Sunday, June 19, 2016

Intracranial Atherosclerosis

What is intracranial artery atherosclerosis?

Intracranial atherosclerosis is deposition of cholesterol and lipids in the wall of the arteries inside the brain. Similar to carotid stenosis in the neck, it is caused by a buildup of plaque in the inner wall of the blood vessels. This narrowing of the blood vessels causes decreased blood flow to the area of the brain that the affected vessels supply. 
There are three ways in which intracranial artery atherosclerosis can result in a stroke:
•       Plaque can grow larger and larger, severely narrowing the artery and reducing blood flow to the brain. Plaque can eventually completely block (occlude) the artery.
•       Plaque can roughen and deform the artery wall, causing blood clots to form and blocking blood flow to the brain.
•       Plaque can rupture and break away, traveling downstream to lodge in a smaller artery and blocking blood flow to the brain.

What are the symptoms?
The symptoms of intracranial artery atherosclerosis are a transient ischemic attack (TIA) or stroke, which can be described with the mnemonic FAST:

F: for facial weakness or droop, especially on one side
A: for arm or leg weakness, tingling, or numbness, especially on one side
S: for slurred speech
T: for time. It is essential to seek immediate medical attention if the above symptoms occur.

Symptoms of a TIA and stroke are similar. TIAs result when blood flow to the brain is temporarily interrupted and then restored. The symptoms typically last a couple of minutes and then resolve completely, and the person returns to normal. However, TIAs should not be ignored; they are a warning that an ischemic stroke and permanent brain injury may be impending.

What are the causes?

Atherosclerosis is a major cause of intracranial artery stenosis. It can begin in early adulthood, but symptoms may not appear for several decades. Some people have rapidly progressing atherosclerosis during their thirties, others during their fifties or sixties. Atherosclerosis begins with damage to the inner wall of the artery caused by high blood pressure, diabetes, smoking, and elevated LDL cholesterol. Other risk factors include obesity, heart disease, family history, and advanced age.

How is a diagnosis made?

Computed Tomography Angiography, or CT angiogram, is a noninvasive X-ray that provides detailed images of anatomical structures within the brain. It involves injecting a contrast agent into the blood stream so that arteries of the brain can be seen. This type of test provides the best pictures of both blood vessels (through angiography) and soft tissues (through CT). It enables doctors to see the narrowed artery and to determine how much it has narrowed.

Magnetic Resonance Angiography (MRA) is similar to the CT angiogram. Contrast dye is injected through an IV to visualize blood vessels in the neck.

Angiogram is a minimally invasive test that uses X-rays and a contrast agent injected into the arteries through a catheter in the groin. It enables doctors to visualize all arteries and veins in the brain. It carries a low risk of permanent neurologic complications. Beyond identifying the area of disease, angiography provides valuable information about the degree of stenosis and shape of the plaque.

Transcranial Doppler Ultrasound is a quick, inexpensive test used to measure the velocity of blood flow through blood vessels in the brain. This technique measures blood flow velocity by emitting a high-pitched sound wave from an ultrasound probe. Different speeds of blood flow appear in different colors on a computer screen. The more sluggish the blood flow, the greater the risk of stroke.

CT or MR Perfusion imaging is a noninvasive test that detects blood flow in the brain and is used in planning surgery. It involves injecting a contrast agent into the bloodstream so that doctors 1) can study how much blood flow is reaching the brain and 2) can determine which areas of the brain are most at risk of stroke.

What treatments are available?

The goal of treatment is to reduce the risk of stroke. Treatment options for intracranial atherosclerosis vary according to the severity of the narrowing and whether you are experiencing stroke-like symptoms or not. Patients are first treated with medication and are encouraged to make lifestyle changes to reduce their risk of stroke. Surgery is limited to patients whose symptoms do not respond to medication.


Blood thinner medications, also called anticoagulants (aspirin, Clopidogrel, Coumadin), allow the blood to pass through the narrowed arteries more easily and prevent clotting. Studies show that aspirin and Coumadin provide similar benefits. Because blood-thinners are associated with an increased risk of bleeding, patients may be monitored for abnormal bleeding. Aspirin has fewer side effects than Coumadin and is associated with a lower risk of bleeding or hemorrhage. Patients taking Coumadin must have their blood monitored periodically; patients taking aspirin and/or Plavix do not require monitoring.

Cholesterol-lowering medications help reduce additional plaque formation in atherosclerosis. These medications can reduce LDL (low-density lipoprotein) cholesterol by an average of 25 to 30% when combined with a low-fat, low-cholesterol diet.

