Seeing the Problem Before It Happens: How Carotid Ultrasound Helps Predict Heart Attacks and Strokes

Table of Contents

• Key Points
• Why This Matters: The Burden of Cardiovascular Disease
• The Problem with Traditional Risk Calculators
• How Carotid Ultrasound Works
• Measuring Plaque: IMT, TPA, and TPV Explained
• What the Research Shows: Large Outcome Studies
• Meta-Analyses: Carotid Plaque Beats IMT
• Direct Comparison: Carotid Plaque vs. Coronary Calcium
• Could Treatment Shrink Carotid Atherosclerosis?
• What Should Be Measured — and What Is Practical?
• Clinical Implications for Patients
• Limitations and Open Questions
• Recommendations and Actionable Advice
• Frequently Asked Questions
• Source Information

Key Points

• Carotid ultrasound measures plaque buildup in neck arteries and predicts heart attacks and strokes better than traditional risk factors or intima-media thickness alone.
• In the BioImage study of 5,808 healthy subjects, carotid total plaque volume was noninferior to coronary calcium for predicting cardiovascular events, without radiation.
• European guidelines suggest considering a carotid scan to refine risk estimates, especially for people classified as intermediate risk by standard calculators.
• A meta-analysis of 41 trials with 18,307 participants found active treatment reduced cardiovascular events and death, but IMT reduction did not correlate with fewer events.
• Total plaque area is considered the most practical measurement for clinical practice because it is reproducible, vendor-independent, and requires no extra software.

Why This Matters: The Burden of Cardiovascular Disease

Whenever illness or injury occurs, a natural question arises: could it have been prevented? That question drives a huge amount of ongoing research into identifying which factors predict future risk — so that risk can be managed and eventually reduced.

The INTERHEART study showed that major, independent cardiovascular risk factors together contribute to 90% of cardiovascular events (heart attacks and strokes). According to the Swiss Federal Statistical Office, cardiovascular and cancer diseases remained the leading causes of death in Switzerland in 2015. National Health Accounts were highest for cardiovascular disease, at 15.6%. Cardiovascular disease together with cancer accounted for 22% of healthcare spending in Switzerland.

Preventing diseases linked to atherosclerosis is therefore a primary healthcare issue. Traditionally, primary care doctors assess atherosclerosis risk by looking for established risk factors. The modification of just seven risk factors has great potential to prevent premature illness and death across the population. Those seven factors are:

• Smoking
• High blood pressure
• High cholesterol
• Obesity
• Sedentary (inactive) lifestyle
• Malnutrition (poor diet)
• Diabetes mellitus (high blood sugar)

Despite this, many patients arrive at hospital with their first ischaemic event. An ischaemic event is a heart attack or stroke caused by blocked blood flow. Yet those same patients had been classified as low-risk by standard risk calculators such as PROCAM and SCORE.

The Problem with Traditional Risk Calculators

Direct visualisation of atherosclerosis may therefore be warranted. Seeing plaque in the arteries could help reclassify people according to their true individual risk, rather than relying on risk formulas alone.

The authors previously studied two populations — one from Olten, Switzerland, and one from Koblenz, Germany. They showed that the sensitivity of global risk calculators such as PROCAM and SCORE is low for detecting advanced carotid atherosclerosis. Sensitivity is the ability to correctly detect disease when it is present. Advanced carotid atherosclerosis was measured as the total carotid plaque area. They also found that agreement between PROCAM and SCORE regarding risk category appears to be limited. This is the rationale for adding ultrasound to atherosclerosis management — the topic of this review.

How Carotid Ultrasound Works

Carotid ultrasound is performed with a linear array probe — a flat-headed scanning device — at a high frequency of at least 7 MHz. This frequency is needed to obtain sufficient resolution to image very small structures. Image resolution depends on the depth of the tissue and the frequency used, and is usually around 0.3 mm.

The anatomical region of interest is the tunica intima, the innermost layer of the artery wall. It is assessed with 2D imaging without Doppler (the colour-flow overlay used in some scans). Intima-media thickness (IMT) is the distance between the endothelium (the inner lining of the artery) and the tunica adventitia (the outer supporting layer).

According to the Mannheim consensus, IMT is preferably measured in the far wall of the last 10 mm of the common carotid artery. The Mannheim consensus is an international agreement on how to standardise these measurements. One major problem with carotid IMT measurements is that researchers use many different methods, as described extensively elsewhere.

