{"product_id":"who-really-needs-carotid-artery-surgery-or-stenting-a-guide-to-identifying-high-risk-patients-with-asymptomatic-carotid-stenosis","title":"Who Really Needs Carotid Artery Surgery or Stenting? A Guide to Identifying High-Risk Patients with Asymptomatic Carotid Stenosis","description":"\u003cp\u003eCarotid artery stenosis—a narrowing of the major neck arteries that supply the brain—is a leading cause of stroke, yet not every patient with this condition needs or benefits from invasive treatment. This article explains how doctors are learning to identify the roughly 10–15% of patients with asymptomatic carotid stenosis who are at sufficiently high risk of stroke that preventive surgery (endarterectomy) or stenting is worthwhile. Researchers have identified eight key \"risk markers,\" ranging from tiny blood clots detected by ultrasound to silent brain infarcts seen on scans, that can help separate high-risk patients from those who are safer being managed with medication and lifestyle changes alone.\u003c\/p\u003e\n\n\u003ch1\u003eWho Really Needs Carotid Artery Surgery or Stenting? A Guide to Identifying High-Risk Patients with Asymptomatic Carotid Stenosis\u003c\/h1\u003e\n\n\u003ch2 id=\"table-of-contents\"\u003eTable of Contents\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\u003ca href=\"#ddn-key-points\"\u003eKey Points\u003c\/a\u003e\u003c\/li\u003e\n\n  \u003cli\u003e\u003ca href=\"#introduction\"\u003eIntroduction: The Stroke Problem and the Carotid Artery Debate\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#study-methods\"\u003eHow This Research Was Conducted\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#microemboli\"\u003eRisk Marker 1: Microemboli Detected by Transcranial Doppler (TCD)\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#echolucency\"\u003eRisk Marker 2: Plaque Echolucency on Duplex Ultrasound\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#progression\"\u003eRisk Marker 3: Progression of Stenosis Severity\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#silent-infarcts\"\u003eRisk Marker 4: Silent Embolic Infarcts on Brain CT or MRI\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#cvr\"\u003eRisk Marker 5: Reduced Cerebrovascular Reserve (CVR)\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#juxtaluminal\"\u003eRisk Marker 6: Size of the Juxtaluminal Hypoechoic Area\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#ipmri\"\u003eRisk Marker 7: Intraplaque Haemorrhage Identified by MRI\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#ulceration\"\u003eRisk Marker 8: Carotid Ulceration\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#guidelines\"\u003eWhat the Guidelines Say: A Summary of Key Risk Factors\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#clinical-implications\"\u003eClinical Implications: What This Means for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#limitations\"\u003eLimitations of the Evidence\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#recommendations\"\u003eRecommendations for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#ddn-faq\"\u003eFrequently Asked Questions\u003c\/a\u003e\u003c\/li\u003e\n\u003cli\u003e\u003ca href=\"#source\"\u003eSource Information\u003c\/a\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003c!-- ddn:keypoints:start --\u003e\n\u003ch2 id=\"ddn-key-points\"\u003eKey Points\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003eRoutine surgery for all asymptomatic carotid stenosis is outdated; individualized risk assessment with imaging is now recommended.\u003c\/li\u003e\n\u003cli\u003eTCD-detected microemboli (≥2 per hour) carry over a 1500% increased 1-year stroke risk in key studies.\u003c\/li\u003e\n\u003cli\u003eCombining TCD microemboli with echolucent plaque on ultrasound identifies a very high-risk group.\u003c\/li\u003e\n\u003cli\u003eStenosis progression despite medical therapy roughly doubles the risk of future stroke or symptoms.\u003c\/li\u003e\n\u003cli\u003eMRI plaque features and silent brain infarcts on CT independently predict elevated stroke risk in asymptomatic patients.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003c!-- ddn:keypoints:end --\u003e\n\n\n\u003ch2 id=\"introduction\"\u003eIntroduction: The Stroke Problem and the Carotid Artery Debate\u003c\/h2\u003e\n\n\u003cp\u003eStroke is a devastating global health problem. In the United States alone, there are almost \u003cstrong\u003e800,000 strokes each year\u003c\/strong\u003e, causing about \u003cstrong\u003e140,000 deaths annually\u003c\/strong\u003e. Approximately 610,000 of these are first-ever strokes. In the United Kingdom, more than 100,000 strokes occur each year, and in 2015 alone, over 40,000 people died of stroke. The statistics are stark: stroke causes twice as many deaths per year in women than breast cancer, and twice as many deaths per year in men than prostate and testicular cancer combined.\u003c\/p\u003e\n\n\u003cp\u003eWorldwide, stroke is the \u003cstrong\u003esecond most common cause of death\u003c\/strong\u003e, accounting for around 6.7 million deaths each year—that's one death every 5 seconds. About 85% of all strokes are ischaemic (caused by a blocked blood vessel), while 15% are haemorrhagic (caused by bleeding in the brain).\u003c\/p\u003e\n\n\u003cp\u003eA substantial proportion of first-ever ischaemic strokes are caused by thromboemboli—blood clots that travel from a narrowed carotid artery in the neck up to the brain. The carotid arteries are the two main blood vessels on each side of the neck that deliver oxygen-rich blood to the brain. When these arteries become narrowed by cholesterol plaque—a condition called carotid stenosis—they can become a source of dangerous clots.