Who Really Needs Carotid Artery Surgery or Stenting? A Guide to Identifying High-Risk Patients with Asymptomatic Carotid Stenosis

Table of Contents

• Key Points
• Background: Why This Question Matters
• Two Opposing Views — and Why Both Are Wrong
• How This Review Was Carried Out
• Marker 1: Microemboli Detected on Transcranial Doppler
• Marker 2: Plaque Echolucency on Duplex Ultrasound
• Marker 3: Progression in the Severity of the Narrowing
• Marker 4: Silent Embolic Infarcts on Brain CT or MRI
• Marker 5: Reduced Cerebrovascular Reserve
• Marker 6: Size of the Juxtaluminal Hypoechoic Area
• Marker 7: Intraplaque Haemorrhage on MRI
• Marker 8: Carotid Ulceration
• What the 2017 European Guidelines Say
• How Many Asymptomatic Patients Could Benefit?
• What This Means for Patients
• Limitations of the Evidence
• Practical Recommendations
• Frequently Asked Questions
• Source Information

Key Points

• Only about 10% to 15% of patients with asymptomatic carotid stenosis might benefit from surgery or stenting; the large majority, around 85% to 90%, are better served by medical therapy alone.
• Treatment should be guided by evidence that a specific patient carries a high risk of stroke on the same side as the narrowed artery. Treatment should not be guided by the percentage of narrowing alone.
• Microemboli detected on transcranial Doppler is the most validated marker; in one study, more than 2 per hour meant a 15.6% versus 1.0% one-year same-sided stroke rate.
• Progression of narrowing over time was one of the clearest danger signals, raising 8-year stroke rates from 9% to 16% in the ACSRS study.
• All patients with asymptomatic carotid stenosis should receive medical treatment; intervention is an addition to it, not a replacement.

Background: Why This Question Matters

Stroke is one of the most common and most feared medical events. In the United States alone, there are almost 800,000 strokes each year. About 610,000 of these are first strokes, and strokes cause roughly 140,000 deaths annually. In the United Kingdom, more than 100,000 people have a stroke each year, and in 2015 alone more than 40,000 people in the UK died of stroke.

The wider picture is just as striking. Stroke causes twice as many deaths each year in women as breast cancer, and twice as many deaths each year in men as prostate and testicular cancer combined. Worldwide, stroke is the second most common cause of death, killing around 6.7 million people each year — that is one death every 5 seconds.

Not all strokes are the same. About 85% are ischaemic (caused by a blocked blood vessel) and 15% are haemorrhagic (caused by bleeding). Clots that travel from a narrowed carotid artery on the same side — an ipsilateral (same-sided) asymptomatic carotid stenosis (ACS) — cause a substantial share of first-ever ischaemic strokes. That is why doctors have long searched for a way to identify which of these narrowed arteries are dangerous and which are not.

Two Opposing Views — and Why Both Are Wrong

Three landmark randomised controlled trials (studies in which patients are randomly assigned to different treatments) found that carotid endarterectomy (CEA — surgery to clear the narrowed artery) produced a 50% relative reduction in the risk of stroke over 5 years compared with best medical treatment (BMT) alone. On the strength of those results, offering CEA routinely to patients with ACS became the treatment of choice in the 1980s and 1990s.

Then the picture changed. In the early and mid-2000s, improvements in BMT caused the annual stroke rate among ACS patients to fall significantly. These improvements included better smoking cessation strategies and widespread use of statins and other measures. Routine surgery for everyone no longer looked like the best option.

Unfortunately, a second view then took hold: that BMT alone is the treatment of choice for every patient with ACS, and that no patient should ever be offered preventive CEA or carotid artery stenting (CAS — placing a mesh tube to hold the artery open). The authors argue that this position is just as mistaken as the old one.

Their key point is that this "BMT-only for everyone" theory is not based on level I evidence (the strongest grade of proof, from randomised trials). It is an extrapolation — an assumption carried across from improved results seen in observational studies and meta-analyses (statistical pooling of many studies). In other words, it has never been properly tested in the group it is being applied to.

How This Review Was Carried Out

This is a review article, not a new clinical trial. The authors gathered and summarised the available published evidence on methods that predict future stroke in people with asymptomatic carotid stenosis.

