Table of Contents
- Key Points
- Background: Why This Research Matters
- How the Study Was Conducted
- Key Findings: Plaque Area and Risk
- Plaque Progression and Regression: What Happens Over Time
- Patient Characteristics and Plaque Area
- Clinical Implications: What This Means for Patients
- How Plaque Area Compares to Other Measurement Methods
- Limitations of the Study
- Recommendations and Future Directions
- Frequently Asked Questions
- Source Information
Key Points
- In a study of 1,686 patients, those with the most carotid plaque had a 5-year risk of stroke, heart attack, or vascular death of 19.5%, versus 5.6% for those with the least.
- After adjusting for other risk factors, the highest plaque group had a 3.5 times higher risk of these combined events than the lowest group.
- Patients whose plaque increased over time had a 15.7% adjusted 5-year risk of combined events, compared with 7.6% for those with stable plaque.
- Measuring carotid plaque area may help doctors target preventive treatment to high-risk patients and evaluate whether treatments are working.
- The study was observational, with a mean follow-up of 2.5 years, so it cannot prove that treating based on plaque measurements directly improves outcomes.
Background: Why This Research Matters
Doctors expect a worldwide increase in cardiovascular and cerebrovascular disease (conditions affecting the heart and blood vessels in the brain). With more patients at high risk of vascular events, doctors need better ways to identify which patients require aggressive medical treatment.
One current approach is to target therapy using traditional risk factors with tools such as Sheffield tables. These tables estimate a patient's risk based on factors like age, sex, blood pressure, smoking, and cholesterol levels. Another suggestion is that doctors use absolute risk reductions (the actual decrease in risk from treatment) to make treatment decisions. For decisions about resource allocation, doctors can use the number of patients that need to be treated to prevent one additional event.
However, estimating risk based on traditional factors is imperfect. The Framingham risk factors (a widely used risk calculation) explain only half of the variance in coronary risk. This means that half of the factors determining whether a person develops heart disease are not captured by these traditional measurements.
Waiting until patients have symptomatic vascular disease is also problematic. About half of patients who experience a stroke or myocardial infarction (heart attack) have no warning symptoms beforehand. It would be desirable, therefore, to have noninvasive methods for identifying patients at higher risk by detecting preclinical atherosclerosis (plaque buildup in arteries before symptoms appear).
Researchers have suggested that several methods may improve the management of hypertension. These methods include intimal-medial thickness (IMT, a measurement of the artery wall), plaque in extracoronary arteries (arteries outside the heart), and coronary calcification (calcium deposits in heart arteries). They also include wall rigidity in the aorta and peripheral arteries, and abnormal endothelium-dependent vasodilation (problems with blood vessel relaxation). Noninvasive detection of atherosclerosis should ideally involve methods that are safe, inexpensive, noninvasive, reliable, and reproducible. Additionally, their results should correlate with the extent of atherosclerotic disease and have high positive and negative predictive value for clinical events.
For the past 7 years, measurements of carotid plaque area at patients' first visit and at follow-up visits have been recorded at the Atherosclerosis Prevention Clinic. These measurements have been used to determine the effectiveness of different therapies. Patients whose carotid atherosclerosis was progressing despite control of traditional risk factors were investigated for new risk factors. These new risk factors included plasma homocysteine (an amino acid in the blood) and lipoprotein(a) (a type of cholesterol particle).
The relationship between cardiovascular reactivity to mental stress and carotid plaque area has been previously reported. Recently, it was reported that among patients whose plaque was progressing rapidly despite treatment of traditional risk factors, vitamin therapy for homocysteine halted the progression of carotid atherosclerosis. Measurement of carotid plaque, combined with multiple regression modeling using traditional risk factors, has been used to define the quantitative trait "unexplained atherosclerosis" for genetic research.