\u003c\/p\u003e\n\n\u003cp\u003eBack in the 1980s and 1990s, three landmark randomised controlled trials demonstrated that carotid endarterectomy (CEA)—a surgical procedure to remove the plaque from the carotid artery—conferred a \u003cstrong\u003e50% relative risk (RR) reduction in the 5-year stroke risk\u003c\/strong\u003e compared with best medical treatment (BMT) alone. As a result, offering CEA routinely to patients with asymptomatic carotid stenosis (ACS)—meaning carotid narrowing that hasn't yet caused any symptoms—was considered the treatment of choice.\u003c\/p\u003e\n\n\u003cp\u003eHowever, in the early and mid-2000s, this approach began to change. Due to significant improvements in medical therapy—such as smoking cessation strategies, widespread use of statins, better blood pressure control, and antiplatelet therapy—the annual stroke rate among patients with ACS declined dramatically. It became clear that operating on every patient with asymptomatic carotid stenosis was no longer appropriate.\u003c\/p\u003e\n\n\u003cp\u003eYet, the opposite approach is equally problematic. Some experts argue that \u003cem\u003eonly\u003c\/em\u003e best medical treatment should be offered to all patients with ACS, and that no one with asymptomatic stenosis should ever undergo prophylactic surgery. The authors of this review point out that this theory is \u003cstrong\u003enot based on Level I Evidence\u003c\/strong\u003e—the highest tier of medical proof. Rather, it is an extrapolation from observational studies showing improved results with modern medical therapy.\u003c\/p\u003e\n\n\u003cp\u003eThe key question, then, is: \u003cstrong\u003eCan we identify which patients with asymptomatic carotid stenosis are at high enough risk of stroke to justify a preventive intervention?\u003c\/strong\u003e This review article summarises the evidence for eight reliable predictors of future stroke risk in these patients.\u003c\/p\u003e\n\n\u003ch2 id=\"study-methods\"\u003eHow This Research Was Conducted\u003c\/h2\u003e\n\n\u003cp\u003eThis is a \u003cstrong\u003ecomprehensive review article\u003c\/strong\u003e, not a single new clinical trial. The authors—three leading vascular surgery and stroke prevention specialists from the Royal Free Hospital in London, New York University Medical Center, and the Stroke Prevention \u0026amp; Atherosclerosis Research Centre at Western University in Canada—systematically examined and summarised the published scientific evidence on identifying high-risk patients with asymptomatic carotid stenosis.\u003c\/p\u003e\n\n\u003cp\u003eThey reviewed findings from numerous major studies, including large prospective observational studies (which follow patients forward in time), meta-analyses (which statistically combine results from multiple studies), and landmark clinical trials. The evidence base includes data from thousands of patients followed for periods ranging from approximately 1 to 8 years. The article also incorporates guideline recommendations from the 2017 European Society for Vascular Surgery (ESVS).\u003c\/p\u003e\n\n\u003ch2 id=\"microemboli\"\u003eRisk Marker 1: Microemboli Detected by Transcranial Doppler (TCD)\u003c\/h2\u003e\n\n\u003cp\u003eTranscranial Doppler (TCD) is a non-invasive ultrasound technique that uses sound waves to measure blood flow in the brain's blood vessels through the skull. During a TCD examination, doctors can hear and visualise tiny particles—called \u003cstrong\u003emicroemboli\u003c\/strong\u003e—traveling through the bloodstream. These microemboli are essentially very small blood clots or plaque fragments that have broken loose from a carotid artery plaque and are heading toward the brain.\u003c\/p\u003e\n\n\u003cp\u003eImagine a tiny piece of plaque flaking off the artery wall and being carried by the blood toward the brain—that's a microembolus. When these are detected, they indicate an \u003cem\u003eunstable\u003c\/em\u003e plaque that may be at risk of causing a larger, symptomatic stroke.\u003c\/p\u003e\n\n\u003cp\u003eThe predictive value of TCD microemboli detection for identifying high-risk patients is well-established. The research group led by Dr. Spence was the first to report that patients with ACS who had \u003cstrong\u003emore than 2 microemboli per hour\u003c\/strong\u003e on TCD had a \u003cstrong\u003e\u0026gt;1500% increased risk of 1-year ipsilateral ischaemic stroke\u003c\/strong\u003e (meaning stroke on the same side of the brain as the narrowed carotid artery) compared with patients without TCD-detected microemboli. The actual numbers were stark: \u003cstrong\u003e15.6% vs 1.0%\u003c\/strong\u003e annual stroke risk (P\u0026lt;0.0001), a difference so large it is extremely unlikely to be due to chance.\u003c\/p\u003e\n\n\u003cp\u003eIn 2010, the same group reported further encouraging news. As a result of improvements in best medical treatment, there was a marked reduction in TCD-detected microemboli—from \u003cstrong\u003e12.6% before 2003 to 3.7% after 2003\u003c\/strong\u003e (P\u0026lt;0.001)—and a corresponding reduction in cardiovascular events, from \u003cstrong\u003e17.6% to 5.2%\u003c\/strong\u003e (P\u0026lt;0.001), in 468 patients with ACS.\u003c\/p\u003e\n\n\u003cp\u003eThese results were verified in an independent, multicentre international study called the \u003cstrong\u003eAsymptomatic Carotid Emboli Study (ACES)\u003c\/strong\u003e, which followed 467 patients with ACS. As in the earlier study, patients had two 1-hour TCD recordings taken 1 week apart. Patients with one or more TCD emboli had a \u003cstrong\u003e\u0026gt;550% higher risk of 1-year ipsilateral stroke\u003c\/strong\u003e compared with patients without emboli (HR: 5.57; 95% CI 1.61 to 19.32; P=0.007).