They assessed each proposed predictor and graded the strength of the supporting evidence — noting that some predictors rest on adequate, robust data while others rest on weaker evidence. They also drew on the 2017 European Society for Vascular Surgery (ESVS) carotid guidelines, which reviewed the same question. The article reviews eight candidate markers and finishes by estimating how many ACS patients might realistically benefit from an intervention.

Marker 1: Microemboli Detected on Transcranial Doppler

This is the best-validated method available. Transcranial Doppler (TCD) is an ultrasound technique that beams sound through the skull to listen to blood flow in the brain's arteries. When tiny clots or plaque fragments — called microemboli — pass through, the machine registers a high-intensity signal and the operator hears a characteristic clicking sound.

Spence and colleagues first reported that patients with ACS who had more than 2 microemboli per hour on TCD had a more than 1500% increased risk of an ischaemic stroke on the same side within one year. In plain terms, that is 16 times the risk. The actual stroke rates were 15.6% versus 1.0% — about 1 in 6 patients versus 1 in 100. This difference was highly statistically significant (p<0.0001), meaning there is less than a 1 in 10,000 chance it happened by random chance.

In 2010, the same research group reported results from 468 patients with ACS. Thanks to improvements in BMT, both the number of TCD-detected microemboli and the number of cardiovascular events fell sharply:

• TCD-detected microemboli: 12.6% before 2003 versus 3.7% after 2003 (p<0.001)
• Cardiovascular events: 17.6% before 2003 versus 5.2% after 2003 (p<0.001)

A few months later, these findings were confirmed by an independent international multicentre study — the Asymptomatic Carotid Emboli Study (ACES) — which followed 467 patients with ACS. As in the earlier work, each participant had two 1-hour TCD recordings taken 1 week apart. Patients with one or more TCD emboli had a more than 550% higher risk of stroke on the same side within one year compared with patients without emboli (hazard ratio [HR] 5.57; 95% confidence interval [CI] 1.61 to 19.32; p=0.007). A hazard ratio compares the risk of an event between two groups over time.

One early study did not find this link. However, the study was underpowered, meaning it was too small to detect a real difference, with only 202 patients. The study counted a single microembolus as a positive result. The study also repeated the test at 6-monthly intervals. There is now compelling evidence that at least two embolic signals during a 1-hour recording identifies patients with ACS at very high risk of stroke — pointing to a high-risk, unstable plaque or a plaque with a clot sitting on its surface.

A meta-analysis of five prospective studies (n=677 patients) confirmed that TCD-detected embolic signals in ACS patients significantly predicted stroke on the same side (odds ratio [OR] 7.46; 95% CI 2.24 to 24.89; p=0.001). An odds ratio of 7.46 means the odds of stroke were roughly 7.5 times higher in people with embolic signals.

Marker 2: Plaque Echolucency on Duplex Ultrasound

Duplex ultrasound is the standard scan used to measure carotid narrowing. On the image, some plaques look dark or "black" (echolucent) and some look bright (echogenic). Studies from the 1990s showed that echolucent plaques correspond to a lipid-rich necrotic core, a soft, fatty, dead core inside the plaque. Echolucent plaques also correspond to intraplaque haemorrhage, which is bleeding inside the plaque. These are found more often in patients who already have symptoms than in those who do not.

Multiple studies have since asked whether echolucency predicts future stroke in ACS patients. Most found a strong association. The one exception was a study from Denmark, which found echolucency predicted stroke in symptomatic patients but not in asymptomatic ones.

The individual studies, with their relative risks (RR — how many times more likely an event is in one group versus another), were:

• O'Holleran et al (1987): 293 patients, 46 months' follow-up, RR 5.12 (2.01 to 13.04)
• Polak et al (1998): 4,886 patients, 39.6 months, RR 1.96 (1.25 to 2.90)
• Mathiesen et al (2001): 177 patients, 36 months, RR 3.85 (0.46 to 32.28)
• Grønholdt et al (2001): 111 patients, 52.8 months, RR 0.87 (0.34 to 2.23)
• Nicolaides et al (2005): 1,092 patients, 37.1 months, RR 2.23 (1.28 to 3.87)
• Topakian et al (2011): 435 patients, 21.8 months, RR 6.61 (1.42 to 30.75)
• Silvestrini et al (2013): 621 patients, median 27 months, RR 2.37 (1.14 to 4.92)
• Huibers et al (2016): 814 patients, 60 months, RR 2.52 (1.20 to 5.25)

