Carotid sinus hypersensitivity

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

## Overview

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The carotid sinus contains a baroreceptor that senses arterial blood pressure and allows the body to regulate blood pressure and perfusion. Excessive sensitivity of this receptor may lead to reduced heart rate and/or blood pressure that can lead to syncope, called Carotid Sinus Hypersensitivity (CSH). [1] [2] [3] [4] [5] [6] [7]

## Historical Perspective

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Weiss and Baker first described the syndrome in 15 patients in 1933. [8]

## Pathophysiology

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The carotid sinus baroreceptor is located in the internal carotid artery sinus just above the bifurcation of the common carotid artery. It senses arterial blood pressure and in response sends afferent signals to the sensory nucleus of the vagus, via the sinus nerve of Hering, a branch of the glossopharyngeal nerve. Increased afferent signals lead to increased vagal tone and reduced sympathetic tone.

Two general types of CSH have been described, though patients may have mixed features:

Vagal or cardioinhibitory type \- Increased signal leads to a slowed heart rate.

* The slowed rate is usually due to sinus arrest or SA exit block. Some degree of AV block may occur as well in some patients.

Vasodepressor type \- Blood pressure falls without slowing of the heart rate. Loss of sympathetic tone may be particularly important in this subtype.

The mechanism of the hypersensitivity has not been fully elucidated. Carotid sinus denervation does not always result in cure, so there may be several contributing features. Many people believe that the defect lies in the CNS.

* One theory is increased alpha-2 adrenergic receptor mediated activity in the afferent or brainstem pathway of the carotid sinus reflex.
* Other theories include high resting vagal tone, hyperresponsiveness to acetylcholine, inadequate cholinesterase, etc. in affected patients.

The syndrome has been observed in patients with tumors or lymph node enlargement in the region of the carotid sinus. If severe atheromatous narrowing of the carotid arteries is present, compression of the carotid artery can lead to syncope due to inadequate CNS perfusion and not necessarily due to carotid sinus hypersensitivity.

## Differentiating Carotid sinus hypersensitivity from other Diseases

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The differential diagnosis of syncope includes true syncope and other non-syncopal causes. Below is listed one of many classification schemes.

Neurologic-associated causes

* Neurocardiogenic syncope – due to direct cardiac inhibition
* Vasovagal syncope
* Micturition syncope
* Carotid sinus hypersensitivity
* Seizure
* Transient ischemic attack (TIA) / Stroke
* Vertigo
* Hypoglycemia
* Narcolepsy
* Psychogenic – panic attack, anxiety disorder, somatization

Cardiac syncope

* Arrhythmia
* Outflow obstruction – valve disease, myxoma, idiopathic hypertrophic sub-aortic stenosis (IHSS), pulmonary embolism
* Insufficient cardiac output – CAD/USA/Myocardial infarction (MI), cardiac tamponade

Peripheral syncope - inability to maintain peripheral vascular tone

* Volume loss – including orthostatic hypotension and blood loss
* Medication effect – common agents include anticholinergics, nitrates, diuretics, other HTN meds.
* Autonomic and peripheral neuropathies – including diabetic neuropathy and other dysautonomias
* Neurodegenerative changes with orthostatic hypotension

## Epidemiology and Demographics

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CSH appears to be more common in men and in elderly patients. Other studies have suggested that CSH is more common in patients with Coronary artery disease (CAD), Hypertension (HTN) and in those with abnormal EKGs. Studies have also shown that CSH is more common in patients taking digitalis, alpha-methyldopa, clonidine and beta-blockers, presumably due to increased vagal activity. Some studies have suggested that CSH is more common in patients with carotid artery atherosclerosis.

