Description

• The carotid sinuses play a central role in maintaining blood pressure (BP) homeostasis.
• The carotid sinuses are located near the bifurcation of the internal and external carotid arteries and contain baroreceptors that are responsive to changes in arterial pressure.
• An endogenous increase in BP or external pressure applied to a carotid sinus can cause an increase in the baroreceptor firing rate and activate vagal efferents and/or inhibit the sympathetic discharge to the heart and blood vessels which results in a slowing of the heart rate and drop in BP.
• In CSH, stimulation of one or both carotid sinuses, (such as mechanical forces with turning the neck) causes an exaggerated baroreceptor response that can result in dizziness or syncope.
• There are three definitions for CSH (1):
  • Standard criteria: a pause in heart rate of ≥3 s in response to carotid sinus massage (CSM) and/or ≥50 mm Hg drop in systolic BP or both of the above
  • Krediet criteria: a pause in heart rate of ≥6 s in response to CSM and/or a fall in MAP to a value <60 mmHg for ≥6 s
  • Kerr criteria: a pause in heart rate in response to CSM >95th percentile of the population response (7.3 s asystole), and/or vasodepression in response to CSM >95th percentile of the population response (>77 mmHg fall in systolic BP), or both
• CSH is generally divided into three subtypes, based on response to CSM:
  • Cardioinhibitory (70–75%): asystole for at least 3 seconds
  • Vasodepressive (5–10%): fall in systolic BP of at least 50 mm Hg
  • Mixed (20–25%): combination of the first 2 subtypes
• Carotid sinus syndrome (CSS) typically (but not consistently) refers to CSH with syncope and may be classified as:
  • Spontaneous CSS: syncope after accidental mechanical manipulation (trigger) of the carotid sinuses (e.g., shaving, tight collars, or tumors)
  • Induced CSS: syncope diagnosed by CSM although no mechanical trigger is found

Epidemiology

• Disease of elderly; most often occurs in male patients >65 years.
• Associated with a history of coronary artery disease (CAD) and hypertension (HTN), with right CSH > left CSH

Prevalence

• In 2006, CSH was found in 39% of unselected adults >65 years of age using standard diagnostic criteria and found to be comparable with 2019 review of prevalence data (2).
• CSH may be a cause of the symptoms in 30% of elderly patients with unexplained syncope.

Etiology and Pathophysiology

• The exact site that causes the hypersensitivity response remains unknown. Changes in any part of the reflex arc or the target organs may give rise to this condition. It may be a part of a generalized autonomic disorder associated with autonomic dysregulation.
• Associated with resting sympathetic overactivity and increased baroreflex sensitivity
• Bradycardia and asystole seen in cardioinhibitory and mixed CSH subtypes appear to be mediated by vagal efferents, whereas vasodilatation and arterial hypotension in the vasodepressor and mixed subtypes are attributed to decrease sympathetic tone.
• Symptomatic CSH has been shown to be associated with impaired cerebral autoregulation and found to be normal in asymptomatic CSH.
• Atherosclerosis may diminish carotid sinus compliance, resulting in a reduction in afferent impulse traffic in the baroreflex pathway.
• CSH is often idiopathic but can be caused by:
  • Carotid body tumors
  • Inflammatory and malignant lymph nodes in the neck
  • Extensive scarring from prior neck surgery in the area of the carotid sinus
  • Metastatic cancer

Risk Factors

• Advanced age, male gender
• CAD
• HTN
• DM

Commonly Associated Conditions

• Carotid sinus syncope, Sick sinus syndrome
• Atrioventricular block
• CAD
• HTN
• Orthostatic hypotension
• Vasovagal syncope
• Alzheimer disease
• Parkinson disease