A recent meta-analysis pooled 7,557 patients with a mean follow-up of 37.2 months. It found a clear positive association between plaque echolucency and future stroke on the same side: RR 2.31 (95% CI 1.58 to 3.39; p<0.001). Of the total sample, 1,741 patients (23.0%) tested positive for echolucency and 5,816 (77.0%) tested negative. There were 100 strokes in the echolucent-positive group and 141 strokes in the negative group, giving a cumulative stroke incidence of 5.7% versus 2.4%. Among patients with at least 50% narrowing, the risk was even higher (RR 2.61; 95% CI 1.47 to 4.63; p=0.001). A second, independent meta-analysis confirmed the same link.

Combining markers makes prediction even stronger. In ACES, plaque echolucency alone was linked to a more than 600% higher risk of same-sided stroke (HR 6.43; 95% CI 1.36 to 30.44; p=0.019). But when echolucency was combined with TCD-detected emboli, the risk rose to a more than 1000% increase (HR 10.61; 95% CI 2.98 to 37.82; p=0.0003).

Marker 3: Progression in the Severity of the Narrowing

Most experts agree that if the narrowing gets worse on repeated ultrasound scans — despite the patient being on best medical treatment — that is a bad sign. Up to half of patients with ACS may have "resistant atherosclerosis" (plaque that keeps growing despite good treatment), which helps explain why progression happens.

The largest prospective study of ACS patients treated with medical therapy alone is the Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) study. It showed that over 8 years, the cumulative rate of ischaemic stroke on the same side was:

• 0% if the narrowing regressed (got better)
• 9% if the narrowing stayed the same
• 16% if the narrowing progressed

Among patients whose narrowing stayed the same, the 8-year stroke rates by starting severity were 4% for 50%–69% stenosis, 8% for 70%–89%, and 13% for 90%–99%. When the narrowing progressed, those rates rose to 8%, 15% and 25% respectively. In other words, progression roughly doubled the risk at every level of severity.

An independent study from Boston, Massachusetts confirmed this. It followed 794 patients (900 carotid arteries) with moderate 50%–69% ACS for a mean of 3.6 years (range 0.3 to 6.7 years). Despite BMT, the narrowing progressed in 262 of 900 arteries (29.1%), and 36 of those (13.7%) developed symptoms. Symptomatic conversion was significantly more common with progression than without it — 13.7% versus 8.5%; p=0.02. Overall, BMT failed to prevent either disease progression or the development of same-sided neurological symptoms in a substantial share of patients.

An earlier study of 1,065 patients with ACS, monitored by carotid ultrasound, painted a similar picture. During an initial median period of 7.5 months (range 6 to 9 months), the carotid lesions progressed in 93 of 1,065 patients (9%). Over a median follow-up of 3.2 years (interquartile range 2.9 to 3.5), there were 495 major adverse cardiovascular events — a combined measure of heart attack, coronary angioplasty, coronary bypass surgery, stroke, peripheral angioplasty, peripheral vascular surgery, amputation for critical limb ischaemia, and death from any cause — in 421 patients (40%).

Patients whose narrowing progressed had a considerably worse outlook:

• 200% higher risk of the combined cardiovascular outcome (adjusted HR 2.01; 95% CI 1.48 to 2.67; p<0.001)
• More than 200% higher risk of heart attack (HR 2.38; 95% CI 1.07 to 5.35; p=0.044)
• 200% higher risk of stroke (adjusted HR 2.0; 95% CI 1.02 to 4.11; p=0.035)
• 175% higher risk of cardiovascular death (adjusted HR 1.75; 95% CI 1.03 to 2.97; p=0.039)

Plaque burden may matter more than the percentage of narrowing. A Canadian study compared three measurements as predictors of cardiovascular events in 349 patients attending stroke prevention clinics. The three measurements were carotid intima-media thickness (cIMT, the thickness of the artery wall's inner layers), total plaque area, and total plaque volume. After a median follow-up of 3.17 years (range 0.07 to 5.0), there were 50 first events: 20 vascular deaths, 11 strokes, 13 transient ischaemic attacks (TIAs — "mini-strokes" that resolve) and 6 heart attacks.

