Asymptomatic Carotid Stenosis: Medical Management or Revascularization?

Increasingly, primary care physicians encounter patients with no history of stroke or transient ischemic attack who have high-grade stenosis on carotid ultrasound. No guidelines endorse carotid screening in patients without cerebrovascular symptoms, yet these patients are identified in various ways: Some cardiologists and vascular surgeons routinely get carotid studies in patients with coronary disease, some clinicians order ultrasound for patients with asymptomatic carotid bruits, some clinicians inappropriately include routine carotid ultrasound in their “syncope work-up,” and some ultrasound screening companies offer direct-to-consumer carotid studies. Because many of these patients end up with surgery or stenting, a brief look at current thinking on asymptomatic carotid stenosis (ACS) is warranted.

Carotid endarterectomy (CEA) was compared with medical therapy in ACS patients in two large randomized trials — a North American study published in 1995 (JW Gen Med May 16 1995)1 and a European trial published in 2004 (JW Gen Med May 21 2004).2 In both trials, the 5-year risk for stroke (including perioperative stroke or death) was significantly lower with CEA than with medical therapy, but the difference was only about 5 percentage points (5%–6% vs. 11%–12%), and no benefit was seen in women.3 Given the 2%–3% rate of perioperative stroke or death, it took several years for the benefit of CEA to clearly surpass that of medical therapy.

Because medical therapy has improved since these trials were conducted, researchers have examined whether stroke rates in patients with ACS have declined during the past decade. In fact, rates have fallen to around 1% annually in medically treated patients.4^,5 Thus, we must ask whether CEA has any role in patients with ACS. Recently, researchers have proposed several imaging findings that might identify high-risk subgroups — plaque echolucency, plaque ulceration, and embolic signals on transcranial Doppler ultrasound of the ipsilateral middle cerebral artery.

In one study of 435 patients with ACS (>70% stenosis by ultrasound), only 10 patients (2%) had strokes during average follow-up of 2 years.6 However, four of these strokes occurred among the 27 patients with both echolucent plaque and embolic signals (15% stroke rate). In contrast, only 1.5% of patients without these two findings had strokes.

In another study of 253 patients with ACS (>60% stenosis by ultrasound), only 6 patients (2.4%) had strokes during average follow-up of 3 years.7 Three of these strokes occurred in the 42 patients with at least two carotid ulcerations (7%); in contrast, the stroke rate was only 1.4% in the 211 patients with one or no ulcers. Additionally, the stroke rate was 13% in patients with embolic signals (2 of 15 patients), but only 1.7% in those without embolic signals (4 of 238 patients).

The most striking aspect of these two studies is their confirmation of a very low overall incidence of stroke — about 1% annually. Thus, many asymptomatic patients who now undergo CEA (or carotid stenting, which is not safer than CEA) are likely risking harm without commensurate benefit. Use of embolic signals and plaque characteristics to identify candidates for CEA is promising but requires larger studies and assurance that the techniques are reliable in community settings. Editorialists “argue for intensified medical management rather than revascularization procedures in patients with ACS,” until strategies to identify high-risk patients have been thoroughly investigated.8 Their position is compelling.