{"product_id":"using-ultrasound-to-prevent-stroke-a-patients-guide","title":"Using Ultrasound to Prevent Stroke: A Patient's Guide","description":"\u003cp\u003eThis review article explains how ultrasound technology can help prevent stroke in multiple ways. Researchers at Western University in London, Ontario, Canada, found that measuring carotid plaque burden (the total amount of plaque in the neck arteries) is a much stronger predictor of heart attack and stroke risk than traditional measurements like intima-media thickness. By adopting a \"treating arteries\" approach guided by ultrasound, the team achieved a more than 80% reduction in stroke and heart attack risk over 2 years in high-risk patients. The article also shows how ultrasound can identify dangerous plaque features and detect blood clots traveling to the brain, helping doctors target treatment to the patients who need it most.\u003c\/p\u003e\n\n\u003ch1\u003eUsing Ultrasound to Prevent Stroke: A Patient's Guide\u003c\/h1\u003e\n\n\u003ch2\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=\"#background\"\u003eWhy This Research Matters\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#imt\"\u003eMeasuring Atherosclerosis: IMT vs. Plaque Burden\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#tpa\"\u003eTotal Plaque Area (TPA): A Powerful Predictor of Risk\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#treating-arteries\"\u003eA New Approach: Treating Arteries Instead of Risk Factors\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#unexplained\"\u003eUnexplained Atherosclerosis and the Gut Microbiome\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#3d\"\u003e3D Ultrasound: Plaque Volume and Vessel Wall Volume\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#vulnerable\"\u003eIdentifying Dangerous Plaques: Echolucency, Ulceration, and Plaque Texture\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#tcd\"\u003eTranscranial Doppler: Listening to Blood Flow in the Brain\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#implications\"\u003eWhat This Means for Patients\u003c\/a\u003e\u003c\/li\u003e\n  \u003cli\u003e\u003ca href=\"#limitations\"\u003eStudy Limitations\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\u003eCarotid plaque burden, measured by ultrasound, predicts heart attack and stroke risk better than intima-media thickness.\u003c\/li\u003e\n\u003cli\u003eIn a single-center study, a plaque-guided 'treating arteries' approach was associated with an over 80% reduction in 2-year stroke and heart attack risk.\u003c\/li\u003e\n\u003cli\u003eGut microbiome metabolites such as TMAO and p-cresyl sulfate were higher in patients with unexplained atherosclerosis in a study of over 3,000 patients.\u003c\/li\u003e\n\u003cli\u003eTranscranial Doppler can detect microemboli; patients with two or more in one hour had a 15.6% one-year stroke risk versus 1% without.\u003c\/li\u003e\n\u003cli\u003eMost asymptomatic carotid stenosis patients do better with intensive medical therapy; TCD embolus detection helps identify the minority who might benefit from intervention.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003c!-- ddn:keypoints:end --\u003e\n\n\n\u003ch2 id=\"background\"\u003eWhy This Research Matters\u003c\/h2\u003e\n\u003cp\u003eStroke is a leading cause of death and disability worldwide, and its burden is growing as populations age. This review article, written by Prof. J. David Spence of the Stroke Prevention \u0026amp; Atherosclerosis Research Centre at Western University, explains how ultrasound—a safe, radiation-free imaging technique—can be used to prevent stroke in several important ways.\u003c\/p\u003e\n\u003cp\u003eThe review highlights that ultrasound is not just a diagnostic tool. It can guide treatment decisions, identify which patients are at highest risk, help researchers discover new risk factors, and even serve as a target for therapy. The author argues that these methods should be used more widely to reduce the growing burden of stroke in aging populations.\u003c\/p\u003e\n\n\u003ch2 id=\"imt\"\u003eMeasuring Atherosclerosis: IMT vs. Plaque Burden\u003c\/h2\u003e\n\u003cp\u003eAtherosclerosis is the buildup of fatty plaque inside arteries. For decades, doctors measured something called intima-media thickness (IMT)—the thickness of the inner two layers of the artery wall—as an early sign of \"preclinical atherosclerosis\" (atherosclerosis that hasn't yet caused symptoms). However, this review makes a strong case that this widespread practice is based on a misunderstanding.\u003c\/p\u003e\n\u003cp\u003eAccording to the author, IMT as measured by the Mannheim consensus does \u003cstrong\u003enot\u003c\/strong\u003e represent true atherosclerosis. Instead, it is a biologically, pathologically, and genetically distinct phenotype (a different physical trait with different underlying causes). Studies that report IMT predicting risk are actually those that combine plaque thickness with IMT—and those studies should not call their measurement \"IMT\" because they mix together patients with plaque and patients without plaque.