Progression of total plaque volume predicted stroke, death or TIA (p=0.001), stroke, death or heart attack (p=0.008), and stroke, death, TIA or heart attack (p=0.001). Progression of total plaque area only weakly predicted stroke, TIA or death (p=0.097), and did not predict stroke, death or heart attack (p=0.59) or the combined outcome (p=0.143). Change in cIMT predicted neither (p=0.13 and p=0.455 respectively). Using Cox regression analysis — a statistical method that adjusts for other factors — total plaque volume progression remained a significant predictor of events even after accounting for coronary risk factors (p=0.001).

The High Risk Plaque BioImage study added that plaque burden correlated strongly with coronary calcium, a marker of heart artery disease, whereas cIMT did not. Plaque burden was as predictive of events as coronary calcium. In ACS patients specifically, plaque burden — not the percentage of narrowing — predicted stroke risk.

Marker 4: Silent Embolic Infarcts on Brain CT or MRI

Not every stroke causes obvious symptoms. Small areas of brain damage — silent embolic infarcts — can be seen on brain CT (computed tomography) or MRI (magnetic resonance imaging) scans without the patient ever noticing anything. Both the Cardiovascular Health Study and the Rotterdam Scan Study showed that these silent infarcts are linked to a higher stroke risk in the general population.

Two studies, ACSRS and an independent study from Japan, showed that silent embolic infarcts independently predict stroke in ACS patients. In ACSRS, patients with 60%–99% narrowing who had silent infarcts on brain CT had a 300% higher risk of future same-sided stroke compared with those without them. The annual stroke rates were 3.6% versus 1.0% (HR 3.0; 95% CI 1.46 to 6.29; p=0.002).

These results suggest that silent infarcts on brain CT or MRI reliably identify ACS patients at high risk of a future same-sided cerebrovascular event. There is one important caveat: brain CT scans may miss up to 40% of brain infarcts in ACS patients, so MRI is the more sensitive option.

Marker 5: Reduced Cerebrovascular Reserve

As the carotid artery narrows, the pressure pushing blood into the brain drops. The brain's small arteries respond by dilating as much as they can to keep blood flow steady — a self-regulating process called autoregulation. If the pressure falls further, for example during a drop in blood pressure, blood flow can no longer be maintained, and stroke risk rises. Cerebrovascular reserve (CVR) is a measure of how much extra blood flow the brain can call upon.

Normal CVR values range from as low as 15% up to 40%. Values below 10% indicate impaired CVR. Several studies have linked impaired CVR to stroke in ACS patients:

• Gur et al (1996): 44 patients, 21 of 44 with impaired CVR, 24 months' follow-up, OR 22.50 (1.44 to 1054.40)
• Silvestrini et al (2000): 94 patients, 40 of 94 impaired, 28.5 months, OR 3.72 (1.05 to 14.85)
• Markus and Cullinane (2001): 107 patients, 21.7 months, OR 14.4 (2.63 to 78.74)
• Kimiagar et al (2010): 35 patients, 21 of 35 impaired, 48 months, OR 6.50 (0.65 to 315.02)
• King et al (2011): 106 patients, 32 of 106 impaired, 22.7 months, OR 3.62 (0.61 to 21.74)

A meta-analysis of 13 studies (991 patients; mean follow-up 32.7 months) found that impaired CVR was associated with an almost 400% higher stroke risk in asymptomatic patients (random effects OR 3.96; 95% CI 2.60 to 6.04).

The authors note two limitations of that meta-analysis. In most of the included studies, the investigators assessing outcomes were not blinded to the CVR results (they knew which patients had impaired flow, which can introduce bias). Also, the definitions of study endpoints (stroke or TIA) and of asymptomatic versus symptomatic disease varied between studies. Even so, the authors concluded that the link between impaired CVR and stroke or TIA risk is robust. Reduced CVR may therefore help identify high-risk ACS patients.

Marker 6: Size of the Juxtaluminal Hypoechoic Area

In unstable plaques that are causing symptoms, the necrotic core sits twice as close to the inner channel of the artery (the lumen) compared with asymptomatic plaques. Studies using ultrasound have shown a link between the juxtaluminal hypoechoic area — the dark "black" zone right next to the lumen — and the presence of neurological symptoms.

