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Wolff T, Guirguis-Blake J, Miller T, et al. Screening For Asymptomatic Carotid Artery Stenosis [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2007 Dec. (Evidence Syntheses, No. 50.)

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Screening For Asymptomatic Carotid Artery Stenosis [Internet].

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CAS is one of several etiological factors for stroke, an important health problem with a high burden of disease in the U.S. It is important to consider the possibility that screening asymptomatic people with ultrasound to detect clinically important CAS for the purpose of performing CEA could reduce the large burden of suffering due to stroke. Although the percentage of all strokes that could potentially be reduced by screening for CAS is relatively small, this is a large number of strokes when considered across the entire country.

The magnitude of contribution of CAS to the morbidity and mortality associated with stroke is not well characterized nor is the natural progression of CAS. We estimate the prevalence of CAS 60–99% in the general population over 65 years old to be about 1%. CAS is more prevalent in older adults, smokers, those with hypertension, and those with heart disease. Unfortunately, research has found no single risk factor or clinically useful risk stratification tool that can reliably and accurately distinguish people who have clinically important CAS from people who do not.

Duplex ultrasound is a non-invasive screening test. Its reported accuracy is approximately 94% sensitive and 92% specific for CAS of 60%–99%. In a low-prevalence population, the number of false positive tests is high. In the case of screening for CAS, false positive tests are important. If all positive tests are followed by cerebral angiography, about 1% of people will suffer a non-fatal stroke as a result of the angiogram. If positive tests are not followed by confirmatory angiography but rather by MRA or CTA - tests with <100% accuracy - then some people will have unnecessary CEA. CEA is associated with important complications, including a perioperative stroke or death rate of 2.4% to 3.7% and, therefore, some people will be harmed unnecessarily.

Under carefully controlled conditions, treatment with CEA for asymptomatic CAS can result in a net absolute reduction in stroke rates - approximately 5% over 5–6 years (about 2.5% absolute risk reduction for disabling strokes). This benefit has been shown in selected patients with selected surgeons, and must be weighed against a small increase in non-fatal MIs. The net benefit for CEA largely depends on people surviving the perioperative period without complications. The two RCTs that found a benefit to surgery over medical management had 30-day perioperative rates of stroke and death of 2.7 – 2.8%. In large observational studies using administrative databases, the average complication rates ranged from 1.6 to 3.7%; statewide rates varied greatly by state, with a range of 2.3 – 6.7%.

Other issues prevent the determination of a good estimate of benefit from CAS screening in the general primary care setting. First, the patients and surgeons in the RCTs of CEA treatment were highly selected; the patients had high stroke risk. Secondly, the absolute benefit of screening and CEA treatment depends on a low perioperative rate of stroke or death. A small increase in perioperative strokes or death could counteract the benefits. There is no validated strategy for reliably identifying patients that are at high enough risk for stroke to benefit from CEA but with low enough risk for perioperative complications. Thirdly, the beneficial outcome of decreased strokes in the RCTs does not account for additional harms of CEA, including non-fatal myocardial infarction. Additionally, the absolute risk reduction in the CEA trials is relatively small (on the order of 4% to 6% over 6 years in ACST).

Another important limitation of the evidence on the benefit of treatment with CEA is that the medical treatment arm in the RCTs was ill-defined, and likely did not include intensive blood pressure and lipid control, as is standard practice today. It is difficult to determine what effect current standard medical therapy would have on overall benefit from CEA. The use of current medical therapy could have reduced the stroke rate in the medical treatment arm of these trials, thus likely reducing the overall benefit to treatment with CEA.

Another issue regarding the evidence on CEA is the timing of strokes and perioperative death. The timing is different in the arms of the RCTs; the events in the CEA arm occur earlier than those in the medical arm. The Kaplan-Meier curves in ACST cross from net harm to net benefit only at about 1.5 years after CEA for men, and at nearly 3 years after CEA for women.57, 5962 The estimated survival from these curves beyond the actual follow-up time may not be applicable. It is possible that the benefit from CEA will be limited to a specific time period and does not continue unabated into the future, as projected in the trials. Thus, the actual (not projected) risk reduction for CEA over 5–10 years is still uncertain. The evidence would suggest that the absolute benefit of screening and CEA in people with asymptomatic CAS in the general population is small.

Table 2 shows hypothetical outcomes of a screening program for asymptomatic carotid artery stenosis. These calculations are based on a number of assumptions that may limit the widespread applicability to certain populations. These assumptions include: the use of ultrasound as the initial screening test with a sensitivity of 0.94 and specificity of 0.92; the prevalence in general primary care population older than 65 years is 1%; all patients with a positive test go to surgery; and the event rate with CEA (perioperative stroke or death) is 3.1%. Further detail on assumptions is available in Table 2. According to these calculations the best trade-off between benefits and harms comes from a strategy of carotid duplex ultrasound screening followed by MRA confirmation. Given this strategy, about 23 strokes would be prevented over 5 years by screening 100,000 people with a true prevalence of clinically important CAS of 1%. Thus, about 4,348 people would need to undergo screening to prevent one stroke (number needed to screen, NNS) after 5 years. Double this number (8,696) would need to be screened to prevent one disabling stroke. If it were possible to define a higher risk population with an actual prevalence of 5%, and using the screening and confirmation strategy defined above, about 217 strokes would be prevented over 5 years by screening 100,000 people. This translates into a NNS of about 461 to prevent one stroke over 5 years, or a NNS of 922 to prevent one disabling stroke over 5 years. An additional 34 people would have a non-fatal myocardial infarction as a result of screening. However, risk assessment tools that accurately identify persons at high risk of a stroke from CAS are not available and, therefore, it is not possible to identify people from a high-risk group with a prevalence of 5% who might benefit from screening and treatment with CEA.

Table 2. Projected Outcomes of Screening 100,000 Asymptomatic Adults for Carotid Artery Stenosis.

Table 2

Projected Outcomes of Screening 100,000 Asymptomatic Adults for Carotid Artery Stenosis.

Asymptomatic CAS likely contributes a relatively small portion of the overall stroke burden. Although this report did not review the evidence on medical treatment, there are accepted medical strategies to prevent stroke. Until we address the gaps in the evidence that screening and treatment with CEA provides overall benefits to the general population, clinicians' efforts might be more practically focused on optimizing medical management.

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