\u003c\/p\u003e\n\u003cp\u003ePlaque thickness itself does predict risk, but the evidence shows that measuring the \u003cstrong\u003etotal plaque burden\u003c\/strong\u003e (the overall amount of plaque) is far more useful. Key differences highlighted in the review:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003ePlaque area is a much stronger predictor of risk than IMT\u003c\/li\u003e\n  \u003cli\u003ePlaque burden measured by ultrasound is highly correlated with coronary calcium scores (another heart risk test) and is just as predictive of risk—but ultrasound is less costly and does not require radiation\u003c\/li\u003e\n  \u003cli\u003eProgression of IMT does not predict risk, whereas progression of plaque area and 3-dimensional (3D) plaque volume does predict cardiovascular risk\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"tpa\"\u003eTotal Plaque Area (TPA): A Powerful Predictor of Risk\u003c\/h2\u003e\n\u003cp\u003eTotal plaque area (TPA) is measured by tracing the outline of a plaque in a longitudinal (lengthwise) ultrasound image, in the plane where the plaque is biggest. All plaques seen on both sides of the neck, between the collarbone and the angle of the jaw, are measured, and the sum of all plaque areas gives the TPA.\u003c\/p\u003e\n\u003cp\u003eThe measurement is surprisingly easy to perform. It can be taught to any experienced ultrasound technologist, takes only a short time, and is very reliable: the intraclass correlation (a measure of test-retest reliability) for repeat measurement is \u003cstrong\u003e0.94\u003c\/strong\u003e, which is considered excellent. The method was invented in 1986 by Maria DiCicco RVT at the author's laboratory, and was first used in a study of the effects of psychological stress on atherosclerosis.\u003c\/p\u003e\n\u003cp\u003eIn 1995, the research team began measuring TPA routinely in their vascular prevention clinics. By 2002, they had strong evidence that TPA predicted cardiovascular risk among patients referred for prevention. The findings were striking:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eBy quartile (quarter) of plaque area, the 5-year risk of stroke, heart attack (myocardial infarction), or vascular death was \u003cstrong\u003e5.6%, 10.7%, 13.9%, and 19.5%\u003c\/strong\u003e—from the lowest to the highest quartile\u003c\/li\u003e\n  \u003cli\u003eThese results were adjusted (statistically corrected) for age, sex, blood pressure, serum cholesterol, smoking (pack-years), diabetes, plasma total homocysteine, and treatment of blood pressure and cholesterol\u003c\/li\u003e\n  \u003cli\u003eIn other words, TPA was a much stronger predictor of risk than traditional risk scores such as the Framingham risk score\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eThe review also revealed important patterns in how plaque behaves over time. Plaque progression (worsening) occurred in half of the patients despite usual therapy, and patients whose plaque progressed had \u003cstrong\u003etwice the risk\u003c\/strong\u003e of those whose plaque was stable or regressed (shrank). Regression occurred in only 25% of patients. This meant that \"usual therapy\" was failing half of the patients—a sobering realization that led to a new approach to vascular prevention.\u003c\/p\u003e\n\n\u003ch2 id=\"treating-arteries\"\u003eA New Approach: Treating Arteries Instead of Risk Factors\u003c\/h2\u003e\n\u003cp\u003eIn 2003, the research team implemented a fundamentally different approach to vascular prevention. Instead of being satisfied with reaching target levels of risk factors like blood pressure and LDL cholesterol (LDL-C), the new target of therapy was to stop plaque progression or achieve plaque regression. In other words: \u003cstrong\u003e\"Treating arteries instead of treating risk factors.\"\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eThe results were dramatic. By 2010, the proportion of patients with plaque regression versus progression had reversed. Now only about a quarter of patients had plaque progression, and about half had regression. Additional benefits followed:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eThe percentage of patients with microemboli (tiny blood clots detected by transcranial Doppler, discussed later) declined from \u003cstrong\u003e12.6% to 3.7%\u003c\/strong\u003e of patients\u003c\/li\u003e\n  \u003cli\u003eThe rate of carotid plaque progression declined significantly\u003c\/li\u003e\n  \u003cli\u003eThe 2-year risk of stroke and heart attack declined by \u003cstrong\u003emore than 80%\u003c\/strong\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eOne of the most practical advantages of this approach is that plaque responds quickly enough to guide treatment. Even plaque area changes within 3 months—the review includes an example of a 64-year-old patient whose plaque area grew from 20 mm² to 28 mm² after stopping a statin (rosuvastatin) and taking only ezetimibe, then regressed to 19 mm² over 13 weeks after restarting rosuvastatin 5 mg daily with ezetimibe 10 mg daily and CoQ10 200 mg daily to prevent muscle pain.