is indicated by the presence of organic heart disease or an abnormal ECG.Reference Linzer, Pritchett, Pontinen, McCarthy and Divine82 For older people with little or no functional impairment, EPS is indicated for unexplained falls and syncope when a cardiac arrhythmia is suspected, as per the same diagnostic strategies as in younger adults with syncope.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 Twenty-four-hour blood pressure measurements may play a role in the evaluation of hypotensive disorders, especially if drug-induced hypotensive symptoms or postprandial hypotension are suspected. Patients with orthostatic hypotension have a reversal in the diurnal blood pressure pattern.Reference Senard, Chamontin, Rascol and Montastruc83 Variation in blood pressure after changes to medication and postprandial dips in blood pressure are useful aids to diagnosis and treatment.
A recent study showed a positive correlation between the cardioinhibitory response to head-up tilt test and the asystole induced by adenosine triphosphate administration in patients with neutrally mediated vasovagal syncope. The study findings may support therapeutic interventions like pacemaker implantation in patients with neurally mediated vasovagal syncope.Reference Parisi, Messano, Santamaria, Angeloni, Digiannuario and Ciccarone84 However, ESC guidelines do not currently recommend ATP test to select patients for cardiac pacing. All older patients with syncope will require a detailed neurological examination. Psychiatric evaluation in patients with suspected pseudosyncope is recommended when other causes have been ruled out.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 Tilt-table testing with concurrent EEG recording and video monitoring may be used to rule out epilepsy and confirm a diagnosis in the absence of significant haemodynamic changes in the test.
Treatment
Treatment of syncope in the elderly should be based on the aetiology of syncope. The main guiding principle will be to differentiate the more malignant cardiac cause from the more benign cause. With the advancement of cardiac monitoring techniques and more frequent tilt-testing with CSM, more cases of cardiac syncope are being recognized with increasing implantation of pacemaker and other devices like implantable cardioverter defibrillator (ICD) being done as therapy. In the elderly, specific treatment is often necessary and determination of the haemodynamic mechanism of syncope by means of the above tests seems to be the most advisable option for optimal management. The main aim of treatment is to reduce the recurrence of syncope and as a result reduce the impact of physical injuries. For hypotensive conditions, such as neurally mediated syncope and orthostatic hypotension, the main therapeutic interventions are isometric counter-pressure manoeuvre and lower limb compression bandage in addition to patient education about the condition. Avoidance of triggers like hot environment, humid atmosphere, prolonged standing, and reduced water intake, increasing fluid and salt intake, withdrawal of offending drugs and other general preventive measures should be advised. In resistant cases, drug therapy with fludrocortisone, midodrine and paroxetine has been found to be effective, though data are limited for older patients. High-risk patients need to be identified by the risk scores and may require more specific treatment like pacemakers. Substitution of salt and intake of isotonic drinks expands the circulating blood volume and may improve venous return. Lying or sitting down when initial symptoms appear may avert or attenuate syncope or traumatic falls.
Physical counter-pressure manoeuvres like hand grip, leg crossing and tensing of muscles are a risk-free, effective and low-cost treatment method in patients with vasovagal syncope and recognizable prodromal symptoms, and should be advised as first-line treatment in patients.Reference Van Dijk, Quartieri, Blanc, Garcia-Civera, Brignole, Moya and Wieling85 The incidence of recurrence of syncope is shown to be reduced by orthostatic training, twice daily training sessions of 40 min tilt positioning at home by standing against a wall.Reference Di Girolamo, Di Iorio, Leonzio, Sabatini and Barsotti86 Cessation of tilt training causes a recurrence of positive results of tilt testing, in spite of the lack of spontaneous syncopal episodes. However it has a very poor compliance.Reference Gajek, Zysko and Mazurek87 There is some evidence that modification of cardiovascular risk factors for falls/syncope reduces the incidence of subsequent events in community-dwelling frail elderly, even in those with dementia, but not in institutionalized elderly.Reference Shaw, Bond, Richardson, Dawson, Steen, McKeith and Kenny88
Pharmacological therapy
There are only limited data from placebo-controlled trials on the efficacy of drugs in the management of vasovagal syncope. Of the various drugs like β-blockers, disopyramide, scopolamine, theophylline, ephedrine, etilefrine, clonidine, fludrocortisone, midodrine and selective serotonin re-uptake inhibitors (SSRI), only the latter three have any effect on vasovagal syncope. As per the guidelines of the ESC, β-blockers should not be used to treat reflex syncope due to lack of compelling evidence.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1
Fludrocortisone is a synthetic mineralocorticoid that acts by retaining sodium on the distal tubules of the kidney and hence expands the blood volume, thereby preventing relative central hypovolaemia. In addition, it increases pressor sensitivity to circulating catecholamines.Reference Bannister, Mathias and Bannister89 Uncontrolled studies provide further modest evidence of efficacy and tolerability, though again only small numbers of patients have been studied. The most common side-effects include hypertension, hypokalaemia and symptomatic fluid retention, and cardiac failure. In the POST 2 trial, fludrocortisone was found to be of no benefit in reducing episodes of moderate to severe vasovagal syncope.Reference Raj, Rose, Ritchie, Sheldon and Investigators90
Midodrine, an alpha-agonist vasoconstrictor, affects smooth muscle cells both in arteries and veins without affecting heart rhythm or causing negative inotropy. Midodrine may be indicated in patients with frequent vasovagal syncope refractory to lifestyle measures.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1 It has to be administered three times per day starting with 5 mg, because of a half-life of only 2–3 h, and dose gradually increased. We have to beware of the phenomenon of supine hypertension, which can increase the risk of stoke. In three small randomized, placebo-controlled trials, midodrine had a beneficial effect on symptom frequency, symptoms during head-up tilt, and quality of life.Reference Kaufmann, Saadia and Voustianiouk91 Studies show that midodrine appears to be more effective in the treatment of orthostatic hypotension caused by autonomic dysfunction, and there is insufficient evidence of its use in the neurally mediated syncope.
