Carotid Sinus Hypersensitivity
Carotid Sinus Hypersensitivity
Carotid sinus hypersensitivity (CSH) is an exaggerated response to carotid sinus baroreceptor stimulation. It results in dizziness or syncope from transient diminished cerebral perfusion. 
Although baroreceptor function usually diminishes with age, some people experience hypersensitive carotid baroreflexes. For these individuals, even mild stimulation to the neck results in marked bradycardia and a drop in blood pressure.
CSH predominantly affects older males. It is a potent contributory factor and a potentially treatable cause of unexplained falls and syncopal episodes in elderly people. [2, 3, 4] Yet, CSH is often overlooked in the differential diagnosis of presyncope and syncope. 
CSH, orthostatic hypotension, and vasovagal syncope are common conditions that are likely to coexist in patients with syncope and falls. 
The carotid sinus reflex plays a central role in blood pressure homeostasis. Changes in stretch and transmural pressure are detected by baroreceptors in the heart, carotid sinus, aortic arch, and other large vessels. Afferent impulses are transmitted by the carotid sinus, glossopharyngeal, and vagus nerves to the nuclei tractus solitarius and the para median nucleus in the brain stem. Efferent limbs are carried through sympathetic and vagus nerves to the heart and blood vessels, controlling heart rate and vasomotor tone.
In CSH, 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.
The hemodynamic changes following carotid sinus stimulation are independent of body position. These changes have a distinct temporal pattern, with an initial fall in the cardiac output driven by heart rate, followed by a later fall in total peripheral resistance. 
CSH may be a part of a generalized autonomic disorder associated with autonomic dysregulation.  Data have been reported on neuronal degeneration with accumulation of hyperphosphorylated tau or alpha-synuclein in neurones in medulla, leading to impairment of central regulation of baroreflex responses and predispose elderly patients to CSH. 
However, the exact mechanism and site of abnormal sensitivity is unknown. The exaggerated response may be due to changes in any part of the reflex arc or the target organs. A potential mechanism for the symptomatic presentation of CSH (eg, syncope, blood pressure/heart rate changes) may be impaired cerebral autoregulation. 
Clinically and historically, 3 types of CSH have been described, as follows:
The cardioinhibitory type comprises 70-75% of cases. The predominant manifestation is a decreased heart rate, which results in sinus bradycardia, atrioventricular block, or asystole due to vagal action on sinus and atrioventricular nodes. This response can be abolished with atropine. 
The vasodepressor type comprises 5-10% of cases. The predominant manifestation is a vasomotor tone decrease without a change in heart rate. The significant resulting drop in blood pressure is due to a change in the balance of parasympathetic and sympathetic effects on peripheral blood vessels. This response is not abolished with atropine.
The mixed type comprises 20-25% of cases. A decrease in heart rate and vasomotor tone occurs.
A proposal by a group of international experts suggests that the classification of CSH into 3 types as above should be revised. It has been suggested that all patients with CSH should be classified as “mixed” between vasodepression and cardioinhibition. This is because isolated cardioinhibitory CSH (asystole without fall in arterial pressure) does not occur. 
The terms spontaneous carotid sinus syndrome and induced carotid sinus syndrome have also been introduced to categorize patients who are presumed to have CSH, as follows:
The term spontaneous carotid sinus syndrome refers to a clinical situation in which the symptoms can be clearly attributed to a history of accidental mechanical manipulation of the carotid sinuses (eg, taking pulses in the neck, shaving) and CSH is reproduced by carotid sinus massage. Spontaneous carotid sinus syndrome is rare and accounts for about 1% of causes of syncope.
The term induced carotid sinus syndrome refers to a clinical situation in which a patient has no clear history of accidental mechanical manipulation of the carotid sinuses and has a negative result from workup for syncope, except for a hypersensitive response to carotid sinus massage, which can be attributed to the patient’s symptoms. Induced carotid sinus syndrome is more prevalent than spontaneous carotid sinus syndrome and accounts for the bulk of patients with an abnormal response to carotid sinus massage observed in the clinical setting.
