6 Asymptomatic Extracranial Carotid Artery Stenosis
Abstract
Extracranial internal carotid artery (ICA) stenosis is responsible for up to one-third of all strokes. The prevalence of ICA stenosis is between 0.1 and 9% in the general population, but in individuals older than 65 years the prevalence may be as high as 60%. Asymptomatic ICA stenosis is diagnosed during physical examination and detection of a carotid bruit; however, bruit is not always present. Computed tomography (CT) and magnetic resonance (MR) angiography are noninvasive screening tools useful in the diagnosis of ICA stenosis. CT angiography or digital subtraction angiography are necessary, especially for interventional planning. All patients should receive best medical treatment including glycemic control and blood pressure control, smoking cessation, and antiplatelet therapy. Surgical intervention is recommended for symptomatic patients and angiography (>60% stenosis) or ultrasonography (>70% stenosis) is recommended for “asymptomatic” patients (who have not had an ipsilateral ischemic infarct or transient attack within the past 6 months) and these patients have a low risk for surgery. For patients with high-risk features (age older than 80 years, severe medical comorbidities, previous neck surgery or radiation, carotid bifurcation or stenotic plaque at or above C2 or into the common carotid artery into the intrathoracic segment, or “twisted carotid”) carotid artery stenting or angioplasty is an excellent alternative.
Introduction
Extracranial carotid artery stenosis is a common cause of ischemic stroke, noted to be responsible for 20% of cases. Epidemiological studies report a prevalence estimated between 0.1 and 9% among the general population, but in those older than 65 years and/or with risk factors including smoking, hypertension, coronary artery disease, and recent strokes, the prevalence may be as high as 60%. Carotid artery disease has been the source of significant debate among the neurological and cardiovascular medicine communities, including the propriety of surgical reconstruction and/or the use of novel endovascular remedies. While all carotid artery stenosis treatment is prophylactic by nature to prevent cerebral embolic events, a challenging area of management is the indications for treatment of lesions that have not demonstrated the propensity to embolize by causing a previous stroke, hence deemed asymptomatic stenosis.
Major controversies in decision making addressed in this chapter include:
Whether or not treatment is indicated.
Endarterectomy versus stenting for asymptomatic carotid artery stenosis.
Complications, outcome, and durability of the treatment.
Whether to Treat
Throughout the 1990s and early 2000s, many large, multicenter, randomized trials were conducted to shed light on the appropriate indications for surgical reconstruction of asymptomatic carotid disease. CASANOVA, published in 1991, compared carotid endarterectomy (CEA) to medical therapy alone in patients with asymptomatic carotid stenosis measuring 50 to 90%, as seen on angiography. Due to an unacceptably high surgical complication rate, very complicated study protocols, and exclusion of patients with greater than 90% stenosis, no difference was seen in the number of strokes or deaths between the two study arms. Published in 1992, the MACE study was a single-center study that compared CEA alone with aspirin therapy, and reinforced the importance of use of aspirin peri- and postoperatively. Given the significantly higher number of myocardial infarctions (MIs) and transient cerebral ischemic events in the surgical group, the study was terminated early, after only 71 patients had been randomized. The consensus was that these complications were attributable to the lack of aspirin use in the surgical arm, which was further supported in subsequent studies. The Veterans Affairs Cooperative Study Group in 1993 published a multicenter prospective randomized study with two treatment arms, CEA plus aspirin–antiplatelet therapy and antiplatelet therapy alone. The surgical arm demonstrated a reduction of ipsilateral neurological events (8 vs. 20.6%), although the study was not statistically powered and failed to show a reduction of ipsilateral strokes or death. Nevertheless, after a long-term 4-year follow-up period, the ipsilateral stroke rate in the surgical group was 4.7% compared to 9.4% in the medical group ( 1 , 2, 3, 4, 5 in algorithm ). The Asymptomatic Carotid Surgery Trial (ACST), published in 2004, is the largest trial on this topic to date, consisting of more than 3,000 patients with greater than 60% asymptomatic stenosis diagnosed by duplex ultrasound, who were randomized to CEA with medical management versus medical management alone. Exclusion criteria included poor surgical risk, prior ipsilateral CEA, and probable cardiac emboli. Surgeons were required to have demonstrated a perioperative morbidity and mortality rate of less than 6% to be involved in the trial, and this rate was just over 3% in the study. The mean follow-up was 3.4 years. The overall 5-year risk of all strokes and deaths, including perioperative stroke and death, was 6.4 and 11.8% in the surgical and medical groups, respectively. Fatal or disabling stroke rates were 3.5 versus 6.1%. Fatal stroke rates alone were 2.1 versus 4.2%. So, in consideration of “asymptomatic” carotid patients (who have not had an ipsilateral ischemic infarct or transient ischemic attacks (TIAs) within the past 6 months), we recommend consideration of surgery (CEA) for otherwise low-risk patients with higher than 60% stenosis by angiography or for those with higher than 70% stenosis by ultrasonography ( 5 in algorithm ).
