Depending on the degree of stenosis, the narrowing of the carotid arteries can significantly reduce the volume of blood that supplies the brain and cause symptoms related to transient attacks of ischemia. it is important to bear in mind that a vast percentage of the individuals suffering from carotid stenosis are asymptomatic, despite having a massive degree of arterial constriction.
Patients who are diagnosed with carotid stenosis often have a prior medical history that includes amaurosis fugax, TIAs or crescendo TIAs (transient ischemic attacks) and infarctions. A useful clinical sign that is strongly indicative of carotid artery disease is the bruit that can be heard on the site of the stenosis by auscultation.
Carotid stenosis is most successfully depicted through the use of intraarterial digital subtraction angiography (DSA), a procedure that has replaced conventional angiography to a vast extent. DSA is a less time-consuming procedure, that allows for the use of smaller catheters, the reduction of the amount of contrast material required . Magnetic resonance angiography (MRA) is also an option.
Another imaging modality that can be applied is the carotid duplex ultrasound (CDUS), which can illustrate regionally increased blood flow that corresponds to areas of stenosis   . This examination can detect the degree of carotid narrowing, as well as further information that will help to classify the condition and draw a successful treatment plan  . The transcranial Doppler can also be used in order to depict the primary intracerebral arteries of the brain. The former two procedures are usually used simultaneously, because they yield better results, as far as the hemodynamic status of the patient is concerned .
Computerized tomography angiography (CTA) can be used to provide an illustration of the lumen of the carotid artery and the neighboring tissues and skeletal structures, while also enabling the three-dimensional regional depiction. This modality is chosen when an ultrasound is inapplicable or its results are not reliable. Such cases include severe accompanying calcification, a short neck or high bifurcation .
Carotid stenosis can be treated either solely pharmacologically or surgically, depending on the particular circumstances and degree of stenosis.
Pharmacological treatment consists of anticoagulants and anti-platelet medications. Aspirin is commonly used at the dosage of 30 to 1300 mg/day, in order to prevent the production of thromboxane A2 by the platelets; it has been found to contribute positively to the prevention of strokes and transient ischemic attacks . Ticlopidine is also an anti-platelet agent that is believed to be more beneficial than aspirin but has been associated with a considerable risk of developing neutropenia and diarrhea. Clopidogrel is used instead, given its significantly reduced risk of neutropenia.
As far as surgical treatment is concerned, the options comprise carotid angioplasty (stenting) and endarterectomy. Regarding carotid angioplasty and stenting (CAS), its fewer complications has allowed the procedure to be widely used in patients who cannot undergo open surgery. Guidelines stipulate the use of CAS currently in cases of patients presenting with symptoms and a stenosis of more than 70% and in cases of patients with no symptoms and a stenosis that exceeds 80%. Both patient groups need to be unsuccessful candidates for an endarterectomy.
Carotid endarterectomy (CEA), on the other hand, is believed to be accompanied by a smaller risk of stroke or mortality, even though the difference between CEA and CAS is not staggering. It is a procedure that has been applied for a longer period of time compared to CAS and is nowadays reserved for low-risk patients with few comorbidities.
The most common complications associated with carotid stenosis are a potential stroke and injuries to the cranial nerves, caused by the surgical interventions, carried out in order to treat the condition. By far, the nerves most frequently subjected to traumatizations are the hypoglossal and laryngeal nerve; the risk of such a complication affects approximately 2 to 7 % of all patients that undergo an endarterectomy. Strokes are equally common, occurring at a rate of 1 to 5% of all patients . Furthermore, an individual that has undergone endarterectomy is faced with a 1-20% risk of recurring stenosis and a 1 to 3% risk of a second surgical procedure.
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) stipulates that the risk of a patient developing a stroke in the 2 years following endarterectomy was 2%, whereas pharmacological therapy was associated with a considerably higher risk (12%) . Ipsilateral stroke was expected to occur at a rate of 6% for patients treated with surgery and 26% for patients treated exclusively with medications. On the other hand, the Asymptomatic Carotid Atherosclerosis Study (ACAS) has presented slightly different rates, with the 5-year risk for ipsilateral stroke being 5.1% for the patients treated with surgery, as opposed to 10% for these individuals treated pharmacologically .
Further studies have outlined that carotid angioplasty carried out with an embolic protection wire has been linked with a 2.5% risk of stroke within the initial 30 days following the procedure . Medications such as cilostazol (anti-platelet agent) are believed to considerably diminish the progression of carotid stenosis after an angioplasty .
Carotid stenosis is otherwise known as carotid artery disease. The narrowing of the carotid arteries is a result of atherosclerotic deposits on the walls of the vessels and, consequently, the etiologic factors are those pertaining to atherosclerosis itself. Various risk factors have indeed been associated with the formation of atherosclerotic plaques within the vascular walls, such as:
The coronary arteries are usually the first to be affected by atherosclerosis, with the carotid arteries being affected later on.