The primary aim of the present study was to examine the relationship between baseline carotid plaque area and the subsequent risk of a combined outcome. That combined outcome was stroke, myocardial infarction, and vascular death. This relationship was examined in this patient population. The effect of carotid plaque progression (or regression) on subsequent risk was a secondary aim.
How the Study Was Conducted
The patients for this study were being followed up in the Premature Atherosclerosis Clinic and the Stroke Prevention Clinic. These clinics are at the University Campus of the London Health Sciences Center in London, Canada. Patients in the Premature Atherosclerosis Clinic were referred because of vascular disease not explained by usual risk factors such as age. Patients were also referred because of a strong family history of vascular disease. Those referred to the Stroke Prevention Clinic were referred mainly because of a stroke or a transient ischemic attack (TIA, a temporary stroke-like event). In some cases, patients were referred because of asymptomatic carotid stenosis (narrowing of the neck artery without symptoms).
Carotid plaque area was measured using a high-resolution duplex ultrasound scanner. Plaque was defined as a local thickening of the intima (the innermost layer of the artery wall) of 1 mm or more in thickness. Measurements were made in magnified longitudinal views of each plaque seen in the right and left common, internal, and external carotid arteries.
The plane in which the measurement of each plaque was made was chosen by panning around the artery until the view showing the largest extent of that plaque was obtained. The image was then frozen and magnified, and the plaque was measured by tracing around the perimeter with a cursor on the screen. The microprocessor in the scanner then displayed the cross-sectional area of the plaque. The operator then moved on to the next plaque and repeated the process until all visible plaques were measured. The sum of cross-sectional areas of all plaques seen between the clavicle (collarbone) and the angle of the jaw was taken as total plaque area.
Intraobserver reliability (the consistency of measurements by the same person) was 0.94 for repeated measurements. For the purpose of demonstrating generalizability of the results to other ultrasound laboratories and clinics, the researchers carried out a study of interobserver reliability (consistency between different operators). In this study, plaque area measurements in 25 patients were repeated a week apart by 2 technicians using 2 different machines.
The senior technologist had been carrying out these measurements for 8 years. The senior technologist performed all the measurements on which this article was based, using a new, high-resolution TL HDI 5000 scanner. The junior technologist, who had been doing such measurements for 1 year, used an ATL Mark 9 duplex scanner. The reliability (intraclass correlation) was 0.85, with the senior technician using the higher-resolution machine systematically measuring more plaque.
Outcome events of stroke and myocardial infarction were ascertained first by a questionnaire at the patients' annual visits and second by inspection of hospital charts for any admissions. Deaths were confirmed by death certificates either from the hospital charts or faxed from family physicians' offices. In 2 cases, family physicians had retired and records were unavailable; in those cases, cause of death was reported by the widow. Both were sudden deaths classified as cardiovascular death.
Determination of outcomes was not blinded in a small number of cases (some strokes were evaluated by one of the study authors). However, in most cases outcomes occurred in settings other than the clinic. Because of the long length of follow-up, patients included in the present study were followed up in 2 studies to which they gave informed consent. Which study they were followed up in depended on when they were first seen. Protocol review numbers from the University of Western Ontario Ethics Review Board were 02391 and 07270. Only patients for whom complete data were available were included in the present study.
Statistical analyses assessed associations between baseline risk factors and the level of carotid plaque area through analysis of variance for continuous variables and a chi-squared test for dichotomous variables. The 5-year risks of combined outcome of stroke, myocardial infarction, and vascular death were estimated from discrete-time event-free survival curves with a complementary log-log regression model. This model was also used to adjust for all the baseline characteristics listed in the study tables. The corrected-group-prognosis method was used to compute adjusted risk estimates and adjusted event-free survival curves. The 5-year risks of stroke alone and of combined stroke and myocardial infarction were estimated with the same approach. The effect of plaque progression (and regression) on the risk of the combined outcome was analyzed as a time-dependent covariate, also after adjustment for all baseline characteristics. The relationships between baseline characteristics and plaque progression were assessed with a complementary log-log regression model. All statistical analyses were carried out with SAS 8.0 software.