\u003c\/p\u003e\n\n\u003cp\u003eOne earlier small study—a prospective observational cohort with only 202 patients—showed contradictory results, but it was underpowered (too small to detect a real difference). The authors note two likely reasons for its negative results: it accepted a single microembolus as a positive test (whereas the evidence supports needing at least two), and the test was repeated at 6-monthly intervals rather than more frequently.\u003c\/p\u003e\n\n\u003cp\u003eA meta-analysis of \u003cstrong\u003efive prospective studies\u003c\/strong\u003e (totalling 677 patients) confirmed that the presence of TCD-detected embolic signals is a significant predictor of ipsilateral stroke, with an odds ratio (OR) of \u003cstrong\u003e7.46 (95% CI 2.24 to 24.89; P=0.001)\u003c\/strong\u003e. An odds ratio of 7.46 means that patients with microemboli have about seven and a half times the odds of having a stroke compared to those without—a very substantial increase in risk. The 2017 ESVS guidelines recommend considering carotid intervention based on the presence of TCD microemboli.\u003c\/p\u003e\n\n\u003ch2 id=\"echolucency\"\u003eRisk Marker 2: Plaque Echolucency on Duplex Ultrasound\u003c\/h2\u003e\n\n\u003cp\u003eOn a duplex ultrasound, doctors can examine the characteristics of the plaque inside the carotid artery. An important feature is \u003cstrong\u003eecholucency\u003c\/strong\u003e—how \"dark\" or \"black\" the plaque appears on the ultrasound image. Early studies from the 1990s demonstrated that echolucent (dark-appearing) plaques correspond to a lipid-rich necrotic core (a soft, fatty, unstable centre) or intraplaque haemorrhage (bleeding inside the plaque)—features more commonly found in patients who have already had symptoms rather than in those with asymptomatic disease.\u003c\/p\u003e\n\n\u003cp\u003eMultiple studies have evaluated whether plaque echolucency predicts future stroke risk in patients with ACS. The majority of studies independently reported a \u003cstrong\u003estrong association between plaque echolucency and increased stroke risk\u003c\/strong\u003e. Here are the key studies:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eO'Holleran et al (1987):\u003c\/strong\u003e 293 patients, 46 months follow-up, relative risk (RR) of ipsilateral stroke 5.12 (95% CI 2.01 to 13.04)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePolak et al (1998):\u003c\/strong\u003e 4,886 patients, 39.6 months follow-up, RR 1.96 (95% CI 1.25 to 2.90)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eMathiesen et al (2001):\u003c\/strong\u003e 177 patients, 36 months follow-up, RR 3.85 (95% CI 0.46 to 32.28)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eGrønholdt et al (2001):\u003c\/strong\u003e 111 patients, 52.8 months follow-up, RR 0.87 (95% CI 0.34 to 2.23) — the only exception, from Denmark, suggesting echolucency was associated with stroke risk in symptomatic but not asymptomatic patients\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eNicolaides et al (2005):\u003c\/strong\u003e 1,092 patients, 37.1 months follow-up, RR 2.23 (95% CI 1.28 to 3.87)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eTopakian et al (2011):\u003c\/strong\u003e 435 patients, 21.8 months follow-up, RR 6.61 (95% CI 1.42 to 30.75)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSilvestrini et al (2013):\u003c\/strong\u003e 621 patients, median 27 months follow-up, RR 2.37 (95% CI 1.14 to 4.92)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHuibers et al (2016):\u003c\/strong\u003e 814 patients, 60 months follow-up, RR 2.52 (95% CI 1.20 to 5.25)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eA recent meta-analysis pooling data from \u003cstrong\u003e7,557 patients\u003c\/strong\u003e with a mean follow-up of 37.2 months demonstrated a positive association between plaque echolucency and the risk of future ipsilateral stroke, with a relative risk of \u003cstrong\u003e2.31 (95% CI 1.58 to 3.39; P\u0026lt;0.001)\u003c\/strong\u003e. Of the total study sample, 1,741 patients (23.0%) had a positive ultrasound test for echolucency. During follow-up, 100 ipsilateral strokes occurred in the echolucent-positive group, while 141 occurred in the echolucency-negative group—a cumulative incidence of ipsilateral stroke of \u003cstrong\u003e5.7% vs 2.4%\u003c\/strong\u003e, respectively.\u003c\/p\u003e\n\n\u003cp\u003eFor patients with ≥50% carotid stenosis, the stroke risk was even higher (RR: 2.61; 95% CI 1.47 to 4.63; P=0.001). This association was verified in an independent meta-analysis as well.\u003c\/p\u003e\n\n\u003cp\u003ePerhaps most importantly, the predictive value of echolucent plaque morphology increases even further when combined with TCD-detected emboli. In the ACES study, carotid plaque echolucency alone was associated with a \u003cstrong\u003e\u0026gt;600% increased risk\u003c\/strong\u003e of ipsilateral stroke (HR: 6.43; 95% CI 1.36 to 30.44; P=0.019). But the combination of plaque echolucency \u003cem\u003ewith\u003c\/em\u003e TCD-detected emboli was associated with a \u003cstrong\u003e\u0026gt;1000% increased risk\u003c\/strong\u003e of ipsilateral stroke (HR: 10.61; 95% CI 2.98 to 37.82; P=0.0003). In other words, these two markers together signal a very dangerous plaque.\u003c\/p\u003e\n\n\u003ch2 id=\"progression\"\u003eRisk Marker 3: Progression of Stenosis Severity\u003c\/h2\u003e\n\n\u003cp\u003eIf a patient's carotid stenosis is getting more severe on successive ultrasound examinations despite receiving best medical treatment, that is not a good sign. The authors note that up to half of patients with ACS may have what is called \"resistant atherosclerosis\"—disease that continues to progress despite appropriate medical therapy.