\u003c\/p\u003e\n\u003cp\u003eThe author emphasizes the core philosophy with a memorable analogy: \u003cem\u003e\"Treating arteries without measuring plaque would be like treating hypertension without measuring blood pressure.\"\u003c\/em\u003e\u003c\/p\u003e\n\n\u003ch2 id=\"unexplained\"\u003eUnexplained Atherosclerosis and the Gut Microbiome\u003c\/h2\u003e\n\u003cp\u003eAfter treating more than 4,000 patients with this plaque-guided approach, the team noticed something important: some patients had atherosclerosis that could not be explained by traditional risk factors. These patients had \"unexplained atherosclerosis\" and were extraordinarily resistant to even intensive medical therapy.\u003c\/p\u003e\n\u003cp\u003eSurprisingly, neither baseline levels of LDL-C (\"bad cholesterol\") nor changes in LDL-C over a year predicted whether plaque would progress or regress. Even among patients with LDL-C below \u003cstrong\u003e1 mmol\/L (19 mg\/dL)\u003c\/strong\u003e—an extremely low level—half still had plaque progression. (These were the patients being treated most intensively, which explains why they had the lowest cholesterol.) Two factors that did predict resistance to therapy were \u003cstrong\u003eage and kidney (renal) function\u003c\/strong\u003e.\u003c\/p\u003e\n\u003cp\u003eThis observation pointed toward a new hypothesis: metabolic toxins that the kidneys normally clear from the body might account for a large proportion of \"unexplained atherosclerosis.\" Patients with kidney failure are known to have extremely high cardiovascular risk. They also have high blood levels of several potentially harmful substances:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eTotal homocysteine (an amino acid linked to heart and stroke risk)\u003c\/li\u003e\n  \u003cli\u003eAsymmetric dimethylarginine (ADMA, which blocks nitric oxide, a molecule that relaxes blood vessels)\u003c\/li\u003e\n  \u003cli\u003eThiocyanate (a potent factor that increases oxidative stress, which damages cells)\u003c\/li\u003e\n  \u003cli\u003eToxic metabolites produced by the intestinal microbiome (gut bacteria) from dietary precursors such as carnitine (found in red meat) and phosphatidylcholine (found in egg yolk)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eIn 2016, the team estimated that plasma total homocysteine only accounted for about \u003cstrong\u003e20%\u003c\/strong\u003e of the effect of kidney impairment on atherosclerosis. They hypothesized that toxic metabolites of the intestinal microbiome might account for a greater proportion.\u003c\/p\u003e\n\u003cp\u003eIn 2018, they reported a breakthrough finding. Among a clinic population of \u003cstrong\u003e3,056 patients\u003c\/strong\u003e, they identified the 5% extremes: patients with \"unexplained atherosclerosis\" (much more plaque than predicted by traditional risk factors) and \"protected\" patients (much less plaque than expected despite high levels of traditional risk factors). Key results:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003ePlasma levels of trimethylamine N-oxide (\u003cstrong\u003eTMAO\u003c\/strong\u003e), p-cresyl sulfate, and two other gut-derived metabolites were significantly higher in patients with unexplained atherosclerosis than in patients whose atherosclerosis was explained by traditional risk factors\u003c\/li\u003e\n  \u003cli\u003eThese same metabolites were significantly lower in \"protected\" patients who had little or no plaque despite high risk factor levels\u003c\/li\u003e\n  \u003cli\u003eIn linear regression analysis, both TMAO and p-cresyl sulfate were significant predictors of plaque burden\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eSpecific metabolite results (see Figure 3 in the original article):\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eTMAO: P=0.005 (statistically significant)\u003c\/li\u003e\n  \u003cli\u003eP-cresyl sulfate: P=0.0001 (highly significant)\u003c\/li\u003e\n  \u003cli\u003eP-cresyl glucuronide: P=0.0001 (highly significant)\u003c\/li\u003e\n  \u003cli\u003ePhenylacetyl glutamine: P=0.0001 (highly significant)\u003c\/li\u003e\n  \u003cli\u003eHippuric acid: P=0.14 (not significant)\u003c\/li\u003e\n  \u003cli\u003eIndoxyl sulfate: P=0.08 (borderline, not significant)\u003c\/li\u003e\n  \u003cli\u003ePhenyl sulfate: P=0.35 (not significant)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eFor context, a P value below 0.05 means there is less than a 5% probability that the result occurred by random chance. A P value of 0.0001 means there is only a 0.01% chance the finding was due to luck.