Serotonin re-uptake inhibitors (SRI) act by reducing the central sympathetic nervous system activity. Some open-label studies and one randomized, placebo-controlled trial demonstrated that SRI may reduce recurrent vasovagal syncope. One study showed that 17.6% of patients who randomly received paroxetine had syncope recurrence in comparison with 52.9% of the placebo group.Reference Di Girolamo, Di Iorio, Sabatini, Leonzio, Barbone and Barsotti92 More evidence is required for the use of this drug in VVS.
Cardiac pacing
The role of cardiac pacing is controversial in the treatment of syncope in the elderly as pacemaker is an invasive treatment modality. The main question is whether a pacemaker is indicated in the first instance and if so, which is the pacing modality to be used. There is more evidence for their role for cardiac arrhythmias in contrast to reflex syncope. There is an argument to insert pacemaker early in unexplained syncope and to avoid the agony of prolonged invasive cardiac monitoring. A recently published meta-analysis of all studies for the role of pacemakers in reflex syncope suggested a non-significant 17% reduction in syncope from the double-blinded studies, and an 84% reduction in studies where the control group did not receive a pacemaker.Reference Sud, Massel, Klein, Leong-Sit, Yee, Skanes, Gula and Krahn93
The ISSUE 2 study, which is a non-randomized trial, hypothesized that spontaneous asystole recorded by continuous cardiac monitoring and not tilt-test results should form the basis for patient selection for a pacemaker insertion. Among the symptomatic bradyarrhythmias in the elderly, sinus node disease and atrioventricular block are the main indications for permanent pacemaker implantation, as evidenced by recent large randomized, multicentre trials. In actual terms, more than 80% of all pacemakers implanted today are in the elderly.Reference Kozak, Owings and Hall94 The European Society of Cardiology recommends that pacemaker implantation may play a role in special circumstances like patients with frequent recurrent reflex syncope, e.g. when no prodrome occur, an age >40 years and documented spontaneous bradycardia or asystole during monitoring.Reference Moya, Sutton, Ammirati, Blanc, Brignole and Dahm1
Several retrospective and observational studies have suggested that atrial-based dual chamber pacing (single-chamber AAI or dual-chamber DDD pacing) is superior to ventricular pacing (VVI) for the improvement of cardiac symptoms, morbidity and mortality, and reduces incidence of pacemaker syndrome and prevents atrial fibrillation. The United Kingdom Pacing and Cardiovascular Events (UKPACE) trial,Reference Toff, Camm and Skehan95 a randomised controlled trail (RCT), showed no difference in the cardiovascular events in patients randomized to receive a single-chamber ventricular pacemaker or dual-chamber. Similar results were noted in the Mode Selection Trial in Sinus Node Dysfunction (MOST),Reference Lamas, Lee and Sweeney96 except for reduction in the incidence of atrial fibrillation in the dual-chamber group. It was an RCT that compared physiological (dual-chamber) and ventricular pacing in symptomatic sinus node dysfunction.