\u003c\/p\u003e\n\n\u003cp\u003eThe largest prospective study of patients with ACS undergoing medical intervention alone—the \u003cstrong\u003eAsymptomatic Carotid Stenosis and Risk of Stroke (ACSRS)\u003c\/strong\u003e study—demonstrated clearly that progression of stenosis severity predicts future stroke. The 8-year cumulative ipsilateral ischaemic stroke rate was:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003e0%\u003c\/strong\u003e in patients with regression (improvement) of stenosis\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e9%\u003c\/strong\u003e if the stenosis was unchanged\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e16%\u003c\/strong\u003e if there was progression of stenosis\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eBreaking this down further, among patients with \u003cem\u003eunchanged\u003c\/em\u003e stenosis, the 8-year cumulative ipsilateral cerebral ischaemic stroke rates for patients with baseline stenosis of 50%–69%, 70%–89%, and 90%–99% were \u003cstrong\u003e4%, 8%, and 13%\u003c\/strong\u003e, respectively. In contrast, in the presence of progression, the stroke rates jumped to \u003cstrong\u003e8%, 15%, and 25%\u003c\/strong\u003e respectively—showing that progression magnifies the risk at every level of stenosis severity.\u003c\/p\u003e\n\n\u003cp\u003eAn independent study from Boston, Massachusetts, verified these findings. This study followed \u003cstrong\u003e794 patients (900 carotid arteries)\u003c\/strong\u003e with moderate (50%–69%) ACS for a mean of 3.6 years (range: 0.3 to 6.7 years). Stenosis progression occurred in \u003cstrong\u003e262 of 900 (29.1%)\u003c\/strong\u003e carotid arteries despite best medical treatment, and 36 (13.7%) of these patients developed symptoms. The symptomatic conversion rate in patients with progression was considerably higher than in those without progression: \u003cstrong\u003e13.7% vs 8.5%\u003c\/strong\u003e, respectively (P=0.02). The researchers concluded that medical treatment failed to prevent carotid disease progression or the development of symptoms in a significant proportion of patients.\u003c\/p\u003e\n\n\u003cp\u003eAn earlier study of 1,065 patients with ACS followed with carotid ultrasound also confirmed these findings. During the initial study period (median 7.5 months), progression of carotid lesions was demonstrated in 93 of 1,065 patients (9%). During a median follow-up of 3.2 years, \u003cstrong\u003e495 major adverse cardiovascular events\u003c\/strong\u003e (a composite including heart attack, coronary interventions, bypass surgery, stroke, peripheral vascular procedures, amputation due to critical limb ischaemia, and all-cause death) were recorded in 421 patients (40%).\u003c\/p\u003e\n\n\u003cp\u003ePatients with progressive ACS had a \u003cstrong\u003e200% higher risk\u003c\/strong\u003e of composite major adverse cardiovascular events compared with patients with non-progressive disease (adjusted HR: 2.01; 95% CI 1.48 to 2.67; P\u0026lt;0.001). This included:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eA \u0026gt;200% higher risk of myocardial infarction (heart attack) (HR: 2.38; 95% CI 1.07 to 5.35; P=0.044)\u003c\/li\u003e\n  \u003cli\u003eA 200% higher risk for stroke (adjusted HR: 2.0; 95% CI 1.02 to 4.11; P=0.035)\u003c\/li\u003e\n  \u003cli\u003eA 175% higher risk for cardiovascular death (adjusted HR: 1.75; 95% CI 1.03 to 2.97; P=0.039)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eOne particularly important insight from this body of research is that \u003cstrong\u003etotal plaque burden\u003c\/strong\u003e may be a better predictor of cardiovascular outcomes than traditional measurements. A study from Canada compared progression and regression of three measurements—carotid intima-media thickness (cIMT), total plaque area, and total plaque volume—as predictors of cardiovascular outcomes in 349 patients attending stroke prevention clinics. After a median follow-up of 3.17 years, there were 50 first events: 20 vascular deaths, 11 strokes, 13 transient ischaemic attacks (TIAs, or \"mini-strokes\"), and 6 heart attacks.\u003c\/p\u003e\n\n\u003cp\u003eThe results were striking:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eProgression of total plaque volume\u003c\/strong\u003e 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).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eProgression of total plaque area\u003c\/strong\u003e only weakly predicted stroke, TIA, or death (P=0.097), and did not predict stroke, death, or heart attack (P=0.59).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eChange in cIMT\u003c\/strong\u003e did not predict stroke, death, or heart attack (P=0.13).\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe study concluded that measurement of total plaque volume is a \u003cstrong\u003esuperior predictor\u003c\/strong\u003e of cardiovascular events compared with either total plaque area or cIMT. In fact, in patients with ACS, plaque burden—not percent stenosis—predicted the risk of stroke. The High Risk Plaque BioImage study also found that plaque burden was strongly correlated with coronary calcium (a measure of heart disease burden) while IMT was not, and plaque burden was as predictive of events as coronary calcium.\u003c\/p\u003e\n\n\u003ch2 id=\"silent-infarcts\"\u003eRisk Marker 4: Silent Embolic Infarcts on Brain CT or MRI\u003c\/h2\u003e\n\n\u003cp\u003eSometimes, tiny emboli (clots) break off from a carotid plaque and travel to the brain, causing small areas of brain damage that are too small to produce noticeable symptoms. These are called \u003cstrong\u003esilent embolic infarcts\u003c\/strong\u003e—\"silent\" because the patient doesn't experience any symptoms, but the damage is visible on brain imaging scans such as CT (computed tomography) or MRI (magnetic resonance imaging).