\u003c\/p\u003e\n\u003cp\u003eThis research opens an exciting new frontier: modifying the diet to change the gut microbiome could potentially reduce atherosclerosis risk in ways that go beyond traditional cholesterol-lowering treatments.\u003c\/p\u003e\n\n\u003ch2 id=\"3d\"\u003e3D Ultrasound: Plaque Volume and Vessel Wall Volume\u003c\/h2\u003e\n\u003cp\u003eWhile 2D plaque area measurements (TPA) are useful, researchers have also developed 3D ultrasound methods to measure total plaque volume (TPV) and vessel wall volume (VWV). These methods, developed by Fenster and colleagues, use manual segmentation (tracing) of cross-sectional slices of plaques.\u003c\/p\u003e\n\u003cp\u003eThe review acknowledges that these measurements have practical challenges. They are tedious to perform, about a third of people cannot master them (some are too perfectionist and cannot make boundary decisions; others are too careless), and it takes several months of training to become certified to do the measurements reliably.\u003c\/p\u003e\n\u003cp\u003eHowever, measuring change in 3D plaque volume is the \u003cstrong\u003emost efficient way\u003c\/strong\u003e to assess how well a therapy is working on atherosclerosis. Here's why:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eIMT changes by only about 1.5 mm per year, and the spatial resolution of carotid ultrasound is about 3 mm—so it is not possible to measure IMT change within an individual in a clinically meaningful time frame\u003c\/li\u003e\n  \u003cli\u003eConsensus sample sizes for IMT studies of anti-atherosclerotic therapies are about \u003cstrong\u003e300 patients per group\u003c\/strong\u003e, followed for 2 years\u003c\/li\u003e\n  \u003cli\u003eCoronary plaque studies using intravascular ultrasound (IVUS) need about \u003cstrong\u003e200 patients per group\u003c\/strong\u003e followed for 2 years\u003c\/li\u003e\n  \u003cli\u003eCarotid plaques are focal (localized), so they can change in 3 dimensions: length, thickness, and circumferential extent. They also grow along the vessel in the direction of blood flow \u003cstrong\u003e2.4 times faster\u003c\/strong\u003e than they thicken\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eThis means 3D plaque volume requires far smaller sample sizes and shorter study durations. In one study of patients with asymptomatic carotid stenosis (ACS), significant plaque volume reduction was seen with atorvastatin compared to placebo in only \u003cstrong\u003e3 months\u003c\/strong\u003e, using only \u003cstrong\u003e17 patients on placebo and 21 on atorvastatin\u003c\/strong\u003e. Specifically:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003ePlacebo group: plaque volume \u003cstrong\u003eprogressed by 16.81 ± 74.10 mm³\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eAtorvastatin group: plaque volume \u003cstrong\u003eregressed by −90.25 ± 85.12 mm³\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eThe difference was highly statistically significant (P\u0026lt;0.0001)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eFor patients who don't yet have carotid plaque, 3D ultrasound measurement of vessel wall volume (VWV) is superior to IMT because the dynamic range is much greater and the ability to detect change over time is far better. In a dietary study, blood pressure reduction with weight loss was strongly associated with reduced VWV over 2 years in a relatively small study of only \u003cstrong\u003e140 participants\u003c\/strong\u003e.\u003c\/p\u003e\n\n\u003ch2 id=\"vulnerable\"\u003eIdentifying Dangerous Plaques: Echolucency, Ulceration, and Plaque Texture\u003c\/h2\u003e\n\u003cp\u003eIn patients with asymptomatic carotid stenosis (ACS)—meaning narrowing of the neck arteries that hasn't yet caused a stroke—the risk of stroke is now lower with intensive medical therapy than with either stenting or surgery (endarterectomy). This makes it critically important to identify the few patients (perhaps 10–15%) who could still benefit from intervention. Ultrasound helps identify these high-risk patients by detecting specific \"vulnerable\" plaque features.\u003c\/p\u003e\n\n\u003ch3\u003eEcholucency and Juxtaluminal Black Plaque Area\u003c\/h3\u003e\n\u003cp\u003eEcholucent plaques appear dark on ultrasound, meaning they are soft and fat-rich rather than dense and calcified. Of particular concern is the \u003cstrong\u003ejuxtaluminal black plaque area (JBA)\u003c\/strong\u003e—a dark area right next to the artery opening, which may represent thrombus (blood clot) and predicts a higher risk of stroke.\u003c\/p\u003e\n\u003cp\u003eNicolaides and colleagues studied \u003cstrong\u003e324 patients with 50–99% carotid stenosis\u003c\/strong\u003e. They found that a gray scale median (GSM) of ≤15 (very dark plaque) and JBA ≥8 mm² were independent predictors of the presence of hemispheric symptoms (symptoms related to one side of the brain). This model identified a high-risk group with an \u003cstrong\u003eodds ratio of 6.7 (95% confidence interval, 4.08–10.91; P\u0026lt;0.001)\u003c\/strong\u003e—meaning these patients were nearly 7 times more likely to have symptoms.