The variability of carotid IMT measurements is lowest in the far wall of the common carotid artery when carotid plaque is excluded. However, this improvement in reproducibility comes with a real cost: it reduces the ability to predict cardiovascular events.

Carotid ultrasound has several practical advantages for clinical use. It is rapid and reliable, it is vendor-independent (meaning no additional software costs for tracing plaque on the image), and results can be obtained without extra software.

Measuring Plaque: IMT, TPA, and TPV Explained

The definition of atherosclerotic plaque versus non-atherosclerotic intimal thickening has not been applied uniformly in the literature. For clinical purposes, the most commonly used definition is an IMT increase of more than 1.5 mm, or a focal thickening of more than 50% compared with adjacent structures.

Researchers have proposed many different ways to quantify carotid plaque. These are summarised in the article's reference table and include:

• Increase of IMT greater than 1.0 mm (Spence, 1991)
• Doubling of IMT (Spence, 1991; Mannheim Consensus)
• Thickening of IMT greater than 1.2 mm (Handa)
• Subjective visual assessment (Polak; Peters, for plaque burden from none to severe)
• Encroaching into the lumen by 0.5 mm (Mannheim Consensus)
• Increase of IMT of 1.5 mm or more (Mannheim Consensus; Spence)
• Texture changes (Singh)
• Plaque present yes or no (Nambi)
• Number of plaques (Plichart)
• Plaque thickness in millimetres (Rundek)
• Plaque area in square millimetres (Spence)
• Plaque volume in cubic millimetres (Baber)
• Echo lucency (brightness on grayscale imaging) (Stein)
• Plaque vascularity using a contrast agent (Coli)

Two newer measures are central to this review. The first is total plaque area (TPA) — the sum of the longitudinal area of all plaques in the carotid wall. It is measured from the clavicles up to the jaw, using multiple angles. This captures the full longitudinal circumference of all plaques in the carotid tree, including the proximal brachial artery if possible.

The second is total plaque volume (TPV). This recently became available using the Philips iU 22 ultrasound system, equipped with a single-sweep volumetric transducer. That probe covers 3.8 cm of the carotid artery and visualises the distal part of the common carotid artery, the bulb, and the proximal parts of the internal carotid artery. Off-line software calculates plaque areas from all the transversal images to produce the total plaque volume.

Because the field of view is only 3.8 cm, some plaques located proximal or distal to the transducer are missed. Those plaques are instead captured by the total plaque area derived from longitudinal carotid images. The advantage of the longitudinal plaque imaging (TPA technique) is its high reproducibility, its vendor independence, and the fact that no additional software is needed. The correlation between TPA and TPV is strong: the correlation coefficient is r² = 0.921 (p <0.0001).

The most complete picture of total plaque burden therefore comes from TPA, followed by TPV and then IMT. However, TPV can capture plaques located laterally in the vessel wall that the TPA method cannot see. For this reason, TPA should also incorporate lateral plaque seen on transversal images.

What the Research Shows: Large Outcome Studies

Outcome studies linking the amount of carotid atherosclerosis to heart and brain ischaemic events are numerous. The largest cohorts — each with at least 4,000 participants — are summarised below.

One of the first studies on the prognostic impact of carotid ultrasound imaging appeared in 1991. In 1,288 Finnish men, coronary event risk rose as follows:

• Intimal thickening: 2.2-fold increase in risk (p = not significant)
• Small carotid plaques: 4.2-fold increase (p <0.01)
• Stenotic plaque (narrowing of the artery): 6.7-fold increase (p <0.01)

In 1995, Japanese researchers found that carotid stenosis and plaque ulcerations predicted ischaemic stroke. In 1996, Belcaro and colleagues found that increases in plaque burden in the carotid and femoral arteries predicted cardiovascular events and death in 2,322 asymptomatic people after six years of follow-up. The same finding held in 13,221 low-risk subjects (the CAFES-CAVE study) after 10 years.

Spence showed in 2002 that TPA predicted cardiovascular events, with risk increasing in the higher quartiles of total plaque area. That analysis included 1,686 patients, most of whom had already had a stroke or transient ischaemic attack (TIA — a "mini-stroke" that resolves). Of these, 684 were originally primary care patients. For that primary care group, adding posterior test probabilities based on the Bayes theorem improved discrimination for predicting future heart attacks after 3.3 years of follow-up. The area under the curve was 0.68 for the NCEP III risk score. The area under the curve is a measure of how well a test separates people who will have events from those who won't. The area under the curve rose to 0.75 for the TPA-based posterior test probability (p = 0.038).