CSH is found in 0.5-9.0% of patients with recurrent syncope.
CSH is observed in up to 14% of elderly nursing home patients and 30% of elderly patients with unexplained syncope and drop attacks.
CSH is more common in males than in females.
CSH is predominantly a disease of elderly people; it is virtually unknown in people younger than 50 years.
The long-term mortality rate is similar to the general population and patients with unexplained syncope. Untreated symptomatic patients have a syncope recurrence rate as high as 62% within 4 years.
Patients treated with a pacemaker have fewer syncopal attacks but may experience a recurrence rate as high as 16% in 4 years.
CSH is associated with an increased risk of falls, drop attacks, bodily injuries, and fractures in elderly patients.
In the general population, the rates of mortality, sudden death, myocardial infarction, or stroke are unaffected by the presence of CSH.
Educate patients on how to recognize premonitory symptoms and avoid triggering events. In addition, educate patients regarding therapeutic actions such as methods to increase central fluid volume in the body
Seifer C. Carotid sinus syndrome. Cardiol Clin. 2013 Feb. 31(1):111-21. [Medline].
Parry SW, Steen N, Bexton RS, Tynan M, Kenny RA. Pacing in elderly recurrent fallers with carotid sinus hypersensitivity: a randomised, double-blind, placebo controlled crossover trial. Heart. 2009 May. 95(5):405-9. [Medline].
Gillespie LD, Robertson MC, Gillespie WJ, et al. Interventions for preventing falls in older people living in the community. Cochrane Database Syst Rev. 2009 Apr 15. CD007146. [Medline].
Smebye KL, Granum S, Wyller TB, Mellingsæter M. Medical findings in an interdisciplinary geriatric outpatient clinic specialising in falls. Tidsskr Nor Laegeforen. 2014 Apr 8. 134(7):705-9. [Medline].
Ziegelstein RC. Near-syncope after exercise. JAMA. 2004 Sep 8. 292(10):1221-6. [Medline].
Tan MP, Newton JL, Chadwick TJ, Parry SW. The relationship between carotid sinus hypersensitivity, orthostatic hypotension, and vasovagal syncope: a case-control study. Europace. 2008 Dec. 10(12):1400-5. [Medline].
Krediet CT, Jardine DL, Wieling W. Dissection of carotid sinus hypersensitivity: the timing of vagal and vasodepressor effects and the effect of body position. Clin Sci (Lond). 2011 Nov. 121(9):389-96. [Medline].
Tan MP, Kenny RA, Chadwick TJ, Kerr SR, Parry SW. Carotid sinus hypersensitivity: disease state or clinical sign of ageing? Insights from a controlled study of autonomic function in symptomatic and asymptomatic subjects. Europace. 2010 Nov. 12(11):1630-6. [Medline].
Miller VM, Kenny RA, Slade JY, Oakley AE, Kalaria RN. Medullary autonomic pathology in carotid sinus hypersensitivity. Neuropathol Appl Neurobiol. 2008 Aug. 34(4):403-11. [Medline].
Tan MP, Chadwick TJ, Kerr SR, Parry SW. Symptomatic presentation of carotid sinus hypersensitivity is associated with impaired cerebral autoregulation. J Am Heart Assoc. 2014 Jun 19. 3(3):e000514. [Medline].
Lacerda Gde C, Pedrosa RC, Lacerda RC, et al. Cardioinhibitory carotid sinus hypersensitivity: prevalence and predictors in 502 outpatients. Arq Bras Cardiol. 2008 Mar. 90(3):148-55. [Medline].
Wieling W, Krediet CT, Solari D, et al. At the heart of the arterial baroreflex: a physiological basis for a new classification of carotid sinus hypersensitivity. J Intern Med. 2013 Apr. 273(4):345-58. [Medline].
Kuo FY, Hsiao HC, Chiou CW, Liu CP. Recurrent syncope due to carotid sinus hypersensitivity and sick sinus syndrome. J Chin Med Assoc. 2008 Oct. 71(10):532-5. [Medline].