\u003c\/p\u003e\n\n\u003cp\u003eBoth the Cardiovascular Health Study and the Rotterdam Scan Study demonstrated that the presence of silent embolic infarcts on brain CT or MRI is associated with an increased risk of stroke in the general population. Two further studies—the ACSRS study and an independent study from Japan—showed that silent embolic infarcts are an \u003cstrong\u003eindependent predictor of stroke\u003c\/strong\u003e in patients with asymptomatic carotid stenosis.\u003c\/p\u003e\n\n\u003cp\u003eIn the ACSRS study, patients with \u003cstrong\u003e60%–99% ACS\u003c\/strong\u003e who had silent embolic infarcts on brain CT scans had a \u003cstrong\u003e300% higher risk\u003c\/strong\u003e of future ipsilateral stroke compared with patients without silent infarcts. The annual stroke rate was \u003cstrong\u003e3.6% vs 1.0%\u003c\/strong\u003e, respectively (HR: 3.0; 95% CI 1.46 to 6.29; P=0.002). This means that a silent infarct on a brain scan is essentially a warning sign that the carotid plaque is actively shedding material into the brain.\u003c\/p\u003e\n\n\u003cp\u003eHowever, the authors note a limitation: brain CT scans may miss up to \u003cstrong\u003e40% of brain infarcts\u003c\/strong\u003e in patients with ACS. MRI is far more sensitive for detecting these small silent strokes.\u003c\/p\u003e\n\n\u003ch2 id=\"cvr\"\u003eRisk Marker 5: Reduced Cerebrovascular Reserve (CVR)\u003c\/h2\u003e\n\n\u003cp\u003eThe brain has a remarkable ability to protect itself. When the carotid artery becomes narrowed, the pressure of blood flowing to the brain decreases. In response, the tiny blood vessels in the brain (cerebral arterioles) dilate—widen—to their maximum to maintain adequate blood flow. This protective mechanism is called \u003cstrong\u003ecerebrovascular reserve (CVR)\u003c\/strong\u003e, and doctors can measure it.\u003c\/p\u003e\n\n\u003cp\u003eNormal CVR values range from as low as 15% up to 40%. Values below \u003cstrong\u003e10%\u003c\/strong\u003e suggest impaired CVR, meaning the brain's blood vessels are already maximally dilated and cannot compensate further if blood pressure drops.\u003c\/p\u003e\n\n\u003cp\u003eSeveral studies have demonstrated that impairment in CVR is associated with the development of stroke in patients with ACS:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eGur et al (1996):\u003c\/strong\u003e 44 patients, 21 with impaired CVR, 24 months follow-up, odds ratio (OR) 22.50\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSilvestrini et al (2000):\u003c\/strong\u003e 94 patients, 40 with impaired CVR, 28.5 months follow-up, OR 3.72 (95% CI 1.05 to 14.85)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eMarkus and Cullinane (2001):\u003c\/strong\u003e 107 patients, 21.7 months follow-up, OR 14.4 (95% CI 2.63 to 78.74)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eKimiagar et al (2010):\u003c\/strong\u003e 35 patients, 21 with impaired CVR, 48 months follow-up, OR 6.50 (95% CI 0.65 to 315.02)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eKing et al (2011):\u003c\/strong\u003e 106 patients, 32 with impaired CVR, 22.7 months follow-up, OR 3.62 (95% CI 0.61 to 21.74)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eA meta-analysis combining \u003cstrong\u003e13 studies with 991 patients\u003c\/strong\u003e and a mean follow-up of 32.7 months demonstrated an almost \u003cstrong\u003e400% higher stroke risk\u003c\/strong\u003e in asymptomatic patients with impaired cerebral blood flow (random effects OR: 3.96; 95% CI 2.60 to 6.04). Although the authors acknowledge limitations—including that investigators were not always blinded to CVR results and definitions of end-points varied between studies—they concluded that the association between CVR impairment and risk of stroke\/TIA is robust. Reduced CVR may therefore identify patients with ACS who are at high risk for stroke.\u003c\/p\u003e\n\n\u003ch2 id=\"juxtaluminal\"\u003eRisk Marker 6: Size of the Juxtaluminal Hypoechoic Area\u003c\/h2\u003e\n\n\u003cp\u003eIn unstable, symptom-causing plaques, the necrotic core (the soft, fatty centre of the plaque) is \u003cstrong\u003etwice as close to the blood vessel lumen\u003c\/strong\u003e compared with asymptomatic carotid plaques. This proximity matters because a plaque component that is closer to the surface is more likely to rupture and release debris into the bloodstream.\u003c\/p\u003e\n\n\u003cp\u003eCross-sectional studies using ultrasound have demonstrated an association between the \u003cstrong\u003ejuxtaluminal hypoechoic (black) area\u003c\/strong\u003e—the dark-appearing region of the plaque directly adjacent to the blood flow channel—and the presence of neurological symptoms. The ACSRS study formally tested whether the presence and size of this juxtaluminal hypoechoic area, in the absence of a visible echogenic (bright) cap, predicts future ipsilateral ischaemic stroke in patients with ACS.\u003c\/p\u003e\n\n\u003cp\u003eThe results showed a powerful \"dose-response\" relationship. The 5-year ipsilateral cerebral or retinal ischaemic event rate was:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003e3%\u003c\/strong\u003e in patients with a juxtaluminal hypoechoic area smaller than 4 mm²\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e21%\u003c\/strong\u003e in patients with an area between 4 and 8 mm²\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e36%\u003c\/strong\u003e in patients with an area between 8 and 10 mm²\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003e43%\u003c\/strong\u003e in patients with a juxtaluminal black area larger than 10 mm²\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe average annual stroke rates were 0.6%, 4.2%, 7.2%, and 8.6%, respectively—a dramatic stepwise increase in risk as the dark area grows. This supports the theory that the size of the juxtaluminal hypoechoic area is a reliable predictor of future ipsilateral ischaemic stroke.