Other landmark findings include:

• 2003 (Hollander, Rotterdam study): In 6,913 prospectively followed healthy subjects, carotid IMT (including regions with plaque) was a stronger predictor of subsequent stroke than carotid plaque alone.
• 2004 (van der Meer, Rotterdam study): In 6,389 subjects assessed for structural changes, all measures — carotid and femoral plaque, carotid IMT with plaque included, and aortic plaque — had equal predictive power for ensuing heart attacks.
• 2007 (Stein, Tromsø study): In 6,226 originally healthy people, TPA was a stronger and statistically significant marker of incident heart attacks than IMT, especially in women, after correction for several conventional risk factors. This observation remained significant after extended follow-up of 15 years.
• Xie et al. (China): In 1,734 subjects screened for future heart attacks and strokes, all measures of carotid structural change (IMT at six sites, TPA, and number of plaques) were effective for risk prediction after adjustment for conventional risk factors.
• 2010 (Lorenz, Atherosclerosis Progression Study): In 4,904 low-risk patients followed for 10 years, carotid IMT measured at the common carotid artery, the bulb, and the internal carotid artery was less predictive than the Framingham and SCORE risk models — but only 5% of these subjects actually had carotid plaques.
• 2010 (Chambless, ARIC study): In 13,145 subjects followed for 15 years, the AUC increased significantly when carotid IMT or carotid plaque was added to traditional risk factors.
• 2011 (Mathiesen, Tromsø study): In 6,584 subjects, TPA — but not common carotid IMT — predicted incident ischaemic stroke after multivariate adjustment.
• 2011 (Polak, Framingham Offspring Study): In 2,965 members followed for 7 years, both internal carotid IMT and internal carotid plaque formation (defined as IMT of 1.5 mm or more) significantly improved the AUC compared with the Framingham risk equation.

The article notes that Naqvi has published an excellent, comprehensive overview of outcome studies performed with carotid ultrasound.

Below are the specific hazard ratios (HR — how many times more likely an event is in one group versus another) from the major cohort studies:

• CAFES-CAVE (10,000 people, death): No plaque — 0.1% event rate; carotid plaque — 3.0% event rate
• Rotterdam (6,389 people, heart attack): Plaque yes/no — HR 1.6, 95% confidence interval (CI) 1.2–2.2
• Rosvall (5,163 people, heart attack): Plaque yes/no — HR 1.8, 95% CI 1.5–2.9; IMT lowest third vs highest third — HR 1.5, 95% CI 0.8–2.6
• Rosvall (5,163 people, stroke): Plaque yes/no — HR 1.3, 95% CI 0.8–2.1; IMT tertiles — HR 2.5, 95% CI 1.2–5.4
• ARIC men (5,552 people, heart attack): IMT ≥1.0 mm — HR 1.9, 95% CI 1.3–2.7
• ARIC women (7,685 people, heart attack): IMT ≥1.0 mm — HR 5.1, 95% CI 3.1–8.4
• ARIC women (7,685 people, stroke): IMT <0.6 vs >1.0 mm — HR 8.5, 95% CI 3.5–20.7
• ARIC men (6,349 people, stroke): IMT <0.6 vs >1.0 mm — HR 3.6, 95% CI 1.5–9.2
• Tromsø (6,257 people, heart attack): TPA tertiles — HR 2.5, 95% CI 2.1–3.0
• Tromsø men (6,226, heart attack): TPA tertiles — HR 1.6, 95% CI 1.04–2.4; IMT quartiles — HR 1.7, 95% CI 0.98–3.1
• Tromsø women (6,226, heart attack): TPA tertiles — HR 4.0, 95% CI 2.2–7.2; IMT quartiles — HR 2.9, 95% CI 1.1–7.7
• Tromsø men (6,844, stroke): TPA tertiles — HR 1.7, 95% CI 1.2–2.5; IMT quartiles — HR 1.4, 95% CI 0.8–2.4
• Tromsø women (6,844, stroke): TPA tertiles — HR 1.6, 95% CI 1.04–2.5; IMT quartiles — HR 1.3, 95% CI 0.7–2.3
• MESA (6,698 people, cardiovascular disease): IMT quartile — HR 1.7, 95% CI 1.2–2.5
• MESA (4,955 people, cardiovascular disease): Carotid score — HR 1.2, 95% CI 1.2–1.4

Meta-Analyses: Carotid Plaque Beats IMT

Several more recent reviews and meta-analyses (studies that pool data from many smaller studies) have tried to put different imaging methods into perspective.