Carotid stenosis caused by atherosclerotic lesions is responsible for approximately 20% of all ischemic strokes, both transient and non-transient, and is believed to be the culprit behind 13 out of 100,000 strokes annually   . It has been strongly associated with prolonged working hours, especially regarding men with pre-existing ischemic heart disease and calcified aortic stenosis. The increasing frequency of carotid stenosis clearly corresponds to the increase is weekly working hours, irrespective of the occupation. Studies have generally proposed that, should the average time a person spends in the workplace be decreased, the public would definitely benefit in terms of cardiovascular health.
Carotid stenosis involves the narrowing of the carotid diameter, caused by atherosclerotic plaques on the lumen of the internal carotid artery. The atheromatous deposits usually affect the posterior carotid wall, and can extend as far as the common carotid artery as well, giving the vessel a characteristic hourglass-type shape.
The risk factors associated with the aforementioned deposits are the same that have been incriminated for atherosclerosis and comprise smoking, hypercholesterolemia, hypertension, diabetes mellitus and obesity. Carotid stenosis is a condition that tends to affect individuals in their senior years and male patients seem to be at a greater risk of succumbing to a related cerebrovascular event, compared to women  .
Carotid stenosis can lead to complications through two separate mechanisms: thromboembolism and low-flow. The narrowing of the arterial wall's diameter renders the blood flow to the brain inadequate; thus, a stroke may occur. On the other hand, the plaques themselves constitute excellent substrates for the development of thrombi, which may cause additional stenosis or embolism      .
Almost 1 out of 5 transient ischemic attacks are caused by carotid stenosis. The actual pathophysiological mechanism may involve either inadequate blood flow or the dislocation of an embolus. Usually, when embolism is responsible for the onset of a stroke, the symptoms that are released involve the brain region supplied by the middle cerebral artery or the anterior cerebral artery. However, transient ischemic attacks that are caused by diminished blood flow through the carotid arteries usually involve periodic, repetitive occasions of variable symptomatology  .
In the extreme case that a complete occlusion of the internal carotid artery has occurred, the mechanism through which a cerebrovascular event can ensue depends on the potency of the collateral blood flow through the circle of Willis. The time following the event is the most critical period and involves the biggest risk of a stroke; as the time passes, collateral circulation gradually develops and restores the blood flow to the brain    . Delayed phenomena of stroking have nevertheless been observed and can be diagnosed even months after the initial event; they have been attributed to the dislocation of a thrombus distally to the clot . It is generally believed that patients who present with no symptomatology despite suffering from carotid stenosis have a less potent cerebrovascular reserve, in contradistinction to those who present with symptoms .
Carotid stenosis depends upon the same risk factors as atherosclerosis and can therefore be prevented with various lifestyle changes that reduce the risk of developing atherosclerotic plaques. Patients are advised to monitor their cholesterol closely, refrain from the consumption of excessive amounts of alcohol, cease smoking, lose weight and exercise more. Individuals who present with a high blood pressure should also be monitored and treated for their condition, as it greatly contributes to carotid stenosis.
People with a family history of carotid stenosis or stroke should consult their physician, who will carry out the necessary examinations to detect a possible carotid artery disease. These include a precautionary carotid ultrasound, an MRA, a CTA and an ophthalmologic exam that will help to diagnose dysfunctional vessels within the eyes.
Carotid artery stenosis is the narrowing of the carotid artery due to the deposition of atherosclerotic plaques in the arterial vessel. It is one of the primary causes of transient ischemic attacks and strokes. In a great majority of the cases the condition produces no symptomatology, despite the presence of a stenosis of extensive degree .
Carotid stenosis is the narrowing of the carotid arteries, which is caused by the deposition of atherosclerotic plaques within the carotid arteries. These plaques consist of fat, calcium, connective tissue and white cells and can lead to a significant constriction of the carotid artery and a reduction in the flow of blood to the brain.
Therefore, patients who are at a higher risk of developing carotid stenosis are those whose lifestyle and family history renders them likely candidates for atherosclerosis. These factors include the following:
Carotid stenosis is a condition that can lead to a transient cerebral event, namely an attack that involves decreased amount of blood reaching the brain, or an infarction. A transient ischemic attack may resolve or leave no residual damage, but an infarction can severely damage the brain and lower the quality of the patient's life. Despite a great degree of stenosis that can be present (>80%), carotid stenosis does not always cause symptoms. For this reason, people with risk factors for atherosclerosis should refer to their physician, who will screen for the condition.
Carotid stenosis is diagnosed with various imaging modalities, such as an ultrasound, an angiography etc. It is either treated exclusively with medications, such as anti-platelet agents and anticoagulants, or surgically, via the removal of the narrowed part of the carotid artery or the positioning of a dilatory device known as a stent, within the arterial wall.