Carotid artery stenosis
|Carotid artery stenosis|
|Carotid Artery Disease|
Signs and symptoms
The common carotid artery is the large artery whose pulse can be felt on both sides of the neck under the jaw. On the right side it starts from the brachiocephalic artery (a branch of the aorta), and on the left side the artery comes directly off the aortic arch. At the throat it forks into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain, and the external carotid artery supplies the face. This fork is a common site for atherosclerosis, an inflammatory build-up of atheromatous plaque inside the common carotid artery, or the internal carotid arteries that causes them to narrow.
The plaque can be stable and asymptomatic, or it can be a source of embolization. Emboli break off from the plaque and travel through the circulation to blood vessels in the brain. As the vessels get smaller, an embolus can lodge in the vessel wall and restrict the blood flow to parts of the brain. This ischemia can either be temporary, yielding a transient ischemic attack, or permanent resulting in a thromboembolic stroke.
Clinically, risk of stroke from carotid artery stenosis is evaluated by the presence or absence of symptoms and the degree of stenosis on imaging.
Transient ischemic attacks (TIAs) are a warning sign, and may be followed by severe permanent strokes, particularly within the first two days. TIAs by definition last less than 24 hours and frequently take the form of a weakness or loss of sensation of a limb or the trunk on one side of the body, or the loss of sight (amaurosis fugax) in one eye. Less common symptoms are artery sounds (bruits), or ringing in the ears (tinnitus).
The common carotid artery is the large vertical artery in red. The blood supply to the carotid artery starts at the arch of the aorta (bottom). The carotid artery divides into the internal carotid artery and the external carotid artery. The internal carotid artery supplies the brain. Plaque often builds up at that division, and causes a narrowing (stenosis). Pieces of plaque can break off and block the small arteries above in the brain, which causes a stroke. Plaque can also build up at the origin of the carotid artery at the aorta.
Carotid artery stenosis is usually diagnosed by color flow duplex ultrasound scan of the carotid arteries in the neck. This involves no radiation, no needles and no contrast agents that may cause allergic reactions. This test has good sensitivity and specificity.
Typically duplex ultrasound scan is the only investigation required for decision making in carotid stenosis as it is widely available and rapidly performed. However, further imaging can be required if the stenosis is not near the bifurcation of the carotid artery.
One of several different imaging modalities, such as a computed tomography angiogram (CTA) or magnetic resonance angiogram (MRA) may be useful. Each imaging modality has its advantages and disadvantages - Magnetic resonance angiography and CT angiography with contrast is contraindicated in patients with renal insufficiency, catheter angiography has a 0.5% to 1.0% risk of stroke, MI, arterial injury or retroperitoneal bleeding. The investigation chosen will depend on the clinical question and the imaging expertise, experience and equipment available.
The need for screening for carotid artery stenosis depends on whether someone is experiencing symptoms arising from the stenosis or has risk factors for the development of carotid artery disease.
While routine population screening is not advised, the American Heart Association recommends screening for people who don’t have symptoms of carotid stenosis but have been diagnosed with related medical conditions or have risk factors for carotid artery disease. Screening is recommended for people who have:
- Vascular disease elsewhere in the body, including:
- Two or more of the following risk factors:
The American Heart Association also recommends screening if a physician detects a carotid bruit, or murmur, over the carotid artery by listening through a stethoscope during a physical exam.
For people with symptoms, the American Heart Association recommends initial screening using ultrasound (see diagnosis below).
- Medications alone (an antiplatelet drug (or drugs) and control of risk factors for atherosclerosis).
- Medical management plus carotid endarterectomy or carotid stenting, which is preferred in patients at high surgical risk and in younger patients.
- Control of smoking, high blood pressure, and high levels of lipids in the blood.
The goal of treatment is to reduce the risk of stroke (cerebrovascular accident). Intervention (carotid endarterectomy or carotid stenting) can cause stroke; however, where the risk of stroke from medical management alone is high, intervention may be beneficial.
Clinical guidelines (such as those of National Institute for Clinical Excellence (NICE)) recommend that all patients with carotid stenosis be given medication, usually blood pressure lowering medications, anti-clotting medications, anti-platelet medications (such as aspirin or clopidogrel), and especially statins (which were originally prescribed for their cholesterol-lowering effects but were also found to reduce inflammation and stabilize plaque).
In selected trial participants with asymptomatic severe carotid artery stenosis, carotid endarterectomy reduces the risk of stroke in the next 5 years by 50%, though this represents a reduction in absolute incidence of all strokes or perioperative death of approximately 6%. In most centres, carotid endarterectomy is associated with a 30-day stroke or mortality rate of < 3%; some areas have higher rates.
NICE and other guidelines also recommend that patients with symptomatic carotid stenosis be given carotid endarterectomy urgently, since the greatest risk of stroke is within days. Carotid endarterectomy reduces the risk of stroke or death from carotid emboli by about half.
For people with stenosis but no symptoms, the interventional recommendations are less clear. Such patients have a historical risk of stroke of about 1–2% per year. Carotid endarterectomy has a surgical risk of stroke or death of about 2–4% in most institutions. In the large Asymptomatic Carotid Surgery Trial (ACST) endarterectomy reduced major stroke and death by about half, even after surgical death and stroke was taken into account. According to the Cochrane Collaboration the absolute benefit of surgery is small. For intervention using stents, there is insufficient evidence to support stenting rather than open surgery, and several trials, including the ACST-2, are comparing these 2 procedures.
Surgery and stenting
The largest clinical trial performed, CREST, randomized patients at risk for a stroke from carotid artery blockage to either open surgery (carotid endarterectomy) or carotid stent placement with embolic protection. This trial followed patients for 4 years and found no overall difference in the primary end point of both treatment arms (myocardial infarctions, any perioperative strokes or ipsilateral strokes within 4 years, or death during procedure). Patients assigned to the surgical arm experienced more perioperative myocardial infarctions compared to the stenting group; however, the difference was not statistically significant (6.8% vs or 7.2% HR for stenting is 1.1 CI 0.81–1.51 P value 0.51) whereas patients assigned to the carotid stent arm experienced more periprocedural strokes compared to endarteretomy (6.4% vs 4.7% HR for stenting 1.5 P-0.03). There was no mortality difference and no difference for major (disabling) strokes between surgery and stenting. It was noted that there did seem to exist an age cutoff where below 75 years old endarterectomy provided more positive outcomes and over 75 stenting offered a better risk profile. The CREST trial was not designed for subgroup analysis and thus not powered enough to draw any statistically significant conclusions. A later study published in 2013 evaluated how these perioperative complications affect long-term survival. This study showed that experiencing a stroke within the first year conferred a two-fold lower survival rate (Hazard Ratio(HR) 6.6 [CI 3.7–12]) than those who experienced a perioperative myocardial infarction at two years post intervention (HR 3.6 [CI 2–6.8]). This difference in mortality, however, converges and becomes negligible at 5 years (HR 2.7 [CI 1.7–4.3] vs HR 2.8 [CI 1.8–4.3]). A 2010 study found benefits (reduced strokes) from carotid endarterectomy in those without symptoms who are under 75.
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