Simons analysed the prognostic impact of carotid IMT compared with carotid plaques using c-statistics (a statistical measure of prediction accuracy). Carotid IMT was not superior to the Framingham risk score for predicting ischaemic heart disease.

In 2012, Den Ruijter and colleagues published a meta-analysis of 14 population-based cohorts with data from 45,828 subjects, comparing common carotid IMT with the Framingham risk score. They found a modest improvement in reclassification and hazard ratio, but not for AUC:

• Framingham AUC: 0.76 (95% CI 0.75–0.76)
• Carotid IMT AUC: 0.76 (95% CI 0.75–0.77)
• Comparison of AUCs: no statistically significant improvement

Inaba and colleagues published a meta-analysis of 11 population-based studies that included 54,336 patients. Compared with carotid IMT, carotid plaque was a significantly better predictor of future heart attacks:

• Carotid plaque AUC: 0.64 (95% CI 0.61–0.67)
• Carotid IMT AUC: 0.61 (95% CI 0.59–0.64)
• Relative diagnostic odds ratio: 1.4 (95% CI 1.1–1.8); p = 0.04

Direct Comparison: Carotid Plaque vs. Coronary Calcium

Early outcome studies compared one imaging method against traditional risk factors. Two large-scale studies — BioImage and MESA — went further and directly compared coronary calcification (calcium deposits in the heart's arteries) with carotid ultrasound imaging.

The BioImage study involved 5,808 healthy subjects and was published in 2015 by Baber and colleagues. It directly compared the total volume of carotid plaques acquired with the Philips iU 22 ultrasound system. This was compared against the presence and amount (score) of coronary calcium. Coronary calcium measures the total calcified plaque burden across the whole coronary tree. In a low- to intermediate-risk population, carotid total plaque volume was noninferior (no worse than) coronary calcium for predicting cardiovascular events — and it avoided radiation.

The MESA study included 6,779 healthy subjects and was published by Gepner and colleagues in 2015. It compared the presence of coronary calcium with the presence of carotid plaques and carotid IMT above the 75th percentile. Only coronary calcium and carotid plaque presence were predictive; carotid IMT was not. For predicting stroke or transient ischaemic attack, only the presence of carotid plaques was predictive after 9.5 years of observation.

For context, here are the key coronary artery calcification (CAC) findings:

• Raggi (10,377 people, death): AUC 0.72–0.78, p = 0.001
• Detrano (6,772 people, major adverse cardiovascular events): AUC 0.79–0.83, p = 0.009
• Arad (4,903 people, major events): AUC 0.68–0.79, p = 0.001
• Erbel (4,129 people, major events): AUC 0.65–0.76, p = 0.001
• MESA (6,814 people, major events): AUC 0.75–0.80, p = 0.001
• MESA (6,698 people, cardiovascular disease): highest vs lowest quartile — HR 4.4, 95% CI 2.8–6.8
• MESA (4,955 people, cardiovascular disease): HR 1.78, 95% CI 1.16–1.98
• MESA (6,814 people, cardiovascular disease): CAC score of 0 — event rate 1.3–5.6%; CAC score above 300 — event rate 13.1–25.6%

Could Treatment Shrink Carotid Atherosclerosis?

A meta-analysis of 41 randomised trials, including 18,307 participants and published in 2010, showed that active treatment significantly reduced cardiovascular events and all-cause death. However, there was no significant relationship between the reduction in IMT and cardiovascular events. This was later confirmed in a second meta-analysis by Goldberger and colleagues.

The picture was not confirmed in the IMPROVE-IT study, which included 3,703 high-risk patients (average Framingham risk score 22%). There, carotid IMT and its progression — but not carotid plaque — led to significant improvements in risk reclassification.

This means that measuring plaque burden may be more useful than measuring IMT alone when tracking whether treatment is working.

What Should Be Measured — and What Is Practical?

Regardless of traditional risk factors, structural arterial changes revealed by atherosclerosis imaging are associated with adverse cardiovascular outcomes. Screening with atherosclerosis imaging has not received a class I recommended indication in primary care (the strongest level of medical recommendation). Yet most cardiovascular events occur in people who are not classified as high risk by traditional risk factors. By inference, additional testing might help with further risk stratification.

Adding carotid plaque quantification to cardiovascular risk prediction has significantly improved discrimination and reclassification of subjects in primary care. Carotid plaque is caused by atherosclerosis involving foam cells, smooth muscle cells, calcifications, macrophages, lipid cores, and a fibrous cap. However, the definition of plaque on ultrasound is not uniform.