\u003c\/p\u003e\n\n\u003ch2 id=\"ipmri\"\u003eRisk Marker 7: Intraplaque Haemorrhage Identified by MRI\u003c\/h2\u003e\n\n\u003cp\u003eMagnetic resonance imaging (MRI) can look inside the carotid plaque itself and identify its specific components with remarkable detail. Three plaque features have been studied as potential predictors of stroke:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eIntraplaque haemorrhage (IPH)\u003c\/strong\u003e—bleeding inside the plaque\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eLipid-rich necrotic core (LRNC)\u003c\/strong\u003e—a soft, fatty, unstable core\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eThinning or rupture of the fibrous cap (TRFC)\u003c\/strong\u003e—weakening of the protective covering of the plaque\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003cp\u003eSeveral studies have evaluated whether MRI assessment of these plaque components can predict stroke in patients with ACS:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eTakaya et al (2006):\u003c\/strong\u003e 154 patients, 38.2 months follow-up, IPH hazard ratio (HR) 5.2 (95% CI 1.6 to 7.3)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSingh et al (2009):\u003c\/strong\u003e 98 patients, 24.9 months follow-up, IPH HR 2.48 to 4.71\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSadat et al (2010):\u003c\/strong\u003e 61 patients, 16.9 months follow-up, IPH HR 1.27 to 26.77; TRFC HR 7.39 (95% CI 1.61 to 33.82); LRNC HR 1.75 (95% CI 0.55 to 5.54)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eMono et al (2012):\u003c\/strong\u003e 65 patients, 18.9 months follow-up, IPH HR 0.03; TRFC HR 1.103 (95% CI 0.11 to 10.70); LRNC HR 7.2 (95% CI 1.12 to 46.28)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eKwee et al (2013):\u003c\/strong\u003e 126 patients, 12.0 months follow-up, IPH HR 3.5 (95% CI 1.06 to 11.96); TRFC HR 5.8 (95% CI 1.91 to 17.32); LRNC HR 3.2 (95% CI 1.08 to 9.50)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eHosseini et al (2013):\u003c\/strong\u003e 179 patients, 17.5 months follow-up, IPH HR 12 (95% CI 4.8 to 30.1)\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003cp\u003eThe majority of these studies showed that carotid plaques with intraplaque haemorrhage, lipid-rich necrotic core, or thinning\/rupture of the fibrous cap are \u003cstrong\u003esignificantly more likely\u003c\/strong\u003e to result in ipsilateral ischaemic events, with this increased risk present across a wide range of stenosis severity.\u003c\/p\u003e\n\n\u003cp\u003eA meta-analysis combining \u003cstrong\u003e9 studies with 779 patients\u003c\/strong\u003e verified these findings. The hazard ratios for intraplaque haemorrhage, lipid-rich necrotic core, and thinning\/rupture of the fibrous cap as predictors of subsequent stroke or TIA were \u003cstrong\u003e4.59 (95% CI 2.91–7.24)\u003c\/strong\u003e, \u003cstrong\u003e3.00 (95% CI 1.51–5.95)\u003c\/strong\u003e, and \u003cstrong\u003e5.93 (95% CI 2.65–13.20)\u003c\/strong\u003e, respectively. This meta-analysis concluded that MRI characterisation of these specific plaque elements can provide additional measures of stroke risk not provided by simple measurement of luminal stenosis alone.\u003c\/p\u003e\n\n\u003ch2 id=\"ulceration\"\u003eRisk Marker 8: Carotid Ulceration\u003c\/h2\u003e\n\n\u003cp\u003eSometimes the surface of a carotid plaque develops an actual crater or ulceration—a break in the inner lining of the artery. Researchers have studied whether the \u003cstrong\u003evolume of these ulcerations\u003c\/strong\u003e predicts risk. In one study, the total ulcer volume (TUV) was computed from tracing ulcer contours on cross-sectional ultrasound images, with each slice having a thickness of 1 mm.\u003c\/p\u003e\n\n\u003cp\u003eThe research demonstrated that patients with a total ulcer volume of \u003cstrong\u003e≥5.00 mm³\u003c\/strong\u003e had significantly worse outcomes during follow-up compared with those with no ulcerations or smaller ulcers. The Kaplan–Meier survival analysis (a statistical method that tracks how many people reach a given endpoint over time) for participants with TUV ≥5.00 mm³ versus those with no ulcerations or TUV \u0026lt;5 mm³ showed a statistically significant difference (log-rank P=0.009) for the combined endpoint of stroke, TIA, or cardiovascular death.\u003c\/p\u003e\n\n\u003cp\u003eIndeed, the 2017 European Society for Vascular Surgery guidelines list a prior \u003cstrong\u003econtralateral stroke or TIA\u003c\/strong\u003e (a stroke or mini-stroke on the opposite side of the brain) as a clinical feature associated with increased risk of late stroke, with a hazard ratio of \u003cstrong\u003e3.0 (95% CI 1.9 to 4.73; P=0.0001)\u003c\/strong\u003e—suggesting that a history of cerebrovascular events anywhere in the brain may signal a generally more vulnerable vascular system.