ACSRS tested whether the presence and size of this black area, when there is no visible bright cap over it, predicts future same-sided ischaemic stroke in ACS patients. Over 5 years, the rate of ischaemic events in the eye or brain on the same side was:

• 3% when the juxtaluminal black area was smaller than 4 mm² (average annual rate 0.6%)
• 21% when it was 4 to 8 mm² (average annual rate 4.2%)
• 36% when it was 8 to 10 mm² (average annual rate 7.2%)
• 43% when it was larger than 10 mm² (average annual rate 8.6%)

These results support the idea that the size of the juxtaluminal hypoechoic area can predict future same-sided ischaemic stroke.

Marker 7: Intraplaque Haemorrhage on MRI

MRI can reveal what is inside a plaque, not just how narrow the artery is. Several studies have tested whether specific plaque components seen on MRI predict stroke in ACS patients. Some studies blinded the MRI readers to patient outcomes, while others did not. The majority found that plaques containing intraplaque haemorrhage (IPH — bleeding inside the plaque) were significantly more likely to cause same-sided ischaemic events. Plaques containing a lipid-rich necrotic core (LRNC — a soft fatty dead core) were also significantly more likely to cause same-sided ischaemic events. Plaques with thinning or rupture of the fibrous cap (TRFC — the protective covering of the plaque) were also significantly more likely to cause same-sided ischaemic events. This increased risk held across a wide range of narrowing severity.

The individual MRI studies reported:

• Takaya et al (2006): 154 patients, 38.2 months — IPH HR 5.2 (1.6 to 7.3); TRFC 2.2 to 132.0; LRNC 0.6 to 33.7
• Singh et al (2009): 98 patients, 24.9 months — IPH 2.48 to 4.71
• Sadat et al (2010): 61 patients, 16.9 months — IPH 1.27 to 26.77; TRFC 7.39 (1.61 to 33.82); LRNC 1.75 (0.55 to 5.54)
• Mono et al (2012): 65 patients, 18.9 months — IPH 0.03 (0.00 to 86.62); TRFC 1.103 (0.11 to 10.70); LRNC 7.2 (1.12 to 46.28)
• Kwee et al (2013): 126 patients, 12.0 months — IPH 3.5 (1.06 to 11.96); TRFC 5.8 (1.91 to 17.32); LRNC 3.2 (1.08 to 9.50)
• Hosseini et al (2013): 179 patients, 17.5 months — IPH 12 (4.8 to 30.1)

A meta-analysis of 9 studies (779 patients) confirmed the value of these features. The hazard ratios for predicting later stroke or TIA were 4.59 (2.91–7.24) for intraplaque haemorrhage, 3.00 (1.51–5.95) for lipid-rich necrotic core, and 5.93 (2.65–13.20) for thinning or rupture of the fibrous cap.

The meta-analysis concluded that MRI characterisation of these plaque elements provides extra information about stroke risk that simply measuring how narrow the artery is does not provide. In practical terms, plaque MRI may help select high-risk groups who could benefit from revascularisation (restoring blood flow by surgery or stenting).

Marker 8: Carotid Ulceration

An ulcer is a crater or depression on the surface of the plaque. Ulcers can harbour clots and release them into the bloodstream. Research showed that the volume of ulceration predicted cardiovascular events. This volume was measured by tracing the contours of ulcers on cross-sectional imaging slices 1 mm thick. The volumes of all slices containing ulceration were then summed. Patients whose total ulcer volume (TUV) reached 5.00 mm³ or more had significantly worse event-free survival than those with no ulceration or a TUV below 5 mm³ (log-rank p=0.009). The events counted were stroke, TIA or cardiovascular death during follow-up.