Several factors influence which test a clinician chooses:

• Expertise and availability — unavoidable requirements
• Cost
• Radiation burden
• Validity
• Reproducibility
• Feasibility
• Test rapidity
• The ability to track atherosclerosis over time to observe treatment effects

In the authors' opinion, carotid total plaque area (TPA) is probably the most suited for clinical practice. They recommend following this with a search for femoral bifurcation plaque and aortic plaque. They also recommend use of the ankle-arm index, which compares blood pressure at the ankle and arm. Another option is measurement of plaque height with ultrasound in various vascular beds.

More sophisticated tests are often time-consuming and costly, or involve radiation exposure — though it has recently been shown that radiation exposure can be reduced. The acquisition of IMT is technically demanding. It requires an ECG signal to time images during diastole (the heart's resting phase) and a room temperature of 22–25°C. Plaque should not be excluded from measurements, in order to improve predictive accuracy for cardiovascular events.

Laclaustra reported a comparative study that used the presence (score above 0) and extent (score above 300) of coronary calcium as the gold standard. That study compared traditional risk factors, 3D carotid plaque volumes, and 3D femoral plaque volumes for correctly detecting coronary calcium within the same subject. Both carotid and femoral plaque were better markers for the presence and extent of coronary calcifications than traditional risk factors. There was a tendency toward better performance of femoral over carotid plaque, especially in smokers.

Clinical Implications for Patients

Cardiovascular risk increases with the carotid plaque burden quantified as total plaque area. What does this mean for patients?

• If you have been told you are "low risk" or "intermediate risk" based on a calculator, a carotid ultrasound may reveal plaque you didn't know about. A carotid ultrasound may change your true risk category.
• Carotid plaque measurement appears more informative than intima-media thickness for predicting heart attacks and strokes.
• Carotid plaque volume has predictive power comparable to coronary calcium scoring, but without radiation exposure.
• The European Joint ESC guidelines now say a carotid artery scan should be considered for adjusting risk levels, especially in intermediate-risk subjects.
• Tracking plaque over time — its presence, progression, stability, or regression — may be a valuable clinical tool for optimising the intensity of preventive therapies.

Ways to incorporate imaging results into clinical decision-making include using "arterial age" instead of chronological age in risk equations. Another way is calculating post-test risk using the sensitivity and specificity of a given carotid plaque burden result. For example, the Bayes theorem formula for the post-test probability of disease when a test is positive is: (prevalence × sensitivity) ÷ [prevalence × sensitivity + (1 – prevalence) + (1 – specificity)]. The formula for a negative test is: [prevalence × (1 – sensitivity)] ÷ [prevalence × (1 – sensitivity) + specificity × (1 – prevalence)].

In subjects with low or intermediate cardiovascular risk, the search for atherosclerosis may be appropriate. Ultrasound of the carotid or femoral arteries could be the primary method applied, depending on local expertise.

Limitations and Open Questions

This review is not a single new study; it is a synthesis of existing research, and several limitations are apparent across that body of work.

• The definition of carotid plaque on ultrasound is not uniform, which makes comparisons between studies difficult.
• Carotid IMT measurements are affected by a diversity of methods. Variability is only lowest when plaque is excluded from the common carotid far wall. That is the very approach that reduces event prediction.
• Carotid total plaque volume covers only a 3.8 cm field of view, so some plaques proximal or distal to the transducer are missed.
• Active treatment reduced cardiovascular events and death in a meta-analysis of 41 trials. But IMT reduction did not correlate with event reduction in that analysis. This leaves it unclear exactly how to monitor treatment success.
• Screening with atherosclerosis imaging has not been given a class I recommendation in primary care.

These gaps suggest that standardised plaque definitions and further head-to-head outcome studies remain needed.

Recommendations and Actionable Advice

Based on this review, the following practical steps can be considered by patients and their clinicians:

1. Know your risk category. If a standard calculator such as PROCAM or SCORE places you at low or intermediate risk, remember this. Many people who have a first heart attack or stroke were classified this way.
2. Ask about carotid ultrasound. The latest European Joint ESC guidelines state that carotid artery scanning should be considered for adjusting the level of risk, especially in intermediate-risk subjects.
3. Focus on total plaque area if a scan is done. The authors consider TPA the most practical measurement for clinical practice, because it is highly reproducible, vendor-independent, and does not require extra software.
4. Consider femoral and aortic plaque screening too. Where local expertise allows, ultrasound of the carotid or femoral arteries may be appropriate; femoral plaque performed at least as well as carotid plaque in one comparison, especially in smokers.
5. Track change over time. Assessing plaque presence, progression, stability, and regression may help optimise the intensity of preventive therapy, because carotid IMT reduction alone did not track with better outcomes in pooled trial data.
6. Continue to control the seven modifiable risk factors: smoking, blood pressure, cholesterol, obesity, sedentary lifestyle, poor nutrition, and diabetes.