\u003c\/p\u003e\n\u003cp\u003eMarkus and colleagues reported that the combination of echolucency with microemboli detected on transcranial Doppler was associated with a marked increase in stroke risk.\u003c\/p\u003e\n\n\u003ch3\u003eUlceration\u003c\/h3\u003e\n\u003cp\u003ePlaque ulceration—a crater or break in the surface of the plaque—is another dangerous feature. The North American Symptomatic Carotid Endarterectomy (NASCET) Study first showed that plaque ulceration detected by angiography predicted a higher risk of stroke. However, angiograms only show the inside of the artery lumen. The best way to assess carotid ulceration is actually \u003cstrong\u003e3D ultrasound\u003c\/strong\u003e, which can see the plaque surface in detail.\u003c\/p\u003e\n\u003cp\u003eIn 2011, the author's team reported findings from patients with ulcers visible on 3D ultrasound:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003ePatients with \u003cstrong\u003e3 or more ulcers\u003c\/strong\u003e in either or both carotid arteries had a risk very similar to that of patients with microemboli on transcranial Doppler\u003c\/li\u003e\n  \u003cli\u003e4% of patients had ≥3 ulcers, 6% had microemboli, and 10% had either microemboli or ≥3 ulcers\u003c\/li\u003e\n  \u003cli\u003ePatients with 3 or more ulcers in either carotid were more likely to have a \u003cstrong\u003estroke or death within 3 years (18% vs. 2%; P=0.03)\u003c\/strong\u003e, regardless of which side the ulcers were found on\u003c\/li\u003e\n  \u003cli\u003eThe 3-year risk of stroke or death was \u003cstrong\u003e20% with microemboli vs. 2% without (P\u0026lt;0.003)\u003c\/strong\u003e\n\u003c\/li\u003e\n  \u003cli\u003eThe annual rate of ipsilateral stroke (stroke on the same side as the carotid disease) was 0.8%\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eIn 2014, the team assessed ulcer volume as a predictor of cardiovascular risk among \u003cstrong\u003e349 patients\u003c\/strong\u003e followed for \u003cstrong\u003e5 years\u003c\/strong\u003e. Patients with total ulcer volume ≥5 mm³ had a significantly higher risk of stroke, transient ischemic attack (TIA, a \"mini-stroke\"), or death (P=0.009), and also of stroke\/TIA\/death\/heart attack\/revascularization (P=0.017).\u003c\/p\u003e\n\n\u003ch3\u003ePlaque Texture\u003c\/h3\u003e\n\u003cp\u003eAn emerging field is the analysis of plaque texture using complex mathematical analysis of radiofrequency signals from carotid ultrasound. While these analyses are difficult to conceptualize as mathematical constructs, they provide information on how pixel intensities are distributed within plaques, yielding \"texture parameters\" such as coarseness or contrast.\u003c\/p\u003e\n\u003cp\u003eThese measures have already shown promise:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eThey can differentiate between symptomatic and asymptomatic patients\u003c\/li\u003e\n  \u003cli\u003eThey were superior to assessment of plaque shape\u003c\/li\u003e\n  \u003cli\u003eThey predicted events better than a combination of a history of prior events and plaque features such as plaque area and gray scale median\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eIn a 2014 study, the author's team evaluated \u003cstrong\u003e298 patients\u003c\/strong\u003e with carotid atherosclerosis using 3D ultrasound at baseline and after 1 year. They measured carotid plaque volume and \u003cstrong\u003e376 measures of plaque texture\u003c\/strong\u003e. Patients were followed for up to 5 years (median follow-up 3.12 years, range 0.77–4.66 years) for heart attack, TIA, and stroke.\u003c\/p\u003e\n\u003cp\u003eThe results showed that changes in texture and total plaque volume combined provided the \u003cstrong\u003ebest predictor\u003c\/strong\u003e of vascular events. In multivariate Cox regression:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eChanges in plaque texture: median hazard ratio \u003cstrong\u003e1.4 (P\u0026lt;0.001)\u003c\/strong\u003e—meaning each unit increase in texture change raised risk by 40%\u003c\/li\u003e\n  \u003cli\u003eTotal plaque volume: median hazard ratio \u003cstrong\u003e1.5 per 100 mm³ (P\u0026lt;0.001)\u003c\/strong\u003e—meaning each 100 mm³ increase in plaque volume raised risk by 50%\u003c\/li\u003e\n  \u003cli\u003eThe Framingham risk score was \u003cstrong\u003enot\u003c\/strong\u003e a significant predictor in this model\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"tcd\"\u003eTranscranial Doppler: Listening to Blood Flow in the Brain\u003c\/h2\u003e\n\u003cp\u003eTranscranial Doppler (TCD) is an ultrasound technique that measures blood flow in the brain's blood vessels. It serves several important functions in stroke prevention.