Key Findings: Plaque Area and Risk
A total of 1,686 patients with a baseline carotid plaque area measurement were categorized into 4 ranges of carotid plaque area corresponding approximately to quartile cutpoints:
- 0.00 to 0.11 cm² (n=422 patients)
- 0.12 to 0.45 cm² (n=424 patients)
- 0.46 to 1.18 cm² (n=421 patients)
- 1.19 to 6.73 cm² (n=419 patients)
The mean plaque area of each quartile was 0.03 ± 0.04 cm², 0.27 ± 0.09 cm², 0.78 ± 0.21 cm², and 2.33 ± 1.05 cm², respectively.
During a mean follow-up of 2.5 ± 1.3 years (range, 0.1 to 5 years), a total of 45 strokes, 94 myocardial infarctions, and 41 deaths occurred. Of the 41 deaths, 27 were vascular, 12 were from cancer, and 2 were from other causes.
The combined 5-year risk of stroke, myocardial infarction, and vascular death increased with increasing levels of plaque area. This finding was statistically highly significant (3-df likelihood ratio test, P<0.001).
When the researchers adjusted for all baseline patient characteristics, the 5-year risk of combined outcome by plaque area quartile was:
- Lowest quartile (0.00 to 0.11 cm²): 5.6% risk (reference group)
- Second quartile (0.12 to 0.45 cm²): 10.7% risk, relative risk 1.9 (95% CI, 1.1 to 3.3), P=0.02
- Third quartile (0.46 to 1.18 cm²): 13.9% risk, relative risk 2.5 (95% CI, 1.4 to 4.4), P=0.001
- Highest quartile (1.19 to 6.73 cm²): 19.5% risk, relative risk 3.5 (95% CI, 1.8 to 6.7), P<0.001
This means that patients in the highest quartile of plaque area were 3.5 times more likely to have had a stroke, myocardial infarction, or vascular death. This is compared to patients in the lowest quartile. The increase in risk by plaque area quartile was weakly confounded by other baseline characteristics. This was assessed by the small change between the adjusted and unadjusted relative risks, but the increase remained statistically significant after adjustment.
The unadjusted 5-year risks were slightly higher: 6.3%, 11.3%, 13.2%, and 19.1% across the four quartiles. The unadjusted relative risks were 1.8 (95% CI, 1.1 to 3.0; P=0.03) for the second quartile, 2.1 (95% CI, 1.2 to 3.5; P=0.004) for the third quartile, and 3.0 (95% CI, 1.8 to 4.9; P<0.001) for the highest quartile compared to the lowest quartile.
Outcomes of stroke alone and of combined stroke and myocardial infarction yielded similar patterns of results. For stroke alone, the adjusted 5-year risks were 1.6%, 2.3%, 3.9%, and 4.0% across quartiles. The relative risks for stroke alone were 1.4 (95% CI, 0.4 to 4.6; P=0.58) for the second quartile, 2.4 (95% CI, 0.7 to 7.6; P=0.14) for the third quartile, and 2.4 (95% CI, 0.7 to 8.8; P=0.17) for the highest quartile. These results for stroke alone did not reach statistical significance.
For the combined outcome of stroke and myocardial infarction, the adjusted 5-year risks were 4.8%, 9.3%, 12.3%, and 14.0% across quartiles. The relative risks were 1.9 (95% CI, 1.1 to 3.4; P=0.02) for the second quartile, 2.5 (95% CI, 1.4 to 4.7; P=0.001) for the third quartile, and 2.9 (95% CI, 1.4 to 5.8; P=0.002) for the highest quartile.
Plaque Progression and Regression: What Happens Over Time
A total of 1,085 patients had at least 1 annual carotid plaque area measurement. Plaque area progression (or regression) was defined as an increase (or decrease) of 0.05 cm² or more from baseline. This value corresponded to approximately the median change in carotid plaque area from baseline.