\u003c\/p\u003e\n\n\u003ch2 id=\"guidelines\"\u003eWhat the Guidelines Say: A Summary of Key Risk Factors\u003c\/h2\u003e\n\n\u003cp\u003eThe 2017 European Society for Vascular Surgery (ESVS) carotid guidelines consolidated the evidence into a clear table of clinical and imaging features associated with an increased risk of late stroke in patients with 50%–99% asymptomatic carotid stenosis treated medically. Here are the key risk markers and their associated risk increases:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSpontaneous embolisation on TCD:\u003c\/strong\u003e OR 7.46 (95% CI 2.24 to 24.89); P=0.001\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePlaque echolucency on duplex ultrasound\u003c\/strong\u003e (vs echogenic): OR 2.61 (95% CI 1.47 to 4.63); P=0.001\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSpontaneous embolisation on TCD + uniformly or predominantly echolucent plaque\u003c\/strong\u003e (70%–99% stenoses): OR 10.61 (95% CI 2.98 to 37.82); P=0.0003\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eStenosis progression\u003c\/strong\u003e (50%–99% stenoses): OR 1.92 (95% CI 1.14 to 3.25); P=0.05\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eStenosis progression\u003c\/strong\u003e (70%–99% stenoses): OR 4.7 (95% CI 2.3 to 9.6)\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eSilent infarction on CT\u003c\/strong\u003e (60%–99% stenoses): OR 3.0 (95% CI 1.46 to 6.29); P=0.002\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eImpaired cerebrovascular reserve\u003c\/strong\u003e (70%–99% stenoses): OR 6.14 (95% CI 2.77 to 4.95); P\u0026lt;0.01\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eJuxtaluminal black area on computerised plaque analysis\u003c\/strong\u003e (comparing areas \u0026lt;4 mm², 4–8 mm², 8–10 mm², \u0026gt;10 mm²): trend P\u0026lt;0.001\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eIntraplaque haemorrhage on MRI:\u003c\/strong\u003e OR 3.66 (95% CI 2.77 to 4.95); P\u0026lt;0.01\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eContralateral stroke\/TIA:\u003c\/strong\u003e OR 3.0 (95% CI 1.9 to 4.73); P=0.0001\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"clinical-implications\"\u003eClinical Implications: What This Means for Patients\u003c\/h2\u003e\n\n\u003cp\u003eThis body of evidence fundamentally changes how doctors should think about asymptomatic carotid stenosis. Rather than applying a \"one-size-fits-all\" approach—either operating on everyone or no one—modern practice calls for a \u003cstrong\u003epersonalised risk assessment\u003c\/strong\u003e.\u003c\/p\u003e\n\n\u003cp\u003eAll patients with ACS should receive best medical treatment, which includes statins to lower cholesterol, antiplatelet therapy, blood pressure control, smoking cessation, and diabetes management. But for patients who display one or more high-risk features described above, the risk of stroke may be high enough (often exceeding 2–3% per year, and sometimes much higher) that a preventive carotid intervention—either carotid endarterectomy (the surgical removal of plaque) or carotid artery stenting (inserting a mesh tube to hold the artery open)—is justified.\u003c\/p\u003e\n\n\u003cp\u003eFrom the available evidence, the authors estimate that approximately \u003cstrong\u003e10%–15% of patients with asymptomatic stenosis\u003c\/strong\u003e might benefit from intervention. In 2005, Spence and colleagues reported that in the period from 2000 to 2005, 10% of patients with ACS had two or more microemboli on TCD—a straightforward way to identify a substantial proportion of these high-risk individuals.\u003c\/p\u003e\n\n\u003cp\u003eIt's important to understand what these statistics mean in real terms. A patient with TCD-detected microemboli and an echolucent plaque faces a risk of ipsilateral stroke that is more than ten times higher than a patient without these features. For such patients, the potential benefit of surgery is substantial—far exceeding the risks of the procedure itself, which in experienced centres is around 1–3% for perioperative stroke or death. On the other hand, for low-risk patients with stable, bright (echogenic) plaques, no microemboli, and no evidence of progression, yearly stroke risk may be under 1%, which is lower than the risk of surgery—and so medical management alone is clearly the right choice.\u003c\/p\u003e\n\n\u003cp\u003eThe authors emphasise that TCD embolus detection is currently the \u003cstrong\u003ebest validated method\u003c\/strong\u003e for identifying high-risk patients, and that combining multiple risk markers (such as TCD emboli with plaque echolucency) dramatically increases predictive power.\u003c\/p\u003e\n\n\u003ch2 id=\"limitations\"\u003eLimitations of the Evidence\u003c\/h2\u003e\n\n\u003cp\u003eAs with any medical research, the studies underlying these recommendations have limitations. The authors note several:\u003c\/p\u003e\n\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003eConflicting results in some early studies:\u003c\/strong\u003e One early TCD study with only 202 patients found no significant association, though it was underpowered and used different criteria for a \"positive\" test.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eBlinding issues in CVR studies:\u003c\/strong\u003e In the majority of studies of cerebrovascular reserve, investigators were not blinded to the CVR results, which could potentially bias outcome assessment.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eVariations in study design:\u003c\/strong\u003e Definitions of study endpoints (stroke vs TIA) and definitions of \"asymptomatic\" versus \"symptomatic\" disease varied between studies.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eCT scan limitations:\u003c\/strong\u003e Brain CT may miss up to 40% of brain infarcts in patients with ACS, potentially underestimating the prevalence of silent infarcts when CT is used alone.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eBlinding not always reported in MRI studies:\u003c\/strong\u003e Some MRI studies described blinding of MRI results to researchers assessing ischaemic outcomes, while others did not report such blinding.