Carotid Bruit

Etiology

Atherosclerotic lesions are commonly found in the arteries that arise from the aortic arch vessels. About 80% of these lesions are located at the bifurcation of the common carotid arteries.[1] Carotid artery auscultation is primarily done during an exam to determine if carotid stenosis may predispose the patient to a stroke. In patients with a 2 mm carotid artery luminal narrowing, carotid bruit is present 70% to 89% of the time.[6] However, luminal narrowing of the carotid artery is not the only cause of carotid bruit. Auscultatory sounds from cardiac valvular murmurs that radiate to the neck, cervical venous hums, and intracranial arteriovenous malformations can produce vascular sounds similar to the carotid bruit.[1] Arterial tortuosity, kinking, and high output clinical states may generate bruit even in normal or non-stenotic arteries. For example, in patients with thyrotoxicosis, there is a 5-to 10-fold increase in blood flow to the enlarged thyroid gland, resulting in a systolic bruit directly over the gland.[1] A case of bovine-type aortic arch and compression of the kissing carotid arteries by a retrosternal goiter is also a rare cause of a carotid bruit.[7] 

Vascular occlusions from extrinsic compression, such as carotid body tumors and carotid paraganglioma, have also been reported to cause carotid bruit.[1][8][9] Disruption of the blood vessels can cause bruit and has presented in patients having a carotid artery dissection.[10] Reports of carotid bruit from inflammation of the carotid vessel due to inflammatory conditions like Takayasu arteritis are also in the literature.[11] Non-sclerotic and noninflammatory diseases such as fibromuscular dysplasia commonly affect the internal carotid arteries and cause carotid bruit. These can be found incidentally during the exam. Cervical fibromuscular dysplasia is mostly asymptomatic.[12]

Epidemiology

A carotid bruit is a nonspecific finding with a broad sensitivity described in the literature (24 to 84%).[13] It is present in about 5% of patients aged 45 to 80 years without clinically significant internal carotid disease.[6] Only about one-third of patients with carotid bruit are found to have lesions considered hemodynamically significant 70% to 90% stenosis). In patients with hemodynamically significant carotid narrowing, 50% will be found to have a bruit during carotid auscultation.[3] A carotid bruit can also be present in 20% of healthy children under 15. Nearly 22% of patients diagnosed with cervical fibromuscular dysplasia are found to have carotid bruits, although patients are seldom found to be symptomatic.[14]

Pathophysiology

The bruit typically implies stenosis at or proximal to the area of auscultation. The auscultated sound is usually the result of turbulent, non-laminar blood flow through a stenotic area. The turbulent flow creates vibrations in the arterial wall that transmit to the body surface, where stethoscopic auscultation is possible. Critical stenosis, however, does not occur until the cross-sectional area decreases to 70%, corresponding to a reduction of lumen diameter by half. Kurtz previously described the basic science of bruits: “ As stenosis increases, therefore, potential energy (pressure) proximal to the stenosis changes to increasing kinetic energy (velocity) within the stenosis. With increasing flow velocity, laminar flow through stenosis eventually changes to turbulent flow, producing vibrations and a bruit. Thus, velocity through the stenotic segment and the subsequent character of the bruit depend on the degree of stenosis and the resulting pressure gradient.” Kurtz further explained that the auscultatory quality and timing of the bruit changes with the degree of stenosis and pressure gradients. A soft early systolic murmur is audible when the lumen is about 50% narrowed. This sound can become high-pitched, more intense, and holosystolic when the stenosis approaches 60%. When the diameter reduces to 70%-80%, a bruit can be audible during systole and early diastole. As the occlusion worsens, blood flow turbulence becomes insufficient to cause vibratory sounds, and a bruit may disappear.[1]

Histopathology

A bruit from carotid artery stenosis is due to a carotid atherosclerotic plaque that can be both stable and unstable. These plaques are similar to the other arterial plaques of the body. The genesis of atherosclerosis begins with low-density lipoprotein particles trapped in the subintimal space by glycoproteins. After the low-density lipoprotein particles oxidize, a cascade of inflammatory response ensues, forming solid crystalline cholesterol that expands in volume, compromising the fibrous cap. The fibrous cap maintains the integrity of the plaques and faces the vascular lumen. Rupture of the fibrous cap leads to thrombosis, potential arterial lumen blockage, and distal embolization. High-grade carotid stenosis is often found to have inflammatory cell infiltrates. Additionally, intraplaque hemorrhage has been found in symptomatic patients and is predictive of future neurologic events and plaque rupture. Several factors seem to influence plaque morphology. Smoking may play a role in expediting atherogenesis. Men are also found to have high-risk plaque features compared to women. Interestingly, age did now show a trend toward age-related plaque instability.[4]

History and Physical

Assessing patients for risks of cerebrovascular events starts by taking a careful history and a focused physical exam. The optimum position for listening for a carotid bruit is supine or sitting with the patient. In the sitting position, optimal carotid palpation and auscultation are achievable when approaching the patient from behind. With the patient’s chin pointing straight forward, the stethoscope bell is applied over each carotid artery, sealing the overlying skin. The patient is then instructed to be inspired deeply and hold their breath without bearing down for 15 to 30 seconds. Auscultation continues during, and shortly after, the breath-holding. Breath-holding not only eliminates other adventitious sounds but also accentuates a carotid bruit.[1] 

Evaluation

While a carotid bruit may alert clinicians to carotid artery disease, it is not sensitive and specific enough to diagnose carotid disease.[15] On identification of a bruit, however, the next step is to determine whether the patient needs additional testing or referral; this usually depends upon the assessed vascular risk factors of the patient or the presence of signs and symptoms suggestive of any neuro-vascular disease. Imaging studies such as carotid duplex ultrasound, computed tomography angiography, and magnetic resonance angiography of the neck help confirm the diagnosis and provide an anatomical layout if a surgical invention is warranted.[16] Collaboration with specialists like neurologists and cardiologists is also commonly employed.

Treatment / Management

Upon confirmation of carotid artery disease as the source of the carotid bruit, medical and surgical treatment should begin based on the severity of the stenosis, the presence or absence of neurological symptoms, and the patient's comorbidities.

Differential Diagnosis

Differential diagnosis for carotid bruit includes:

• Cardiac valvular murmurs
• Carotid artery vasculitis
• Carotid body tumors
• Carotid dissection
• Carotid stenosis
• Cervical fibromuscular dysplasia
• Cervical venous hum
• Extrinsic compression of the carotid artery
• High-output clinical states like thyrotoxicosis
• Intracranial arteriovenous malformations

Prognosis

While carotid bruits have generally been regarded as markers of generalized atherosclerosis, the data does not show them as strong predictors of cerebrovascular events. However, carotid bruit auscultation may help select patients who benefit the most from aggressive cardiovascular risk stratification and therapeutic interventions.[17]

Complications

The annual incidence of cerebrovascular accidents in people with asymptomatic bruits is about 1 to 3 percent.[3] Stroke is the second most common cause of mortality worldwide and the third leading cause of death in the United States. Carotid artery disease contributes to 15 to 20% of all ischemic strokes.[4]