Of the 1,085 patients:
- 685 patients (63.1%) had carotid plaque progression
- 306 patients (28.2%) had plaque regression
- 176 patients (16.2%) had no change in carotid plaque area over the period of follow-up
At baseline, 209 patients had no measurable plaque. After 1 year, only 75 patients had no measurable plaque. The distribution of plaque area was heavily weighted to low plaque areas, with few patients having more than 3 cm² of total plaque area.
The occurrence of progression or regression of plaque area was associated with the combined outcome after adjustment for all baseline characteristics. This finding was statistically significant (2-df likelihood ratio test, P=0.003).
The combined 5-year adjusted risk of stroke, myocardial infarction, and vascular death was:
- 9.4% for patients with carotid plaque area regression
- 7.6% for patients with no change in plaque area
- 15.7% for patients with plaque area progression
Patients who progressed were 2.1 times (95% CI, 1.2 to 3.6; P=0.005) more likely to have had a stroke, myocardial infarction, or vascular death than patients who had no change in plaque area.
Among all the baseline characteristics, only increased age, higher cholesterol level, and male sex were statistically significant predictors of plaque progression. However, the relative risks were all close to unity, meaning the associations were weak. The adjusted relative risks for plaque progression were:
- Age (per 10 years): 1.1 (95% CI, 1.1 to 1.2), P<0.001
- Body mass index (per 10 kg/m²): 0.9 (95% CI, 0.7 to 1.0), P=0.12
- Smoking (per 10 pack-years): 1.0 (95% CI, 1.0 to 1.1), P=0.64
- Systolic pressure (per 10 mm Hg): 1.0 (95% CI, 1.0 to 1.1), P=0.28
- Diastolic pressure (per 10 mm Hg): 0.9 (95% CI, 0.9 to 1.0), P=0.11
- Cholesterol (per 1 mmol/L): 1.1 (95% CI, 1.1 to 1.2), P=0.001
- Triglycerides (per 1 mmol/L): 1.0 (95% CI, 0.9 to 1.1), P=0.95
- HDL (per 1 mmol/L): 0.8 (95% CI, 0.6 to 1.0), P=0.06
- Homocysteine (per 5 µmol/L): 1.0 (95% CI, 1.0 to 1.1), P=0.48
- Female sex: 0.8 (95% CI, 0.7 to 0.9), P=0.03
- Diabetes mellitus: 1.1 (95% CI, 0.8 to 1.4), P=0.60
- On lipid-lowering drugs at referral: 1.1 (95% CI, 0.9 to 1.3), P=0.21
- On antihypertensive drugs at referral: 1.2 (95% CI, 1.0 to 1.4), P=0.08
Patient Characteristics and Plaque Area
Baseline patient characteristics were strongly related to carotid plaque area. Carotid plaque area was strongly related to age. A mean difference of 25.4 years was observed between the age of subjects in the fourth and first quartiles.
The striking relationship between age and carotid plaque area showed a marked increase between 45 and 70 years of age and a leveling after 70 years of age. Some measurable plaque is present in most patients 45 years of age and older. Rapid increase in plaque area between 60 and 75 years of age may be associated with the impairment of mitochondrial function or loss of ability to handle oxidative stress. Apparent leveling off after 75 years of age may represent a survivor effect, meaning those with rapid progression may not survive to older age.
