Carotid Sinus Hypersensitivity

Carotid Sinus Hypersensitivity

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Carotid sinus hypersensitivity (CSH) is an exaggerated response to carotid sinus baroreceptor stimulation. It results in dizziness or syncope from transient diminished cerebral perfusion. [1]

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. [5]

CSH, orthostatic hypotension, and vasovagal syncope are common conditions that are likely to coexist in patients with syncope and falls. [6]

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. [7]

CSH may be a part of a generalized autonomic disorder associated with autonomic dysregulation. [8] 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. [9]

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. [10]

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. [11]

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. [12]

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

For patient education resources, see Brain & Nervous System Center as well as Dizziness.

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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

Mikhael F El-Chami, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society

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.

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