Carotid or Vertebral Artery Occlusive Disease
Carotid or vertebral artery disease may be asymptomatic or symptomatic. Factors that are associated with an increased risk for ischemic stroke related to carotid or vertebral artery occlusive disease include age, cigarette smoking, hypertension, ischemic heart disease, diabetes, and hyperlipidemia.
ASYMPTOMATIC CAROTID ARTERY DISEASE
Carotid bruit occurs in 4% to 5% of the population aged 45 to 80 years. However, a carotid bruit is merely a reflection of turbulence in the artery and a relatively poor predictor of underlying internal carotid stenosis in asymptomatic patients. Bruits are noted in approximately 40% of patients with 50% or more linear carotid stenosis (≥75% cross-sectional area stenosis) and 10% of those with less than 50% linear stenosis. Patients who have carotid bruit and have asymptomatic pressure-significant occlusive lesions of the carotid system (high-grade asymptomatic carotid stenoses diagnosed on carotid ultrasonography) are at greater risk for stroke than patients who have bruit and normal carotid ultrasonography (twofold) and the general population (sevenfold).
Various characteristics of bruits, including location, loudness, and pitch, are relatively poor predictors of the underlying stenosis. Bruits with a diastolic component in addition to the usual systolic component generally have an associated underlying high-grade stenosis. An ocular bruit is a relatively good predictor of some degree of underlying internal carotid artery siphon stenosis, although the stenosis may not be severe.
Patients with asymptomatic carotid bruits are at greater risk than the general population for all forms of atherosclerotic vascular disease. The risk for myocardial infarction (MI) is also increased (˜2.5 times) in patients with asymptomatic carotid bruit, and MI is the leading cause of death. However, these patients are at far less risk for ischemic stroke than are patients with symptomatic bruits or stenoses (see below). The risk for stroke in elderly individuals with asymptomatic carotid bruit is relatively small, but it increases significantly in patients of all ages when associated with hypertension.
Asymptomatic carotid artery stenosis (ACAS) is usually defined as a 50% narrowing of the carotid artery or more in the absence of retinal or cerebral ischemia. In the general population, the prevalence of high-grade asymptomatic CAS (≥70%) ranges from 0% to 3.1%, and the annual stroke rate in these patients ranges from 0.5% to 3%, with contemporary medical management including use of statins leading to stroke rates at the low end of this range. The degree of stenosis in the carotid artery is a good predictor of stroke risk. In one study of asymptomatic patients, Doppler ultrasonographic evidence of more than 75% stenosis was associated with a 5.5% (during a
mean of 28 months) annual risk for stroke. The range of stroke risk that was reported for patients with asymptomatic high-grade (≥75% cross-sectional stenosis) carotid stenosis was 2% to 5.5% during the first year, but the risk after the first year decreased, particularly if the stenosis was stable. Stroke risk depends on the percentage of stenosis, progression of stenosis between noninvasive examinations, and the presence or absence of ulceration. In the Asymptomatic Carotid Atherosclerosis Study (ACAS), the stroke risk among asymptomatic patients with 60% or more carotid stenosis was 11% during a mean of approximately 5 years; these patients were treated with aspirin and correction of risk factors. Similar findings were noted in the Asymptomatic Carotid Stenosis Trial (ACST), in which the 5-year stroke risk was 11.8% in the medically treated group, in patients with at least a 60% carotid stenosis. At 10 years, the stroke risk in the medical group (excluding perioperative events) was 16.9%.
mean of 28 months) annual risk for stroke. The range of stroke risk that was reported for patients with asymptomatic high-grade (≥75% cross-sectional stenosis) carotid stenosis was 2% to 5.5% during the first year, but the risk after the first year decreased, particularly if the stenosis was stable. Stroke risk depends on the percentage of stenosis, progression of stenosis between noninvasive examinations, and the presence or absence of ulceration. In the Asymptomatic Carotid Atherosclerosis Study (ACAS), the stroke risk among asymptomatic patients with 60% or more carotid stenosis was 11% during a mean of approximately 5 years; these patients were treated with aspirin and correction of risk factors. Similar findings were noted in the Asymptomatic Carotid Stenosis Trial (ACST), in which the 5-year stroke risk was 11.8% in the medically treated group, in patients with at least a 60% carotid stenosis. At 10 years, the stroke risk in the medical group (excluding perioperative events) was 16.9%.
The presence of ulceration seems to increase the risk for subsequent stroke, depending on the size and the extent of the ulceration. However, these lesions are difficult to define in many cases, even with conventional arteriography. When ulcers are identified on conventional cut-film arteriography, their size can be defined by multiplying the length and the width of the ulcer in millimeters. The presence of small “A” ulcers (<10 mm2) is not associated with an increased risk for stroke, but the presence of “B” ulcers (10-40 mm2) or “C” ulcers (>40 mm2) has been associated with stroke rates of 4.5% and 7.5% per year, respectively (in “C” ulcers, the rate of stroke may be somewhat independent of the associated carotid stenosis). Other plaque characteristics defined on MRI may also predict a higher risk of future stroke, including the presence of lipid-rich necrotic core, intraplaque hemorrhage, and thinning and rupture of a fibrous cap. Some data also suggest that patients with two or more microemboli per hour of transcranial Doppler monitoring may have a higher risk of future stroke. Stroke risk in such patients is approximately 15%, compared to 1% in those without microemboli detection. Data from ACAS indicate that there may be a select group of otherwise relatively healthy patients with 60% or more carotid stenosis (diameter reduction) who have a lower risk for ipsilateral stroke and death with carotid endarterectomy (CEA) than do patients who are treated with aspirin and reduction of risk factors, when CEA is performed with less than 3% surgical morbidity and mortality. The risk for any stroke or death within 30 days postoperatively or any ipsilateral stroke or death after 30 days was 5.1% for surgical patients and 11.0% for those who were treated medically for 5 years. The resultant 66% relative risk reduction in men was statistically significant, but was not so in women (17%). Perioperative morbidity and mortality were higher in women and contributed to the lack of clear benefit in them. With respect to overall stroke rates and ipsilateral major stroke and death, the difference between the groups that had surgery and the groups that did not have surgery was not statistically significant, although there was a trend favoring surgery. In another large, randomized trial, ACST, CEA was compared with conservative management in patients with more than 60% carotid stenosis. The 5-year stroke risk was 6.4% in the CEA group, compared with 11.8% in the medically treated group. Fatal or disabling stroke was also reduced by surgery, with the 5-year risk of 3.5% in the CEA cohort and 6.1% in those who were treated medically (p = 0.004). Women and men both were benefited by CEA.