Pacemaker therapy for carotid sinus hypersensitivity has been studied in several non-randomized studies with encouraging results. In an RCT, Brignole et al. randomized 60 patients with pure or mixed cardioinhibitory response to dual-chamber pacemaker therapy or no treatment. Syncope recurred in 9% of the paced group versus 57% of the control group. In the SAFE PACE study, Kenny et al. randomized 175 patients, who had falls and a cardioinhibitory response to carotid sinus massage, and this resulted in markedly decreased recurrent falls and injuries in 70% of paced patients.Reference Kenny, Richardson and Steen97 The subsequent SAFE PACE 2, an underpowered study, questions the use of pacing in cardioinhibitory CSH, but the study was done in frailer and cognitively impaired patients.Reference Ryan, Nick, Colette and Roseanne98 A small study done by Maggi et al. suggests that a cardioinhibitory response to CSM predicts sinus arrest as the mechanism of syncope and subsequent pacing reduces the frequency of syncope and these patients would benefit from pacing rather than an ILR.Reference Maggi, Menozzi and Brignole99 In summary, the available evidence suggests that patients with recurrent syncope or frequent falls of unknown aetiology may benefit from a pacemaker implantation if they have documented cardioinhibitory or mixed response during carotid sinus massage.Reference Kaszala, Kalahasty and Ellenbogen100
Driving and syncope
With more and more people living longer with healthy lifestyles, driving in the older person suffering from syncope is increasingly relevant. In a survey among 104 patients, 3% of known patients with syncope reported it to have occurred while they were driving.Reference Maas, Ventura, Kretzschmar, Aydin and Schuchert101 Since the publication of the review article by Parry and colleagues on syncope in 2010,Reference Parry and Tan7 the Driver and Vehicle Licensing Agency (DVLA) in the UK has amended its restrictions on driving with syncope.102 As previously reported, driving restrictions do not apply to group 1 (car/motorcycle) or group 2 (heavy goods vehicles, passenger carrying vehicles) if syncope has a clear cause and is associated with ‘the three Ps’: provocation, prodrome and posture. If syncope is not the clear diagnosis for transient loss of consciousness, but remains the most likely cause, then group 1 drivers face no restrictions, whereas group 2 drivers face a 3-month restriction from driving.
If a cardiac cause of syncope is suspected, then both group 1 and 2 drivers face restrictions (6 and 12 months, respectively). The driving bans are subject to thorough investigation and appropriate treatment, e.g. cardiac pacing. Syncope while driving leads to a 6- and 12-month licence revocation for group 1 and 2 drivers, respectively, regardless of cause. Cough syncope faces more stringent regulation, with group 1 drivers being banned for 6 months for a single episode, or 12 months for multiple attacks. Group 2 drivers cannot drive for 5 years from the date of the last attack. Both group 1 and 2 drivers may reapply for the licenses earlier if any precipitating underlying condition is treated, e.g. weight loss, smoking cessation and gastro-oesophageal reflux treated. Clinicians, patients and carers need to be increasingly aware of the DVLA regulations for patients with syncope.
Conclusion
Syncope in the older person remains a diagnostic challenge. The benign neurally mediated syncope is the most common cause, but cardiac syncope as a result of life-threatening arrhythmias or structural heart disease is being increasingly recognized and treated. The recent advances in our understanding of the most appropriate means of identifying and treating such patients, with the help of advances in research and modern technology, along with the latest guidelines have enabled us to provide more optimum care for the older person. With the ever increasing older population and their complex needs, the demands on resources are going to increase further. More cost-effective measures aimed at a focused approach need to be encouraged in all healthcare centres.
The success of dedicated syncope units has taught us that a targeted approach to management of syncope in the older person, with multidisciplinary involvement including geriatricians, cardiologists and neurologists, can avoid unnecessary tests like brain imaging, carotid Doppler ultrasound, advanced cardiovascular investigations, chest radiography and electroencephalography. The increasing number of geriatricians running these services is encouraging and the available evidence suggests that more training in this area will ensure that equitable care can be provided. Ongoing drug trials like the POST 3 TRIAL for midodrine will shed more light on the role of more conservative and safe measures to treat these patients. Patients that require invasive treatments like pacemakers and implantable cardioverter defibrillators need to be appropriately selected and treated. Advancement in monitoring techniques with wireless technology and remote monitoring targeting the appropriate patients with cognitive impairments and reduced mobility can ensure that mortality and morbidity are minimized.
This review article is an attempt to explore the very challenging and intriguing area of syncope and to update the previous knowledge on the subject, where there is still no unanimity in decision making among the various healthcare professionals. The joint multi-professional approach in dedicated units may pave the way for bridging this gap. Further research and randomized controlled trials with specific emphasis on the complex older patient is required to broaden our knowledge and discover the hidden advances in this area.
Acknowledgements
We would like to thank Dr Graeme Fancourt, Consultant Physician for Older People in Glenfield Hospital, University Hospital of Leicester NHS Trust and Dr Irfana Musa, Specialist Registrar in Geriatric Medicine, University Hospitals of Leicester for their contribution and support in writing this article.
Conflicts of interest
The authors have no conflicts of interest to declare.