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eEvolving medical therapy:\u003c\/strong\u003e The natural history of asymptomatic carotid stenosis continues to improve as medical therapy advances, and the authors note that the ongoing trials comparing stenting or endarterectomy with best medical therapy will clarify the picture further.\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"recommendations\"\u003eRecommendations for Patients\u003c\/h2\u003e\n\n\u003cp\u003eIf you or a loved one has been diagnosed with asymptomatic carotid stenosis (a carotid narrowing that hasn't caused a stroke or mini-stroke), here are some practical takeaways from this research:\u003c\/p\u003e\n\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eDon't assume no treatment is needed:\u003c\/strong\u003e While it's true that aggressive medical therapy has dramatically reduced stroke rates, the risk is not zero—and about 10–15% of patients with ACS face a much higher risk than the rest. Write down your exact degree of stenosis (e.g., 70%) and discuss it with a specialist.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eAsk about TCD embolus detection:\u003c\/strong\u003e This non-invasive ultrasound test, which takes about an hour, checks for tiny particles traveling to the brain. Two or more microemboli per hour marks a \u0026gt;1500% increase in 1-year stroke risk—this is the single best-validated predictor.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eAsk about plaque characterisation:\u003c\/strong\u003e Not all plaques are equal. If your plaque appears dark and \"echolucent\" on ultrasound, or\n\n\u003c!-- ddn:faq:start --\u003e\n\u003ch2 id=\"ddn-faq\"\u003eFrequently Asked Questions\u003c\/h2\u003e\n\u003ch3\u003eI have asymptomatic carotid stenosis. Do I need surgery or stenting?\u003c\/h3\u003e\n\u003cp\u003eNot automatically. Modern medical therapy—statins, blood pressure control, antiplatelet drugs, and lifestyle changes—is effective for many patients. However, about 10–15% of people with asymptomatic stenosis have a high enough stroke risk to benefit from preventive intervention. Doctors now use imaging tests to identify these high-risk individuals and personalize treatment decisions.\u003c\/p\u003e\n\u003ch3\u003eMy ultrasound says my plaque is 'echolucent'. What does that mean?\u003c\/h3\u003e\n\u003cp\u003eEcholucent means the plaque appears dark on an ultrasound, suggesting a soft, fatty, unstable center. In pooled data from over 7,500 patients, echolucent plaques were associated with about a 2.3 times higher risk of future stroke compared with brighter plaques. When combined with microemboli detected on TCD, the risk is more than ten times higher.\u003c\/p\u003e\n\u003ch3\u003eIf my carotid narrowing is getting worse despite medication, is my risk higher?\u003c\/h3\u003e\n\u003cp\u003eYes. In the largest study of medically treated asymptomatic carotid stenosis, the 8-year stroke rate was 16% if stenosis progressed, versus 9% if it stayed unchanged and 0% if it regressed. An independent study found that progression roughly doubled the risk of symptoms. Worsening stenosis signals resistant atherosclerosis that may require more than just medical therapy.\u003c\/p\u003e\n\u003ch3\u003eWhat are 'silent' brain infarcts and do they increase stroke risk?\u003c\/h3\u003e\n\u003cp\u003eSilent embolic infarcts are tiny areas of brain damage caused by clots from a carotid plaque, but they are too small to cause noticeable symptoms. They show up on CT or MRI scans. In the ACSRS study, patients with a silent infarct on CT had a 3 times higher annual risk of future stroke compared to those without one.\u003c\/p\u003e\n\u003ch3\u003eCan an MRI of my carotid plaque help predict stroke risk?\u003c\/h3\u003e\n\u003cp\u003eYes. MRI can detect specific plaque features such as intraplaque haemorrhage (bleeding inside the plaque), a lipid-rich necrotic core, and thinning or rupture of the fibrous cap. A meta-analysis found these features increased stroke risk by roughly 3- to 6-fold. This information can add to the risk assessment beyond just measuring how narrow the artery is.\u003c\/p\u003e\n\u003ch3\u003eWhat does 'reduced cerebrovascular reserve' mean and is it dangerous?\u003c\/h3\u003e\n\u003cp\u003eCerebrovascular reserve is the brain's ability to widen its small blood vessels to maintain blood flow when a carotid artery is narrowed. When this reserve is impaired (below about 10%), the brain cannot compensate further. In a meta-analysis of 13 studies, asymptomatic patients with impaired reserve had nearly a 4 times higher risk of stroke.\u003c\/p\u003e\n\u003ch3\u003eWhen should I seek a second opinion about surgery or stenting for asymptomatic carotid stenosis?\u003c\/h3\u003e\n\u003cp\u003eMany patients with asymptomatic carotid stenosis do not benefit from surgery or stenting; only about 10–15% are high-risk enough to justify it. Intervention is generally considered when risk markers are present, such as two or more microemboli per hour on transcranial Doppler, echolucent plaque, stenosis progression, silent brain infarcts, or impaired cerebrovascular reserve. A second opinion can review your imaging and ultrasound findings to determine whether you have these high-risk features or whether medical treatment alone is the safer choice. Diagnostic Detectives Network provides independent expert second opinions.\u003c\/p\u003e\n\u003c!-- ddn:faq:end --\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"DiagnosticDetectives.Com","offers":[{"title":"Default Title","offer_id":47471110062236,"sku":null,"price":0.0,"currency_code":"USD","in_stock":true}],"url":"https:\/\/diagnosticdetectives.com\/de\/products\/who-really-needs-carotid-artery-surgery-or-stenting-a-guide-to-identifying-high-risk-patients-with-asymptomatic-carotid-stenosis","provider":"DiagnosticDetectives.Com","version":"1.0","type":"link"}