Baseline characteristics by quartile of carotid plaque area were as follows:
- Age: 43.5 years in the lowest quartile, 53.7 years in the second quartile, 61.7 years in the third quartile, and 68.9 years in the highest quartile (P<0.001)
- Body mass index: 26.6, 27.6, 27.8, and 27.7 kg/m² (P=0.06)
- Pack-years of smoking: 6.3, 9.7, 14.1, and 20.1 (P<0.001)
- Systolic pressure: 129.2, 135.3, 144.1, and 150.4 mm Hg (P<0.001)
- Diastolic pressure: 79.8, 80.6, 80.5, and 79.6 mm Hg (P=0.52)
- Cholesterol: 5.16, 5.33, 5.24, and 4.90 mmol/L (P<0.001)
- Triglycerides: 1.71, 2.03, 1.86, and 1.84 mmol/L (P=0.001)
- HDL: 1.23, 1.24, 1.33, and 1.28 mmol/L (P<0.001)
- Homocysteine: 11.31, 11.87, 12.97, and 14.94 µmol/L (P<0.001)
- Male sex: 44.8%, 49.1%, 50.4%, and 67.5% (P<0.001)
- Diabetes mellitus: 1.7%, 4.9%, 10.4%, and 18.6% (P<0.001)
- On lipid-lowering drugs at referral: 19.7%, 38.4%, 59.6%, and 73.5% (P<0.001)
- On antihypertensive drugs at referral: 37.7%, 51.9%, 62.7%, and 74.9% (P<0.001)
Except for diastolic blood pressure and body mass index, all other baseline characteristics were significantly associated with increased plaque area.
Clinical Implications: What This Means for Patients
The results of this study demonstrated that baseline carotid plaque area was a strong risk factor for the combined outcome of stroke, myocardial infarction, and vascular death. Baseline carotid plaque area was also a strong risk factor for the combined outcome of stroke and myocardial infarction. Measuring carotid plaque area adds to the arsenal of tools for identifying high-risk patients and is useful for targeting aggressive preventive therapy and testing new therapies.
The fact that plaque progression also predicted outcome indicated that measurement of plaque in follow-up may be used to determine the effectiveness of therapy. The researchers speculate that the trend to better outcomes in patients with stable plaque than in those with regression may be explained by carotid endarterectomy. Carotid endarterectomy is surgical removal of plaque from the neck artery. Carotid endarterectomy often results in large reductions in plaque burden. Carotid endarterectomy patients are at high risk for death or myocardial infarction, even though endarterectomy significantly reduces risk of stroke.
It may seem unusual that adjustment for age, sex, systolic blood pressure, serum cholesterol, and pack-years of smoking did not diminish the predictive value of plaque area measurement. This can be understood in light of previous studies showing that Framingham risk factors explain only half of coronary risk. Previous studies also show that traditional risk factors explain only half of carotid plaque. In a multiple regression model with all the risk factors mentioned above, in addition to treatment of blood pressure and lipids, the R² for plaque area was only 0.51. This means that traditional risk factors explain only about half of the variation in plaque area between patients.
High-risk patients benefit more from treatment, so the ability to identify them prospectively should make aggressive preventive therapy more cost-effective. For example, the number needed to treat to prevent 1 myocardial infarction in 10 years for young overweight women with moderate hypertension would be 500 to 800. For elderly men with isolated systolic hypertension, it would be fewer than 50.
How Plaque Area Compares to Other Measurement Methods
Alternative noninvasive indexes include coronary plaque calcification by CT (computed tomography), measurement of IMT, and measurement of carotid stenosis by Doppler ultrasound. The latter approach may be intuitively attractive but is limited because of the phenomenon of compensatory enlargement. As plaque develops, the artery enlarges to accommodate the plaque, so stenosis (narrowing) is a late event likely resulting from plaque rupture with scarring.
Smoking, blood pressure, and serum cholesterol are much more weakly associated with carotid stenosis than with risk. Smoking, for example, increases the odds ratio for stenosis only to 1.08 (95% CI, 1.03 to 1.16), whereas smoking increases risk of stroke 6-fold.
Measuring plaque as a continuous variable appears to be more powerful than simply detecting the presence or absence of plaque at extracoronary sites or counting the number of sites involved. One study found that extracoronary plaque was a more powerful predictor of coronary risk than coronary calcification by CT. However, the odds ratio for patients with plaque at 3 sites versus none was only 2.37 (95% CI, 1.08 to 5.21). The odds ratio between grade 3 and 0 of coronary calcification was 1.79 (95% CI, 0.94 to 3.40).