Blood pressure medications (diuretics, ACE inhibitors, angiotensin blockers, beta blockers, calcium channel blockers, etc.) help control and regulate blood pressure. Because high blood pressure is a major risk factor of stroke, regular blood pressure screenings are recommended, along with taking your medication regularly.

Surgery / Endovascular Therapy

The aim of surgery is to prevent stroke by removing or reducing the plaque buildup and enlarging the artery to allow more blood flow to the brain. Surgical treatment is considered for patients whose symptoms do not respond to medication. For example, those who continue to have TIAs or strokes, those with a high grade of stenosis, and those with insufficient blood supply to an area of the brain.

Balloon angioplasty / stenting is a minimally invasive endovascular procedure that compresses the plaque and widens the diameter of the artery. Endovascular means that the procedure is performed inside the artery, from within the bloodstream, with a small flexible catheter. The catheter is inserted into the femoral artery in the groin during an angiogram. The catheter is then advanced through the bloodstream to where the plaque-narrowed artery is located. A small balloon is then slowly inflated within the narrowed artery to dilate it and compress the plaque against the artery wall.

The aim is to reduce stenosis by less than 50%, as a small increase of the vessel diameter results in large increases in blood flow to the brain. The balloon is then deflated and removed. In some cases, a self-expanding mesh-like tube called a stent is placed over the plaque, holding open the artery. Complications from angioplasty can include stroke, tearing of the vessel wall from the catheter or balloon, and vasospasm.

Angioplasty is typically recommended for patients who have high-grade artery stenosis (greater than 70%) and recurrent TIA or stroke symptoms despite medication treatment. Angioplasty / stenting can successful reduce the stenosis to less than 30% without complications in 60 to 80% of patients.

Cerebral artery bypass is a surgical procedure that reroutes the blood supply around the plaque-blocked area. This procedure requires making an opening in the skull, called a craniotomy. A donor artery from the scalp is detached from its normal position on one end, redirected to the inside of the skull, and connected to an artery on the surface of the brain. The scalp artery now supplies blood to the brain and bypasses the blocked vessel (see Cerebral Bypass Surgery). Complications from bypass can include stroke, vasospasm, and clotting in the donor vessel.

Bypass is typically recommended when the artery is 100% blocked and angioplasty is not possible. Results of artery bypass vary widely depending on the location and type of bypass. 

Despite treatment with medications, patients who have had a stroke or TIA due to intracranial artery stenosis face a 12 to 14% risk of recurrent stroke during the 2-year period after the initial stroke. In some high-risk groups, the annual risk of recurrent stroke may exceed 20%.

After angioplasty, restenosis can occur in 7.5 to 32.4% of patients and is usually not symptomatic. The long-term outcome of stroke prevention after angioplasty is not yet known, but short-term results are promising and is currently being studied in clinical trials.
It’s important to understand that atherosclerosis is a progressive disease. 

Lifestyle changes, medications help to prevent progression of the disease and occurrence of stroke. Surgery and Endovascular therapy are required in selected cases to prevent stroke.


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Sunday, June 5, 2016

Management of Asymptomatic Carotid Artery Stenosis


Asymptomatic stenosis of the carotid artery is not an uncommon finding encountered by many doctors in clinical practice.

The common question that comes up is

What is the management of these patients?
Should they undergo carotid revascularization surgery?

Current guidelines recommend revascularization in most patients with severe asymptomatic carotid artery stenosis. However, these guidelines are based on older studies that do not reflect the changing natural history of asymptomatic carotid artery stenosis with current optimal medical management.

Conventional treatment

Current recommendations for revascularization for asymptomatic carotid artery stenosis are predominantly based on two landmark studies performed in the 1990s.

The Asymptomatic Carotid Artery Study (ACAS) was a well-conducted study that assessed carotid endarterectomy (CEA) in asymptomatic carotid artery stenosis (>60%) for stroke prevention. The study was halted because of a projected safety favoring carotid endarterectomy (CEA). The perioperative stroke rate was 2.3%. The five-year projected rate of ipsilateral stroke was 11% for the medical group versus 5.1% for the surgical group.

In the Asymptomatic Carotid Surgery Trial (ACST), the 30-day risk of stroke or death was 3.1%. The five-year rates were 6.4% for CEA and 11.7% for medical therapy arm.

However, medical therapy in these trials was not up to current standards, with only a minority of patients receiving lipid-lowering therapy (Statins) and blood pressure (BP) was also significantly higher than today's standards.