Huang, et al, found CSH in 28% of patients with unexplained syncope, and other studies have found it in up to 45% of such patients. Huang Other studies have found CSH in up to 20% of the elderly population, though only a fraction of these individuals actually suffer from signs and symptoms of CSH. [9]

## Natural History, Complications and Prognosis

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Many but not all patients with syncope due to CSH have recurrent symptoms if not treated. In one study, up to 2/3 of patients did not have recurrence, so it is prudent to reserve significant interventions for those patients with recurrent symptoms. Patients with CSH have a higher rate of hip fracture, laceration and recurrent syncope than in age-matched controls. Brignole, et al evaluated 312 patients with CSH, and found similar mortality to controls. Brignole

## Diagnosis

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Persons with CSH may have reproducible signs and symptoms with carotid sinus pressure, and this may be used diagnostically. If patients have audible bruits on exam or known significant carotid atherosclerosis, carotid sinus massage (CSM) is generally not recommended.

The usual criteria for diagnosis are >3 seconds of ventricular asystole and/or a fall of SBP of >50 mmHg during carotid sinus massage.

* The massage is defined as firm steady pressure to the carotid sinus for ~5 seconds with the neck in the hyperextended position while supine.
* The carotid sinus can be found along the carotid artery medial to the sternocleidomastoid (SCM) at the level of the thyroid cartilage.
* Heart rate, blood pressure, EKG and clinical response are monitored for change.
* The procedure is then repeated on the other side. The procedure may be repeated standing to evaluate carotid sinus vasodepressor hypersensitivity.

Patients may have either a heart rate fall, the cardioinhibitory response, or fall in blood pressure, the vasodepressor response. Weiss and Baker also reported that some patients suffered from syncope without any fall in heart rate or blood pressure, they called the primary cerebral type. [10]

The test is not all-together sensitive or specific. If normal patients are tested, some will have a fall in blood pressure and heart rate despite no history of syncope. Other patients with history of syncope will have a fall in HR or BP but no reproducible symptoms at the time of the test.

### History and Symptoms

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Many patients will give a history of syncope or near-syncope with movement of the neck, wearing of a tight collar, shaving, etc. This history is not necessary, however, to make the diagnosis. Patients are usually upright, often standing, and develop a sudden episode of syncope, often with an associated fall. Small convulsive movements often occur with the loss of consciousness. The loss of consciousness is usually <30 seconds, and patients awake quickly with no clouding of consciousness.

The syndrome has been described in patients in chronic Afib, in addition to patients in normal sinus rhythm (NSR).

### Physical Examination

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#### Eyes

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Pressing on the eyes can elicit a vagal response, but this is not part of the syndrome.

#### Ear Nose and Throat

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Caeful examination should be done to assess for carotid bruits and to assure that there is no obvious mass compressing the carotid (such as tumors or lymph nodes).

## Treatment

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### Medical Therapy

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* Anticholinergics - atropine
* Sympathomimetic meds – ephedrine. May be particularly useful in patients with vasodepressor type.
* Volume agents – fludrocortisone
* Selective serotonin reuptake inhibitors (SSRI) – two recent studies have shown a good response to SSRIs in five patients with the vasodepressor type CSH.

### Surgery

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* Patients with cardioinhibitory / vagal type CSH often do quite well with pacemaker placement. Because some patients have AV node blockade, ventricular as well as atrial pacing is often indicated.
* Carotid sinus denervation by surgery or radiation.

## 2012 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities (DO NOT EDIT)[11][12]

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### Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT)[12]

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Class I

"1. Permanent pacing is indicated for recurrent syncope caused by spontaneously occurring carotid sinus stimulation and carotid sinus pressure that induces ventricular asystole of more than 3 seconds. (Level of Evidence: C)[13][14]"
Class III (No Benefit)

"1. Permanent pacing is not indicated for a hypersensitive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms. (Level of Evidence: C)"
"2. Permanent pacing is not indicated for situational vasovagal syncope in which avoidance behavior is effective and preferred. (Level of Evidence: C)"
Class IIa

"1. Permanent pacing is reasonable for syncope without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. (Level of Evidence: C)[13]"
Class IIb

"1. Permanent pacing is reasonable for syncope without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. (Level of Evidence: B)[15][16][17][18]"