What the 2017 European Guidelines Say

The 2017 European Society for Vascular Surgery (ESVS) carotid guidelines list specific clinical and imaging features. These features are associated with an increased risk of late stroke in patients with 50%–99% asymptomatic carotid stenosis treated medically. These are the figures that support using these markers in practice:

• Spontaneous embolisation on TCD: OR 7.46 (2.24 to 24.89); p=0.001
• Plaque echolucency versus echogenic plaque on Duplex ultrasound: 2.61 (1.47 to 4.63); p=0.001
• Spontaneous embolisation on TCD combined with a uniformly or predominantly echolucent plaque (70%–99% stenosis): 10.61 (2.98 to 37.82); p=0.0003
• Stenosis progression (50%–99% stenosis): 1.92 (1.14 to 3.25); p=0.05
• Stenosis progression (70%–99% stenosis): 4.7 (2.3 to 9.6)
• Silent infarction on CT (60%–99% stenosis): 3.0 (1.46 to 6.29); p=0.002
• Impaired cerebrovascular reserve (70%–99% stenosis): 6.14 (2.77 to 4.95); p<0.01
• Juxtaluminal black area on computerised plaque analysis (under 4 mm², 4–8 mm², 8–10 mm², over 10 mm²): trend p<0.001
• Intraplaque haemorrhage on MRI: 3.66 (2.77 to 4.95); p<0.01
• Contralateral (opposite-side) stroke or TIA: 3.0 (1.9 to 4.73); p=0.0001

How Many Asymptomatic Patients Could Benefit?

The authors estimate that approximately 10% to 15% of patients with asymptomatic carotid stenosis might benefit from an intervention. That means the large majority — around 85% to 90% — are better served by medical therapy alone.

Spence and colleagues reported that between 2000 and 2005, 10% of patients with ACS had two or more microemboli on TCD. This is exactly the group that stands to gain most from intervention.

The authors also note that the picture will become clearer after ongoing studies comparing stenting or endarterectomy with best medical therapy publish their results. Until then, they advise that no patient should be offered an intervention unless there is evidence of a high risk of same-sided stroke, drawn from modalities such as those discussed here.

What This Means for Patients

If you have been told you have a narrowed carotid artery but have never had symptoms, this article is directly relevant to you. The take-home message is that your treatment should not be decided by the percentage of narrowing alone.

The percentage matters less than how dangerous the plaque actually appears. Two patients can both have a 70% narrowing and face very different risks. One may have a stable, quiet plaque that is best left alone and managed with medication. The other may have an active, unstable plaque shedding clots — and that patient should be considered for surgery or stenting.

Equally, the authors stress that all patients with asymptomatic carotid stenosis should receive best medical treatment. That is the foundation of care regardless of what else is decided. Intervention is an addition to BMT, not a replacement for it.

Limitations of the Evidence

The authors are explicit that the evidence behind these eight markers is uneven. Some predictors — microemboli on TCD in particular — rest on robust, well-replicated evidence. Others are supported by weaker data.

Specific limitations include:

• A meta-analysis of cerebrovascular reserve studies had a bias problem: in most studies the investigators were not blinded to the CVR results.
• Definitions of study endpoints (stroke versus TIA) and definitions of asymptomatic versus symptomatic disease varied between studies, making comparisons difficult.
• Some MRI plaque studies did not report blinding of the investigators who assessed outcomes, whereas others did.
• Brain CT scans may miss up to 40% of brain infarcts in patients with ACS.
• One early TCD study was underpowered with only 202 patients and used a single microembolus as its threshold, which likely explains its negative results.
• Most importantly, the article is a review of existing evidence, not a new randomised trial. It cannot prove that selecting patients using these markers improves outcomes — that requires the ongoing randomised studies comparing intervention with BMT.

Practical Recommendations

Based on this review, the following principles apply to patients with asymptomatic carotid stenosis:

1. Take best medical treatment seriously. Smoking cessation, statin therapy and control of blood pressure and other risk factors reduced annual stroke rates and microemboli substantially in the studies reviewed.
2. Ask whether your plaque has been characterised, not just measured. Plaque appearance on ultrasound (echolucency), plaque burden, and features on MRI all carry information about risk.
3. Repeat imaging matters. Progression of narrowing over time was one of the clearest signals of danger, raising 8-year stroke rates from 9% to 16% in the ACSRS study.
4. If TCD is available, embolus detection is the single best-validated test. Two or more microemboli in a 1-hour recording identifies very high risk, and the 2017 ESVS guidelines endorse intervention based on TCD microemboli.
5. Do not accept either extreme. Routine surgery for everyone and medical therapy alone for everyone are both described by the authors as suboptimal.
6. Discuss the 10%–15% figure with your clinician. Understanding that only a minority of ACS patients need an intervention helps frame the conversation about your own risk.