Evolving Natural History of Asymptomatic Carotid Artery Stenosis

Recent evidence suggests that the natural history of asymptomatic carotid artery stenosis has improved remarkably, and the risk-benefit analysis of revascularization will need to be re-evaluated. Current optimal medical management consists of high-dose statin drugs, optimal BP control, smoking cessation, antiplatelet therapy (generally aspirin alone), optimal diabetes control and other lifestyle changes. Hence, the annual risk of stroke with current OMT is likely <1%.

Who is a "High-Risk" Patient?

The reality is that the majority of patients with asymptomatic carotid artery stenosis will never become symptomatic and may undergo unnecessary procedures if these studies do show benefit of endarterectomy or stenting

Clinical Features

There are few clinical predictors of increased stroke risk in asymptomatic carotid artery stenosis. Certain clinical characteristics, such as male sex, current smoking, poorly controlled hypertension, and history of contralateral transient ischemic attack (TIA)/stroke impart a higher risk of future stroke. However these are too non-specific to serve as useful guides for deciding about revascularization.

Stenosis Severity

Patients with 50-69% stenosis had a lower risk compared to those with 70-89% and 90-99% stenosis. However, stenosis severity alone is not a strong enough predictor to be used alone in decision making.

Progression of Stenosis

Progression of stenosis on periodic examination has been shown to impart at least twice the risk of stroke in patients.

Plaque Characteristics

Using ultrasound, atherosclerotic plaques can be characterized based on their surface irregularity, ulcerations, echolucency and gray-scale values. Studies show that patients with predominantly echolucent, lipid-rich plaque have significantly higher stroke risk (3%) than those with mostly echodense, fibrotic plaque (0.8-0.4%). Ulceration on plaque surface detected by three-dimensional ultrasound has also been shown to identify high-risk subjects. Magnetic resonance imaging (MRI) has also been used to detect the presence of intraplaque hemorrhage as indicative of a high-risk plaque. Intraplaque hemorrhage detected by MRI is associated with an increased risk of cerebrovascular events

Silent Emboli Detection

Since both progressive stenosis and high-risk imaging features identify unstable plaque more prone to atheroembolic events, another way to identify patients at risk is to assess for active silent emboli or evidence of prior asymptomatic cerebral emboli using transcranial doppler study. However, most patients with these signals did remain stroke free at three years, and thus, this test lacks the specificity for stand-alone clinical use.

Silent Embolic Infarcts on Computed Tomography (CT) or MRI

Presence of ipsilateral silent embolic infarcts on neuroimaging may be predictive of increased risk of ipsilateral stroke.

 Reduced Cerebrovascular Reserve

In patients with severe ipsilateral carotid stenosis, the presence of an incomplete circle of Willis or presence of intracranial or contralateral occlusive disease can reduce cerebral perfusion pressure. Cerebrovascular reserve in such patients can be assessed using TCD velocity measurements in response to acetazolamide or breathing 5% CO2.


The elderly (especially those over 80 years of age) is a group in which the benefit of revascularization for asymptomatic carotid artery stenosis is most controversial because However, age cannot be an absolute contraindication with increasing life expectancy of the overall population; certainly in carefully selected patients, excellent outcomes after both CEA (Carotid Endarterectomy) and CAS (Carotid Artery Stenting) have been demonstrated. Overall CEA has more favorable outcomes for those over 70 years of age and CAS for those under 70 years of age.

Conclusions and Recommendations for Clinical Practice

Both medical and surgical management arms of asymptomatic carotid artery stenosis are rapidly evolving and will continue to result in decreased stroke risk.

  • We recommend that for asymptomatic carotid artery stenosis patients (even those with >80%) stenosis there is enough evidence for a more conservative approach and decisions regarding revascularization should be made after discussing the stroke risk with the patients.
  • Serial ultrasounds should be performed and revascularization offered to those with >70% stenosis with evidence of progression of stenosis severity.
  • All patients with asymptomatic carotid artery stenosis should be on Optimal Medical Management.
  • For the very elderly (>80 years) and life expectancy less than five years, a conservative approach is most reasonable in most situations.
  • Carotid Endarterectomy remains the gold-standard for revascularization of carotid stenosis. Carotid Artery Stenting should be considered in patients with high risk of surgery from associated cardiac co-morbidity.
  • Individual patient and anatomic risks for CEA and CAS are different and should be considered and a multi-specialty approach should be followed.