Occlusive Cerebrovascular Disease

Introduction
Every year, half a million people in the United States suffer a stroke. Fifteen to 30 percent of these episodes are fatal, making stroke the third leading cause of death in this country. Carotid artery stenosis is responsible for as many as 25% of these strokes in the elderly. Most neurologic events are caused by emboli occluding small cerebral arteries. Emboli from the carotid bifurcation may consist of platelet aggregates that form on irregular or ulcerated surfaces or plaque debris liberated by turbulent flow and intraplaque hemorrhage. Less commonly (fewer than 10% of cases), emboli arise from the heart (eg, mural thrombus or atrial myxoma) or from the aortic arch. Stroke can also be caused by intracerebral hemorrhage (from trauma or a ruptured cerebral aneurysm) or by small vessel occlusive disease in the pons, basal ganglia, and internal capsule of the brain (lacunar infarcts).

A transient ischemic attack (TIA) is defined as the sudden onset of a neurologic deficit that resolves completely within 24 hours. A stroke is a neurologic deficit that persists beyond 24 hours. A single TIA or stroke is associated with a 30% risk of subsequent stroke.

Risk factors for carotid disease include hypertension, diabetes mellitus, hypercholesterolemia, advanced age, smoking, and coronary artery disease.

Clinical Findings
A. Symptoms and Signs

Clinical manifestations of carotid artery occlusive disease include contralateral weakness or sensory loss, expressive aphasia, and amaurosis fugax (transient partial or complete loss of vision in the ipsilateral eye). Vertebrobasilar TIAs are characterized by brain stem and cerebellar symptoms, including dysarthria, diplopia, vertigo, ataxia, and hemiparesis or quadriparesis.

Dizziness and unsteadiness, particularly when associated with a quick change in position, are nonspecific symptoms and more often the result of postural hypotension than of vertebrobasilar insufficiency. Syncope is rarely a manifestation of carotid artery occlusive disease. Rather, it is usually a result of a cardiac arrhythmia.

Occlusive disease of the brachiocephalic arteries may be accompanied by cervical bruits, diminished or absent pulses in the neck or arms, Hollenhorst plaques (bright, refractile cholesterol emboli) in the retinal arteries, or a blood pressure difference between the two arms of more than 10 mm Hg. The common carotid pulsation can be examined qualitatively by palpation at the base of the neck. The presence of superficial temporal artery pulsation confirms patency of the ipsilateral external carotid artery. A carotid bruit is a high-pitched, blowing noise localized in the mid neck close to the angle of the mandible. Heart sounds must be auscultated to make certain that the bruit is not caused by a referred murmur of aortic stenosis. Only 30% of patients with cervical bruits have carotid stenosis greater than 60%. The absence of a bruit also does not preclude the possibility of a hemodynamically significant lesion -  thus, bruits are neither sensitive nor specific for carotid occlusive disease. In fact, asymptomatic carotid bruits are stronger predictors of death from coronary artery disease than of death from stroke.

B. Imaging Studies
Duplex ultrasonography has become the study of choice for evaluation of carotid occlusive disease. It provides both physiologic and anatomic information. Percent stenosis is derived from measurement of blood flow velocities, with sensitivity and specificity greater than 90%. Ultrasound also provides some characterization of the plaque itself, including its location and the presence of calcification, ulceration, and intraplaque hemorrhage. Patients with adequate ultrasound studies may be offered surgery without further imaging. Patients with suboptimal ultrasound studies or in whom intracranial tandem lesions may be suspected are referred for gadolinium-enhanced MRA, which provides more detailed information about plaque composition and characterizes the intracranial circulation and the brain parenchyma. When compared with en bloc resected specimens, correlation of percent stenosis is better with ultrasound and MRA than with conventional angiography. This can be explained by the fact that MRA and ultrasound both produce cross-sectional imaging of vessels whose stenotic regions may be eccentric. Symptomatic patients with ipsilateral carotid occlusion by ultrasound should be referred for conventional or CT angiography before electing nonoperative management because a small percentage of these patients will have an internal carotid artery “string sign” and should be revascularized. Catheter angiography carries a 1% risk of procedure-related stroke and is reserved for patients with greatly disparate ultrasound and MRA findings, those suspected of vertebrobasilar insufficiency or intracranial lesions unable to undergo MRA, and those potentially requiring endovascular intervention. As ultrasound is highly operator dependent, whereas MRA is highly equipment dependent; selection of the most accurate imaging modality may vary by institution.