\u003c\/p\u003e\n\n\u003ch3\u003eEmbolus Detection\u003c\/h3\u003e\n\u003cp\u003eDetection of microemboli (tiny particles or clots traveling in the bloodstream) is perhaps the best-validated way to identify which patients with asymptomatic carotid stenosis (ACS) are at high risk of stroke. In 2005, the author's team reported a study of \u003cstrong\u003e319 patients with ACS\u003c\/strong\u003e:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003e\n\u003cstrong\u003e10%\u003c\/strong\u003e had two or more microemboli detected in \u003cstrong\u003eone hour\u003c\/strong\u003e of monitoring\u003c\/li\u003e\n  \u003cli\u003eTheir \u003cstrong\u003e1-year risk of stroke was 15.6%\u003c\/strong\u003e, compared to only \u003cstrong\u003e1%\u003c\/strong\u003e among patients without microemboli\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eThis very clearly distinguishes which patients with ACS could benefit from intervention. Patients with microemboli could benefit from procedures like carotid endarterectomy (surgical removal of plaque) or stenting, which carry a periprocedural risk of stroke or death of about \u003cstrong\u003e3–4%\u003c\/strong\u003e. Patients without microemboli would be better treated with intensive medical therapy alone.\u003c\/p\u003e\n\u003cp\u003eIn 2010, a study of \u003cstrong\u003e468 patients\u003c\/strong\u003e (199 enrolled before 2003 and 269 after 2003) confirmed that intensive medical therapy reduced the percentage of patients with microemboli, as described earlier (from 12.6% to 3.7%).\u003c\/p\u003e\n\n\u003ch3\u003ePatent Foramen Ovale (PFO) Detection\u003c\/h3\u003e\n\u003cp\u003eA patent foramen ovale (PFO) is a small opening between the upper chambers of the heart that fails to close after birth. In some people, this \"hole in the heart\" allows blood clots to pass from the right side of the heart to the left side, where they can travel to the brain and cause a stroke. This is called \u003cstrong\u003eparadoxical embolism\u003c\/strong\u003e.\u003c\/p\u003e\n\u003cp\u003eTCD saline studies (also called bubble studies) are used to detect PFO. During this test, a small amount of saline with tiny bubbles is injected into a vein while the doctor uses TCD to listen for those bubbles crossing to the brain. This technique is actually \u003cstrong\u003emore sensitive than trans-esophageal echocardiography (TEE)\u003c\/strong\u003e for detecting PFO, and the size of the right-to-left shunt (RLS) as assessed by TCD is more predictive of recurrent stroke than merely detecting a PFO.\u003c\/p\u003e\n\u003cp\u003eThe review notes an important clinical challenge: even among patients with cryptogenic stroke (stroke of unknown cause), approximately \u003cstrong\u003ehalf\u003c\/strong\u003e of PFOs are \u003cstrong\u003eincidental\u003c\/strong\u003e—meaning they are not the cause of the stroke. Therefore, before recommending percutaneous closure of a PFO (a procedure to plug the hole), doctors need ways to identify patients who are likely to benefit.\u003c\/p\u003e\n\u003cp\u003eClinical clues that a PFO may have caused a stroke (paradoxical embolism) include:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eProlonged sitting (which increases the risk of blood clots in the legs)\u003c\/li\u003e\n  \u003cli\u003eShortness of breath (dyspnea) at the onset of stroke\u003c\/li\u003e\n  \u003cli\u003eLow oxygen (pO₂) and carbon dioxide (pCO₂) levels at the time of stroke\u003c\/li\u003e\n  \u003cli\u003ePrevious history of deep vein thrombosis (DVT), pulmonary embolism, or varicose veins\u003c\/li\u003e\n  \u003cli\u003eHistory of sleep apnea\u003c\/li\u003e\n  \u003cli\u003eWaking up with stroke symptoms (possibly related to sleep apnea)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eThe author explains that a paradoxical embolus is essentially a pulmonary embolus (blood clot in the lungs) that \"turned left through a PFO instead of turning right to go into the pulmonary artery.\" This is why the clinical clues overlap so much with those of pulmonary embolism.\u003c\/p\u003e\n\n\u003ch2 id=\"implications\"\u003eWhat This Means for Patients\u003c\/h2\u003e\n\u003cp\u003eThis research has several direct implications for patients concerned about stroke risk:\u003c\/p\u003e\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePlaque measurement matters more than cholesterol numbers alone.\u003c\/strong\u003e Two patients with identical cholesterol levels can have very different plaque burdens—and the plaque burden is what determines risk. Asking your doctor about carotid plaque measurement (TPA) can provide a more personalized picture of your risk.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eTreatment can be guided by plaque response.\u003c\/strong\u003e If your plaque is progressing despite treatment, it may be time to intensify therapy or consider additional factors. If your plaque is regressing, you'll know your treatment is working.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eGut health may affect stroke risk.