McIntosh SJ, Lawson J, Kenny RA. Clinical characteristics of vasodepressor, cardioinhibitory, and mixed carotid sinus syndrome in the elderly. Am J Med. 1993 Aug. 95(2):203-8. [Medline].
Ballard C, Shaw F, McKeith I, Kenny R. High prevalence of neurovascular instability in neurodegenerative dementias. Neurology. 1998 Dec. 51(6):1760-2. [Medline].
Kenny RA, Shaw FE, O’Brien JT, Scheltens PH, Kalaria R, Ballard C. Carotid sinus syndrome is common in dementia with Lewy bodies and correlates with deep white matter lesions. J Neurol Neurosurg Psychiatry. 2004 Jul. 75(7):966-71. [Medline].
Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000 May. 83(5):564-9. [Medline].
Morillo CA, Camacho ME, Wood MA, et al. Diagnostic utility of mechanical, pharmacological and orthostatic stimulation of the carotid sinus in patients with unexplained syncope. J Am Coll Cardiol. 1999 Nov 1. 34(5):1587-94. [Medline].
Krediet CT, Parry SW, Jardine DL, Benditt DG, Brignole M, Wieling W. The history of diagnosing carotid sinus hypersensitivity: why are the current criteria too sensitive?. Europace. 2011 Jan. 13(1):14-22. [Medline].
Amin V, Pavri BB. Carotid sinus syndrome. Cardiol Rev. 2015 May-Jun. 23(3):130-4. [Medline].
[Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: 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) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008 May 27. 51(21):e1-62. [Medline].
Kenny RA, Richardson DA, Steen N, et al. Carotid sinus syndrome: a modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001 Nov 1. 38(5):1491-6. [Medline].
Ryan DJ, Nick S, Colette SM, Roseanne K. Carotid sinus syndrome, should we pace? A multicentre, randomised control trial (Safepace 2). Heart. 2010 Mar. 96(5):347-51. [Medline].
Brignole M, Menozzi C, Lolli G, et al. Long-term outcome of paced and nonpaced patients with severe carotid sinus syndrome. Am J Cardiol. 1992 Apr 15. 69(12):1039-43. [Medline].
Moore A, Watts M, Sheehy T, et al. Treatment of vasodepressor carotid sinus syndrome with midodrine: a randomized, controlled pilot study. J Am Geriatr Soc. 2005 Jan. 53(1):114-8. [Medline].
Cattaneo M, Porretta AP, Gallino A. Ranolazine: Drug overview and possible role in primary microvascular angina management. Int J Cardiol. 2015 Feb 15. 181:376-81. [Medline].
Lloyd MG, Wakeling JM, Koehle MS, Drapala RJ, Claydon VE. Carotid sinus hypersensitivity: block of the sternocleidomastoid muscle does not affect responses to carotid sinus massage in healthy young adults. Physiol Rep. 2017 Oct. 5(19):[Medline]. [Full Text].
Evidence Review Committee Members, Varosy PD, Chen LY, Miller AL, et al. Pacing as a treatment for reflex-mediated (vasovagal, situational, or carotid sinus hypersensitivity) syncope: A systematic review for the 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. Heart Rhythm. 2017 Aug. 14(8):e255-e269. [Medline]. [Full Text].
Lilitsis E, Papaioannou A, Hatzimichali A, et al. A case of asystole from carotid sinus hypersensitivity during patient positioning for thyroidectomy. BMC Anesthesiol. 2016 Oct 6. 16(1):85. [Medline]. [Full Text].
Mevan N Wijetunga, MD, FACC, FHRS Cardiac Electrophysiologist, CentraCare Heart & Vascular Center
Mevan N Wijetunga, MD, FACC, FHRS is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology
Disclosure: Nothing to disclose.
Mikhael F El-Chami, MD Associate Professor, Department of Medicine, Division of Cardiology, Section of Electrophysiology, Emory University School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Medtronic; Boston Scientific<br/>Received grant/research funds from Medtronic Inc for principle investigator.
Carotid Sinus Hypersensitivity
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