Treatment

A. Medical Measures
Acute or evolving strokes and strokes associated with major neurologic deficits are initially managed medically, delaying surgery for 5-8 weeks until the deficit is stabl. Patients with transient ischemic attacks may be treated initially with an oral antiplatelet medication (aspirin, 81 mg daily, or clopidogrel, 75 mg daily) to reduce the likelihood of thrombosis and microemboli and then scheduled for elective surgery. However, if the attacks are of increasing frequency, the patient is admitted and placed on a heparin drip while being evaluated for surgery. Postoperatively, most patients are maintained on aspirin indefinitely to reduce the incidence of thrombosis or recurrent disease in the newly endarterectomized vessel.

For patients in whom neurologic symptoms are thought to be secondary to intracerebral disease not amenable to surgical reconstruction, warfarin or clopidogrel may be indicated.

B. Surgery
1. Transient ischemic attacks and stroke

Carotid endarterectomy plus optimal drug therapy and risk factor modification are highly effective in preventing stroke and death in symptomatic patients with carotid stenosis greater than 70%  -  as demonstrated by the North American Symptomatic Carotid Endarterectomy Trial (NASCET). A more modest risk-benefit ratio has been demonstrated for carotid endarterectomy in symptomatic 50-69% stenoses. Surgical success is maximized when preoperative symptoms are related to ischemia of the ipsilateral hemisphere and when the surgery is done by a vascular surgeon who performs carotid endarterectomies regularly with a mortality-complication rate less than 5%. Placement of a temporary carotid shunt during surgery may be necessary to allow cerebral perfusion during cross-clamping. Indications for intraoperative shunting vary by surgeon. Most surgeons shunt patients with previous stroke; some selectively shunt for a measured stump pressure (internal carotid back pressure) under 50 mm Hg or for patients with EEG changes, and others shunt all patients.

2. Asymptomatic carotid stenosis
Patients with asymptomatic carotid stenosis greater than 80% have a 12% risk of stroke. This statistic helps form the basis for the American Heart Association’s recommendation of upper limits of acceptable combined morbidity and mortality for carotid endarterectomy: 3% for asymptomatic patients, 5-7% for those with TIAs or stroke, and 10% for those with recurrent carotid stenosis. The Asymptomatic Carotid Artery Stenosis (ACAS) trial demonstrated that in good-risk asymptomatic patients with greater than 60% stenosis, surgery afforded an overall relative risk reduction of 53% over aspirin alone. These findings are supported by a smaller Veterans Administration Hospital study of patients with asymptomatic carotid artery stenosis. Most vascular surgeons offer surgery to good-risk asymptomatic patients with greater than 80% stenosis in the ipsilateral carotid artery.

3. Percutaneous techniques
Patients who are not good candidates for surgery because of medical comorbidities can be considered for carotid angioplasty and stenting. This is also an option in patients with a history of previous neck surgery or irradiation, in whom there is a higher risk of cranial nerve injury because of fibrosis and scarring. Carotid stenting is associated with a 2-18% risk of periprocedural stroke or transient ischemic attack and an 8-14% per year incidence of recurrent stenosis (compared with less than 4% per year with surgery).

Prognosis
Carotid endarterectomy carries a reported average 1-2% mortality rate and a 1-5% risk of neurologic complication, though institutional variation exists. In symptomatic patients, endarterectomy reduces stroke risk fivefold to tenfold at 5 years. The 5-15% incidence of late stroke after uncomplicated endarterectomy is often related to contralateral carotid or intracranial disease.

Restenosis occurring less than 2 years after carotid endarterectomy is usually not symptomatic because it is due to intimal hyperplasia, which produces a smooth, nonfriable luminal surface. These lesions respond well to angioplasty and stenting, and the risk of procedural neurologic events is lower than for atherosclerotic lesions. Such lesions may regress and intervention is reserved for stenoses of 80% or greater. After 2 years, restenosis is more often related to progression of atherosclerotic disease. These lesions can be friable and prone to intraplaque hemorrhage, just like the original plaque. In general, repeat surgery or stenting is advised for symptomatic restenoses or stenoses greater than 80%.

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Provided by ArmMed Media
Revision date: July 7, 2011
Last revised: by Dave R. Roger, M.D.