\u003c\/strong\u003e The finding that gut microbiome metabolites like TMAO are linked to unexplained atherosclerosis suggests that diet could play a role in stroke prevention beyond traditional risk factors. However, more research is needed before specific dietary recommendations can be made.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eNot everyone with carotid stenosis needs surgery.\u003c\/strong\u003e With modern intensive medical therapy, most patients with asymptomatic carotid stenosis are safer with medication than with stenting or surgery. Tests like TCD embolus detection help identify the 10–15% who might benefit from intervention.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003ePFO closure decisions should be individualized.\u003c\/strong\u003e If you've had a stroke and have a PFO, the presence of additional clues (like DVT history or sleep apnea) can help determine whether the PFO was the culprit or just an incidental finding.\u003c\/li\u003e\n\u003c\/ol\u003e\n\n\u003ch2 id=\"limitations\"\u003eStudy Limitations\u003c\/h2\u003e\n\u003cp\u003eThis article is a narrative review, not a single clinical trial. It draws on multiple studies conducted over several decades, largely from one research center. Some specific limitations worth noting:\u003c\/p\u003e\n\u003cul\u003e\n  \u003cli\u003eMany of the key findings come from a single center (Western University's Stroke Prevention \u0026amp; Atherosclerosis Research Centre) and may not apply equally in all settings\u003c\/li\u003e\n  \u003cli\u003eThe \"treating arteries\" approach was implemented without a randomized controlled trial; the \u0026gt;80% risk reduction was observed by comparing patients before and after 2003, which could be influenced by other changes in care over time\u003c\/li\u003e\n  \u003cli\u003eThe microbiome findings, while statistically significant, are observational and do not prove that TMAO or p-cresyl sulfate \u003cem\u003ecause\u003c\/em\u003e atherosclerosis—only that they are associated with it\u003c\/li\u003e\n  \u003cli\u003e3D plaque volume measurement is technically challenging and requires extensive training; about a third of people cannot master it\u003c\/li\u003e\n  \u003cli\u003eThe plaque texture analysis is an emerging field that is mathematically complex and not yet widely available in clinical practice\u003c\/li\u003e\n  \u003cli\u003eThe PFO section was cut short in the original text, so some details of that discussion are not included here\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2 id=\"recommendations\"\u003eRecommendations for Patients\u003c\/h2\u003e\n\u003cp\u003eBased on this research, here are practical steps patients can discuss with their healthcare providers:\u003c\/p\u003e\n\u003col\u003e\n  \u003cli\u003e\n\u003cstrong\u003eAsk about carotid plaque measurement.\u003c\/strong\u003e If you have risk factors for stroke or heart disease, ask whether a carotid ultrasound to measure plaque area (TPA) would be useful—even if a standard carotid ultrasound was normal. Plaque burden is a stronger predictor than IMT.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eIf you have carotid stenosis, ask about TCD monitoring.\u003c\/strong\u003e Microembolus detection can tell you whether you're in the 10% of patients with a 15.6% 1-year stroke risk (who may need intervention) or the 90% with a 1% risk (who are better treated with medication).\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eIf you've had a cryptogenic stroke and have a PFO, ask whether TCD saline studies would help.\u003c\/strong\u003e The size of the right-to-left shunt, along with clinical clues like DVT history or sleep apnea, can guide whether PFO closure is worth considering.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eFollow up with repeat plaque measurements.\u003c\/strong\u003e Carotid plaque changes over months, not years. Regular monitoring can tell you whether your treatment is actually working.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eDon't rely solely on cholesterol levels.\u003c\/strong\u003e Even patients with very low LDL-C can have plaque progression. If your plaque is progressing despite \"good\" cholesterol numbers, talk to your doctor about additional strategies.\u003c\/li\u003e\n  \u003cli\u003e\n\u003cstrong\u003eConsider the gut-heart connection.\u003c\/strong\u003e While specific dietary recommendations await more research, limiting excess red meat (a source of carnitine) and being mindful of dietary patterns that support a healthy gut microbiome are reasonable steps.\u003c\/li\u003e\n\u003c\/ol\u003e\n\u003cp\u003eThe author's closing message is clear: ultrasound methods for stroke prevention are underutilized. With the burden of stroke increasing in aging populations, wider adoption of these techniques could meaningfully reduce the toll of this devastating disease.\u003c\/p\u003e\n\n\u003c!-- ddn:faq:start --\u003e\n\u003ch2 id=\"ddn-faq\"\u003eFrequently Asked Questions\u003c\/h2\u003e\n\u003ch3\u003eWhy is measuring plaque burden better than measuring intima-media thickness (IMT)?