Reflex Syncope/Neurally Mediated Syncope

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Summary

1) Reflex Syncope/Neurally Mediated Syncope

Vasovagal Syncope

VVS is a neurally mediated reflex in which there is a relatively sudden change in autonomic nervous system activity leading to a fall in BP, HR and cerebral perfusion.²⁹ In young patients a diagnosis can usually be made from history alone. This is not always the case with older patients. Although VVS is the most common cause of syncope in the older patient, it may not follow the benign course commonly observed in the young.^30,31 The classic prodrome usually described as pallor, sweating, nausea and dizziness may be shorter in duration or in some instances non-existent or poorly recognised in the older patient.^30,32–34 In the older person, VVS is more likely due to a dysautonomic response representing an inability of the baroreflex to adapt to physiological challenges, which results in a progressive fall in HR ± BP before the onset of symptoms.³⁵ VVS has multiple triggers including a warm environment, prolonged standing, dehydration especially in those on diuretics or anti-hypertensive and vasodilator medications.³⁴

Investigation

HUT testing is well tolerated in the older patient³⁴ and is indicated in syncope of unknown origin,³⁶ when history is atypical, driving is a concern, or serious injury sustained,³⁷ and as outlined in the ESC guidelines.¹ Even the older, frailer patient with cognitive impairment tolerates HUT,³⁸ including both passive and GTN-provoked HUT.^39,40

The HUT is positive when there is induction of either reflex hypotension/bradycardia or delayed OH associated with syncope or pre-syncope¹ with symptom reproduction. In unexplained falls due to reflex syncope, patients may deny witnessed loss of conscioussness induced by HUT. This was the case in 42 % of older patients in one study.³ Responses are vasodepressor (hypotension), cardioinhibitory (bradycardia) or mixed.⁴¹ An exception to the classification is chronotropic incompetence, where the patient has no compensatory rise in HR on HUT.²⁴

If HUT results in a cardio-inhibitory response and syncope, capture of a real-time event with early insertion of an ILR9 should be sought.⁴² It is also important to remember that HUT does not always replicate real-time syncopal episodes as has been demonstrated in ILR analysis in patients with VVS.⁴³

Implantable Loop Recorder – Use in Reflex Syncope

The International Study on Syncope of Unknown Etiology (ISSUE-2)⁴⁴ trial provided evidence that early ILR insertion to capture syncope in real-time in those with suspected reflex syncope, ensured safe and effective directed therapy in patients experiencing frequent syncope.⁴⁴ The mean age of trial participants was 66 ± 14 years. Other characteristics of participants were syncope beginning in middle or older age, frequent injury and short prodrome. The study demonstrated a reduction in recurrent syncope rates following ILR-guided therapy ie. pacemaker insertion, following asystole or bradyarrhythmia.⁴⁴ Fifty per cent of those with recurrent unexplained syncope had asystole during symptoms.⁴⁴

In the ISSUE-3 trial, patients who were ILR positive (documented asystolic episode) but had negative tilt tests, had the best outcomes from cardiac pacing with a 5 % recurrence of syncope at 2 years.⁴⁵ However, 25 % of those who were ILR positive and actively paced had a recurrence of syncope at 2 years, when those with positive and negative tilts tests were included.^45,46 The study raised questions about the origin of the asystole in the older pacemaker group and whether reflex syncope or age-related conducting tissue disease was responsible.⁴⁷

Management of Vasovagal Syncope

Cardiac and psychotropic medications can cause hypotension and VVS, therefore initial treatment focuses on modification of culprit medications (up to 40 %). Management includes education with advice on adequate fluid intake,⁴⁸ physical counter manoeuvres (PCM),⁷ compression stockings, tilt training⁴⁹ and feedback to patients of haemodynamic changes correlating with symptoms at the time of HUT.

Older patients with VVS are more likely to require cardiac pacing, for example, when spontaneous cardioinhibitory response in the setting of frequent syncope is observed.¹ Cardiac pacing in VVS is given a class IIa recommendation in international guidelines, in those over 40 years with recurrent reflex syncope and documented spontaneous cardioinhibitory response during monitoring; a Class IIb recommendation for refractory symptoms in the same age group in the presence of a documented cardio-inhibitory response on HUT.^1,50 The ISSUE-3 trial refines this to include those VVS patients over 40 years, with syncope beginning in middle or older age,⁵¹ with three or more episodes of syncope in the previous 2 years and spontaneous asystole during monitoring.^46,47 These patients correspond with those defined by the ESC guidelines as patients with high risk of injury or high frequency of syncope recurrence.^1,51

Carotid Sinus Hypersensitivity and Carotid Sinus Syndrome

CSS is exclusively a disorder of ageing and current guidelines advise that carotid sinus massage (CSM) should be performed in patients over 40 years with unexplained syncope.¹ Careful history taking may reveal triggers such as head turning, tight collars, shaving and vagal stimuli,²⁴ although micturition, defaecation and known triggers of VVS can also provoke CSS. Contraindications to CSM include transient ischaemic attack/stroke within 3 months,¹ recent myocardial ischaemia⁵² or evidence of carotid bruit¹ unless significant stenosis has been excluded by carotid dopplers. Using the exclusion criteria, the risk of stroke or transient ischaemic attack (TIA) from CSM has been reported as one per 1,000 episodes of massage.²⁷

Traditionally, carotid sinus hypersensitivity (CSH) has been defined as a ventricular pause lasting >3 seconds and/or a fall in systolic BP of 50 mmHg during CSM without spontaneous syncope.¹ CSS is diagnosed when the above criteria is associated with spontaneous syncope.¹ The CSH response is categorised as cardio-inhibitory, vasodepressor or a combination of both.^27,45 Recently, authors proposed new criteria for exaggerated responses to CSM-asystole ≥6 seconds and a fall in mean arterial BP ≥60 mmHg over 6 seconds⁵³ based on data from a population study where the 95th percentile for CSM response was 7.3 seconds of asystole and 77 mmHg drop in systolic BP.⁸ Wieling et al.⁵⁴ observed that there was no LOC before 6 seconds of asystole providing a pathophysiological reason to extend the guidelines.⁵⁴

CSH may be an epiphenomenon of ageing rather than a disease process given that it is evident in up to 35 % of asymptomatic community-dwelling older people.⁸ Recently, CSH has been associated with cognitive impairment and dementia; however, it is not clear whether it is a risk factor for development of dementia or consequence of neurodegenerative pathology.^55,56

Investigation

CSM should be performed in all patients over 40 with syncope of unknown aetiology¹ and unexplained falls.⁷

Management of Carotid Sinus Hypersensitivity and Carotid Sinus Syndrome

Although the most common presentation of CSS is syncope, patients can also present with falls and drop attacks.^52,57 The ESC guidelines only advise pacing with regard to syncope in CSS.¹ The American Geriatrics Society guidelines on falls prevention in older adults recommend cardiac pacing for CSH and unexplained/non-accidental falls.⁵⁸ Dual-chamber permanent pacemaker insertion for cardio-inhibitory or mixed subtypes of CSS is the treatment of choice.⁵⁹