## Sources

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* The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities [12]

## References

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1. ↑ Weiss, S, et al. The carotid sinus reflex in health and disease; its role in the causation of fainting and convulsions. Medicine 1933;12:297.
2. ↑ Huang, SSKS, et al. CSH in patients with unexplained syncope. Amer Heart J 1988;116:989.
3. ↑ Brignole pmid=1539520 Brignole, M, et al. Long-term outcome in symptomatic CSH. Am Heart J 1992;123:687.
4. ↑ O'Mahony, D. Pathophysiology of CSH in elderly patients. Lancet 1995;346:950.
5. ↑ McIntosh, SJ, et al. Clinical characteristics of vasodepressor, cardioinhibitory, and mixed carotid sinus syndrome in the elderly. Am J Med 1993;95:203.
6. ↑ Fahmy, RN, et al. Revisiting carotid sinus denervation in carotid sinus hypersensitivity. Am Heart J 1994;128:1257.
7. ↑ Sugrue, DD, et al. Symptomatic "isolated" carotid sinus hypersensitivity: natural history and results of treatment with anticholinergic drugs or pacemaker. J Am Coll Cardiol 1986;7:158.
8. ↑ Weiss, S, et al. The carotid sinus reflex in health and disease; its role in the causation of fainting and convulsions. Medicine 1933;12:297.
9. ↑ Huang, SSKS, et al. CSH in patients with unexplained syncope. Amer Heart J 1988;116:989.
10. ↑ Weiss, S, et al. The carotid sinus reflex in health and disease; its role in the causation of fainting and convulsions. Medicine 1933;12:297.
11. ↑ Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD (2013). "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 61 (3): e6–75. doi:10.1016/j.jacc.2012.11.007. PMID 23265327.
12. ↑ 12.0 12.1 12.2 Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207
13. ↑ 13.0 13.1 Brignole M, Menozzi C, Lolli G, Bottoni N, Gaggioli G (1992). "Long-term outcome of paced and nonpaced patients with severe carotid sinus syndrome". Am J Cardiol. 69 (12): 1039–43. PMID 1561975.CS1 maint: Multiple names: authors list (link)
14. ↑ Brignole M, Menozzi C, Gianfranchi L, Oddone D, Lolli G, Bertulla A (1991). "Neurally mediated syncope detected by carotid sinus massage and head-up tilt test in sick sinus syndrome". Am J Cardiol. 68 (10): 1032–6. PMID 1927916.CS1 maint: Multiple names: authors list (link)
15. ↑ Connolly SJ, Sheldon R, Thorpe KE, Roberts RS, Ellenbogen KA, Wilkoff BL; et al. (2003). "Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope: Second Vasovagal Pacemaker Study (VPS II): a randomized trial". JAMA. 289 (17): 2224–9. doi:10.1001/jama.289.17.2224. PMID 12734133.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)  Review in: ACP J Club. 2003 Nov-Dec;139(3):77
16. ↑ Sutton R, Brignole M, Menozzi C, Raviele A, Alboni P, Giani P; et al. (2000). "Dual-chamber pacing in the treatment of neurally mediated tilt-positive cardioinhibitory syncope : pacemaker versus no therapy: a multicenter randomized study. The Vasovagal Syncope International Study (VASIS) Investigators". Circulation. 102 (3): 294–9. PMID 10899092.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
17. ↑ Ammirati F, Colivicchi F, Santini M, Syncope Diagnosis and Treatment Study Investigators (2001). "Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope: a multicenter, randomized, controlled trial". Circulation. 104 (1): 52–7. PMID 11435337.CS1 maint: Multiple names: authors list (link)
18. ↑ Sheldon R, Koshman ML, Wilson W, Kieser T, Rose S (1998). "Effect of dual-chamber pacing with automatic rate-drop sensing on recurrent neurally mediated syncope". Am J Cardiol. 81 (2): 158–62. PMID 9591898.CS1 maint: Multiple names: authors list (link)

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