\u003c\/h3\u003e\n\u003cp\u003ePlaque area is a much stronger predictor of heart attack and stroke risk than IMT. In a 2002 study, 5-year risk rose from 5.6% to 19.5% across increasing plaque-area quartiles, even after adjusting for cholesterol, blood pressure, and smoking. IMT, as measured by the Mannheim consensus, does not represent true atherosclerosis.\u003c\/p\u003e\n\u003ch3\u003eWhat is total plaque area (TPA) and how is it measured?\u003c\/h3\u003e\n\u003cp\u003eTotal plaque area is the sum of all carotid plaque areas, measured by tracing each plaque in a lengthwise ultrasound image. Plaques between the collarbone and the jaw on both sides are included. It is reliable (intraclass correlation 0.94), quick to perform, and was first used in 1986. Higher TPA predicts higher cardiovascular risk.\u003c\/p\u003e\n\u003ch3\u003eWhat does 'treating arteries instead of risk factors' mean?\u003c\/h3\u003e\n\u003cp\u003eInstead of only targeting blood pressure and LDL cholesterol numbers, doctors use repeat plaque measurements to guide therapy. The goal is to stop plaque progression or achieve regression. At one center, this approach reversed the proportion of patients with progression versus regression, and the 2-year risk of stroke and heart attack fell by more than 80% compared with prior treatment.\u003c\/p\u003e\n\u003ch3\u003eCan gut microbiome metabolites explain unexplained atherosclerosis?\u003c\/h3\u003e\n\u003cp\u003eIn a 2016–2018 study of over 3,000 clinic patients, those with unexplained atherosclerosis (more plaque than expected) had higher blood levels of gut-derived metabolites like TMAO and p-cresyl sulfate. These metabolites were lower in patients with less plaque than expected. This suggests diet and gut bacteria may influence stroke risk beyond traditional factors, but causality isn't proven.\u003c\/p\u003e\n\u003ch3\u003eHow does transcranial Doppler (TCD) help prevent stroke?\u003c\/h3\u003e\n\u003cp\u003eTCD uses ultrasound to detect microemboli—tiny blood clots traveling to the brain. In a 2005 study of 319 patients with asymptomatic carotid stenosis, those with two or more microemboli in one hour had a 15.6% one-year stroke risk, versus 1% in those without. This helps identify which patients might need surgery or stenting instead of just medication.\u003c\/p\u003e\n\u003ch3\u003eIf I have asymptomatic carotid stenosis, do I need surgery?\u003c\/h3\u003e\n\u003cp\u003eMost patients with asymptomatic carotid stenosis are safer with intensive medical therapy than with stenting or surgery. Only about 10–15% might benefit from intervention. Tests such as TCD for microemboli or ultrasound for three or more plaque ulcers can identify higher-risk patients, who may then consider procedures, which carry a periprocedural stroke or death risk of about 3–4%.\u003c\/p\u003e\n\u003ch3\u003eHow can I know if a PFO caused my stroke?\u003c\/h3\u003e\n\u003cp\u003eA patent foramen ovale (PFO) is an opening in the heart that can let clots cross to the brain. But half of PFOs in cryptogenic stroke are incidental. TCD saline (bubble) studies help detect PFOs, and the shunt size is more predictive than just presence. Clinical clues like deep vein thrombosis, sleep apnea, or prolonged sitting suggest the PFO was the cause.\u003c\/p\u003e\n\u003c!-- ddn:faq:end --\u003e\n\n\u003ch2 id=\"source\"\u003eSource Information\u003c\/h2\u003e\n\u003cp\u003e\u003cstrong\u003eOriginal article title:\u003c\/strong\u003e Spence 2020 Uses of ultrasound in stroke prevention\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor:\u003c\/strong\u003e Prof. J. David Spence, CM, MD, FRCPC, FAHA\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eAffiliation:\u003c\/strong\u003e Stroke Prevention \u0026amp; Atherosclerosis Research Centre, Robarts Research Institute, Western University, London, ON, Canada\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eJournal:\u003c\/strong\u003e Cardiovascular Diagnosis and Therapy, Vol 10, No 4, August 2020, pages 955–964\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003ePublication details:\u003c\/strong\u003e Review Article on Advanced Imaging in The Diagnosis of Cardiovascular Diseases. Submitted Oct 22, 2019; accepted Dec 09, 2019. doi: 10.21037\/cdt.2019.12.12\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003eNote: This patient-friendly article is based on peer-reviewed research. It is intended for informational purposes and does not replace professional medical advice. Always consult your healthcare provider about your specific medical situation.\u003c\/em\u003e\u003c\/p\u003e","brand":"DiagnosticDetectives.Com","offers":[{"title":"Default Title","offer_id":47423022956700,"sku":null,"price":0.0,"currency_code":"CHF","in_stock":true}],"url":"https:\/\/diagnosticdetectives.ch\/fr\/products\/using-ultrasound-to-prevent-stroke-a-patients-guide","provider":"DiagnosticDetectives.Com","version":"1.0","type":"link"}