Frequently Asked Questions

I have a narrowed neck artery but no symptoms. Do I need surgery or a stent?

Not necessarily. A review of existing evidence estimates that only about 10% to 15% of people with asymptomatic carotid stenosis might benefit from an intervention. The large majority, roughly 85% to 90%, are better served by medical therapy alone. Treatment should be guided by evidence that your specific plaque carries a high risk of stroke on the same side, not by the percentage of narrowing alone.

What does it mean if my ultrasound shows an echolucent (dark) plaque?

In a meta-analysis pooling 7,557 patients with a mean follow-up of 37.2 months, plaque echolucency on duplex ultrasound was linked to a higher risk of future stroke on the same side. The relative risk was 2.31. Among patients with at least 50% narrowing the risk was higher still (relative risk 2.61). Echolucent plaques often contain a soft fatty core or bleeding inside the plaque.

What is transcranial Doppler, and why does it matter for me?

Transcranial Doppler is an ultrasound technique that beams sound through the skull to listen to blood flow in the brain's arteries. It registers tiny clots or plaque fragments called microemboli. In one study, patients with more than 2 microemboli per hour had a 15.6% versus 1.0% one-year stroke rate on the same side. A meta-analysis of five studies confirmed embolic signals predicted same-sided stroke.

If my narrowing gets worse on repeat scans, does that raise my stroke risk?

Yes. In the ACSRS study, over 8 years the cumulative same-sided ischaemic stroke rate was 0% if the narrowing regressed, 9% if it stayed the same, and 16% if it progressed. Progression roughly doubled risk at every level of severity. A separate study of 794 patients found progression occurred in 29.1% of arteries despite medical treatment, and symptoms developed in 13.7% of those.

What does it mean to have reduced cerebrovascular reserve?

Cerebrovascular reserve measures how much extra blood flow the brain can call upon when the carotid artery narrows. Normal values range from 15% to 40%; below 10% indicates impairment. A meta-analysis of 13 studies (991 patients, mean follow-up 32.7 months) found impaired reserve was associated with an almost 400% higher stroke risk in asymptomatic patients. The authors noted some studies were not blinded.

Can an MRI show whether my plaque is dangerous?

Yes. MRI can reveal what is inside a plaque, not just how narrow the artery is. A meta-analysis of 9 studies (779 patients) found hazard ratios for later stroke or TIA of 4.59 for intraplaque haemorrhage, 3.00 for lipid-rich necrotic core, and 5.93 for thinning or rupture of the fibrous cap. This information adds to what measuring narrowing alone provides.

Should I still take medication if I might have surgery or a stent?

Yes. All patients with asymptomatic carotid stenosis should receive medical treatment, which is the foundation of care regardless of what else is decided. Intervention is an addition to medical treatment, not a replacement for it. In the studies reviewed, smoking cessation, statin therapy and control of blood pressure and other risk factors substantially reduced annual stroke rates and microemboli.

I have a narrowed neck artery but no symptoms — when should I get a second opinion before agreeing to surgery or a stent?

Seek a second opinion when the decision rests only on the percentage of narrowing. Roughly 10%–15% of patients with asymptomatic carotid stenosis may benefit from surgery or stenting; the rest are better served by medical therapy alone. Ask whether your plaque has been characterised — appearance on ultrasound, plaque burden, MRI features, silent infarcts, impaired cerebrovascular reserve, or progression on repeat scans. Two or more microemboli in a one-hour transcranial Doppler recording identifies very high risk. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Spence 2018 How to identify which patients with asymptomatic carotid stenosis could benefit from endarterectomy or stenting

Authors: Kosmas I Paraskevas, Frank J Veith, J David Spence

Author affiliations: Department of Vascular and Endovascular Surgery, Royal Free Hospital, London, UK; Department of Vascular Surgery, New York University Langone Medical Center, New York, USA; Department of Vascular Surgery, Cleveland Clinic, Cleveland, Ohio, USA; Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, Canada

Publication details: Stroke and Vascular Neurology, 2018; volume 3: e000129. doi:10.1136/svn-2017-000129. Open access review. Received 8 December 2017; revised 6 February 2018; accepted 7 February 2018; published online first 24 February 2018.

Note: This patient-friendly article is based on peer-reviewed research. It is intended for general information and does not replace personalised advice from your own doctor.