In short, carotid ultrasound is a rapid, radiation-free, and increasingly well-validated tool. When used as an addition to — not a replacement for — traditional risk assessment, it may give both patients and doctors a clearer picture of true cardiovascular risk.

Frequently Asked Questions

What is carotid ultrasound and what does it measure?

Carotid ultrasound is an imaging test that uses sound waves to picture the neck arteries. It measures how much atherosclerosis, or fatty plaque buildup, a person has. It can assess intima-media thickness, total plaque area, and total plaque volume. The test is rapid, reliable, and does not use radiation.

Why might I need a carotid ultrasound if my risk calculator says I'm low or intermediate risk?

Many patients classified as low risk by standard calculators such as PROCAM and SCORE later have a first heart attack or stroke. European guidelines now suggest considering a carotid scan to refine risk estimates, especially for people in the intermediate-risk group. A scan may reveal plaque and change your true risk category.

How does carotid plaque measurement compare with coronary calcium scoring?

Carotid plaque volume has predictive power comparable to coronary calcium scoring, but it avoids radiation exposure. In the BioImage study of 5,808 healthy subjects, carotid total plaque volume was noninferior to coronary calcium for predicting cardiovascular events in a low- to intermediate-risk population. Both approaches can help assess risk.

What is the difference between IMT and total plaque area?

Intima-media thickness (IMT) is the distance between the inner lining and outer supporting layer of the artery wall. Total plaque area (TPA) is the sum of the longitudinal area of all plaques in the carotid wall. Research suggests plaque measures predict heart attacks and strokes better than IMT alone.

Can treatment shrink carotid plaque, and how is it monitored?

A meta-analysis of 41 randomised trials including 18,307 participants showed active treatment significantly reduced cardiovascular events and all-cause death. However, reduction in IMT did not correlate with fewer events. Measuring plaque burden may be more useful than IMT alone when tracking whether treatment is working.

What are the limitations of carotid ultrasound?

The definition of carotid plaque on ultrasound is not uniform, making study comparisons difficult. IMT measurements vary by method. Total plaque volume covers only a 3.8 cm field of view, so some plaques may be missed. Screening with atherosclerosis imaging has not received a class I recommendation in primary care.

What should I do if I have a carotid ultrasound scan?

If a scan is done, focus on total plaque area, which is highly reproducible, vendor-independent, and needs no extra software. Consider femoral and aortic plaque screening where expertise allows. Track plaque presence, progression, stability, and regression over time. Continue controlling the seven modifiable risk factors with your clinician.

If a risk calculator says I'm low or intermediate risk, when should I get a second opinion about a carotid ultrasound?

Many people who have a first heart attack or stroke were classified as low risk by standard calculators such as PROCAM and SCORE. European Joint ESC guidelines say a carotid artery scan should be considered for adjusting risk levels. This is especially true in intermediate-risk subjects. A second opinion is reasonable when a calculator places you at low or intermediate risk. A second opinion is also reasonable when you want your imaging reviewed. A second opinion is reasonable when you are deciding whether carotid plaque measurement should guide preventive treatment. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Bonn Zurich Sonographic assessment of carotidatherosclerosis

Authors: Romanens Michel, Sudano Isabella, Adams Ansgar, Schober Edward A.

Author affiliations: Vascular Risk Foundation, Olten, Switzerland; University Heart Centre, Cardiology Department, University Hospital Zurich, Switzerland; BAD Gesundheitsvorsorge und Sicherheitstechnik GmbH, Bonn, Germany; Fairfond Stiftung für Fairness im Gesundheitswesen, Olten, Switzerland.

Publication details: Swiss Medical Weekly. 2019;149:w20142. Published 17 November 2019. doi:10.4414/smw.2019.20142. Article type: Review article (Biomedical intelligence).

Note: This patient-friendly article is based on peer-reviewed research. It preserves the original data, findings, and conclusions while translating technical language for a general audience. Please discuss any decisions about cardiovascular screening or treatment with your own healthcare provider.