Ease of measurement and low cost are important advantages compared with measuring IMT. Because the magnitude of the quantity being measured is much greater relative to the resolution of the ultrasound scanner, the reliability of the measurements is much greater. Additionally, no special equipment or software is required, and the time to perform the measurements only adds about 25% to the time of a routine carotid ultrasound examination. With the advent of 3-dimensional measurement of carotid plaque volume, the examination has become even easier to perform, requiring only 2 minutes a side for data acquisition.
Carotid IMT, which predicts stroke more strongly than myocardial infarction, is an indirect method of assessing atherosclerosis, which is mainly an intimal process. IMT represents largely medial hypertrophy related to hypertension. A substantial proportion of strokes are due to hypertensive small-vessel disease. Therefore, it is not surprising that IMT predicts stroke more strongly than myocardial infarction. The researchers found the opposite for plaque area.
One study found that IMT was weakly associated with coronary atherosclerosis. They pointed out that in early disease, the media accounts for approximately 80% and the intima for only 20% of IMT. Direct measurement of the atherosclerotic plaque itself, without inclusion of the media, should be a more specific approach to predicting atherosclerosis risk. Indeed, this has been the case in studies in Britain and in Canada. Like IMT, carotid plaque increases with age, but the quantity of plaque area levels off at about 75 years of age. This may be because people with rapid progression of plaque do not survive to old age.
Limitations of the Study
The study had several limitations. Determination of outcomes was not blinded in a small number of cases, meaning some strokes were evaluated by one of the study authors. However, in most cases, outcomes occurred in settings other than the clinic.
The study was observational, following patients over time without randomly assigning them to different treatments. This means the study can show associations between plaque area and outcomes but cannot prove that measuring plaque area and treating based on it directly causes better outcomes.
The mean follow-up was 2.5 years, with a range of 0.1 to 5 years. This relatively short follow-up period may not capture the full long-term risk associated with plaque area.
The study population was drawn from specialized clinics (Premature Atherosclerosis Clinic and Stroke Prevention Clinic), so the results may not be fully generalizable to the general population. Patients in these clinics were referred for specific reasons, such as vascular disease not explained by usual risk factors or a strong family history of vascular disease.
The interobserver reliability study showed that the senior technician using the higher-resolution machine systematically measured more plaque than the junior technician using a different machine. This suggests that measurements may vary between different operators and different ultrasound machines, although the reliability was still good at 0.85.
Recommendations and Future Directions
The researchers have adopted regression of plaque as the therapeutic goal in their clinic. They have found that follow-up measurements of plaque can determine whether therapy is successful. Follow-up measurements of plaque can also determine whether more intensive investigation and treatment of new risk factors may be required. These new risk factors include homocysteine and lipoprotein(a), and this may be required for patients whose plaque is progressing rapidly.
The results of this study lead to the hypothesis that ultrasound-based management of vascular patients may improve the cost-utility of preventive therapy. This approach would permit expensive therapies to be targeted on patients with a low number needed to treat and provide feedback on the success of therapy.
This hypothesis needs to be tested in a randomized, controlled trial. One approach would be to use cluster randomization of physician or clinic practices to usual care versus care based on ultrasound evaluation, with cost-utility as the primary outcome.
Furthermore, the quantity of baseline plaque and rate of progression predict outcomes. Therefore, plaque measurement represents a way to efficiently evaluate new therapies with much smaller sample sizes than would be required for studies based on clinical events. For new therapies that have been shown to be antiatherosclerotic in animal studies, plaque measurement would permit dose-finding studies. This applies to therapies that do not have other intermediate outcomes such as effects on plasma lipids. Plaque measurement would also provide preliminary evidence of efficacy. This could lead to human studies that could not otherwise be contemplated.
The researchers note that trying to treat atherosclerotic patients without knowing how their arteries are doing is rather similar to trying to treat hypertension without measuring blood pressure. It is also similar to trying to treat dyslipidemia (abnormal cholesterol levels) without measuring follow-up lipid levels.
Frequently Asked Questions
What is carotid plaque area and how is it measured?
Carotid plaque area is the total cross-sectional area of plaque in the neck arteries, measured with a high-resolution duplex ultrasound scanner. Plaque is defined as a local thickening of the artery's inner layer of 1 mm or more. The technician traces each plaque on the screen, and the scanner sums all areas between the collarbone and jaw angle.
Can measuring plaque in my neck arteries predict my risk of stroke or heart attack?
In a study of 1,686 patients at an atherosclerosis prevention clinic, those with the most carotid plaque had a 5-year risk of stroke, heart attack, or vascular death of 19.5%, compared with 5.6% for those with the least plaque. This 3.5-fold difference remained after adjusting for other risk factors.
What does it mean if my plaque area increases over time?
In the same study, patients whose plaque area increased by at least 0.05 cm² from baseline had a 15.7% adjusted 5-year risk of stroke, heart attack, or vascular death, compared with 7.6% for those whose plaque stayed the same. Progression was linked to a 2.1 times higher risk than no change.
How does carotid plaque area compare to other tests like intima-media thickness or coronary calcium?
The article states that measuring plaque as a continuous variable appears more powerful than simply detecting plaque presence or counting sites. It is easier and less costly than intima-media thickness, requires no special software, and adds about 25% to a routine carotid ultrasound. Plaque area predicted heart attack and stroke combined, while intima-media thickness predicts stroke more strongly.
What are the limitations of using carotid plaque area to guide treatment?
The study was observational, so it cannot prove that measuring plaque and treating based on it directly causes better outcomes. Follow-up averaged only 2.5 years, and patients came from specialized clinics, so results may not apply to everyone. Measurements can also vary between operators and machines, though reliability was still good.
What are the recommendations for using plaque measurements in practice?
The researchers adopted plaque regression as a therapeutic goal in their clinic. They suggest that follow-up plaque measurements can show whether therapy is working and whether testing for new risk factors, such as homocysteine or lipoprotein(a), is needed. They propose that ultrasound-based management be tested in a randomized controlled trial.
My carotid ultrasound showed a lot of plaque in my neck arteries — when should I get a second opinion about my stroke and heart attack risk and whether my preventive treatment is working?
Carotid plaque area predicts the combined risk of stroke, heart attack, and vascular death: patients with the most plaque had a 19.5% five-year risk versus 5.6% for those with the least, and plaque that worsened over time carried a 15.7% risk versus 7.6% when it stayed stable. Because treatment decisions and follow-up measurements depend on how much plaque you have and whether it is progressing, an independent review of your ultrasound images and risk factors can help confirm your risk category and whether your preventive therapy is adequate. Diagnostic Detectives Network provides independent expert second opinions.
Source Information
Original Article Title: Spence 2002 Carotid Plaque Area A Tool for Targeting and Evaluating Vascular Preventive Therapy
Authors: J. David Spence, MD; Michael Eliasziw, PhD; Maria DiCicco, RVT; Daniel G. Hackam, MD; Ramzy Galil; Tara Lohmann, BSc
Author Affiliations: Robarts Research Institute and University of Western Ontario, London (J.D.S., M.D.); Department of Community Health Sciences and Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta (M.E.); McMaster University, Hamilton (D.G.H., R.G.); and McGill University, Montreal (T.L.), Canada
Publication: Stroke. 2002;33:2916-2922. Published by the American Heart Association.
DOI: 10.1161/01.STR.0000042207.16156.B9
Funding: This work was supported by a grant from the Heart and Stroke Foundation of Ontario (grant B3738).
This patient-friendly article is based on peer-reviewed research.