We note that all of the studies cited earlier were completed in the pre-statin therapy era. There is evidence that statin therapy, in concert with routine antiplatelet therapy, affords a greater measure of protection in the medical management of asymptomatic carotid stenosis. To evaluate this, three new randomized controlled trials are in progress, the SPACE 2, ACST-2, and CREST-2. All of these will evaluate the role of prophylactic CEA for asymptomatic disease in the era of modern pharmacotherapy ( 1 , 2, 3 in algorithm ).
Anatomical Considerations
It is important to note anatomical parameters that may increase the degree of surgical difficulty. On preoperative imaging, the features we look for include the presence of a high carotid bifurcation or stenotic internal carotid artery (ICA) plaque distal to the second cervical vertebra or above the angle of the mandible, or common carotid artery (CCA) plaque extending proximal into the intrathoracic segment. In the era of carotid stenting, transmandibular extended approaches or dislocation of the temporomandibular joint that might have been necessary to access the high distal ICA are no longer appropriate. We also look for the “twisted carotid” variant where the ICA is medially rotated under the external carotid artery (ECA), which renders adequate distal ICA exposure more difficult; this relationship is easy to predict preoperatively by studying the anteroposterior and lateral angiograms ( 4, 5 in algorithm ). Other anatomical factors that add significant perioperative risk of a CEA and should be taken in consideration in the decision-making process are previous ipsilateral neck surgery including CEA, radial neck dissection, and open tracheostomy. Nonanatomical factors include age older than 80 years, previous radiation, contralateral vocal cord paralysis, and severe neck stiffness ( 4, 5, 6 in algorithm ).
Workup
Clinical Evaluation
Many patients with carotid artery stenosis will present without any threatening neurological complaints. These lesions often reach the attention of clinicians after careful physical examination and the detection of a carotid bruit. While physical exam findings are valuable tools, the absence of a cervical bruit does not rule out carotid disease, and between a quarter and a third of patients with high-grade stenosis will have no auscultatable carotid bruit. A careful history-taking is essential, focusing on specific symptomatology of cerebral embolic disease, including visual changes, language difficulty, facial paresis, dysarthria, numbness, or weakness. Although this chapter addresses the appropriate clinical rationale for reconstruction of “asymptomatic” carotid disease, “symptomatic” carotid stenosis with concomitant ipsilateral ischemic disease is a much more compelling trigger for fast-track surgery, as the 2-year risk of stroke in untreated symptomatic and asymptomatic carotid artery disease is 26 and 6%, respectively.
Imaging
Rational choice of imaging facilitates confirmation of the presence and degree of carotid artery stenosis. Carotid ultrasound is used as a tool to screen patients, or to follow patients either on medical management or postoperatively. Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) have become increasingly useful in noninvasive screening of carotid artery disease. In many cases, CTA can be substituted for digital subtraction angiography (DSA) in planning surgery. MRA can be insensitive to resolve the difference between high-grade stenosis and/or complete occlusion, and also it does not sufficiently show the extent of distal ICA disease, which is necessary information to plan a safe and effective surgery. CTA is much better at resolving these questions, but can underestimate the degree of stenosis in the presence of calcium at the carotid bulb (this is critically important), which is often seen in carotid atheroma cases. Therefore, we create a surgical plan based on CTA alone, but we have a low threshold for the addition of formal DSA imaging (the majority of our patients do have bulb calcification on the CTA), and both studies can give us anatomical clues ( 4 in algorithm ).
Treatment
Conservative Management
Initial conservative management of carotid artery disease should attempt to avoid progression or development of concurrent cardiovascular disease. The mainstays of risk modification include glycemic control, blood pressure control, serum lipid monitoring, and smoking cessation. All patients presenting with carotid artery disease should be started on aspirin. There is Level A evidence and a Class I recommendation that low-dose aspirin (75–325 mg) reduces the risk of stroke in this patient population ( 1 in algorithm ). Medical treatments for carotid artery stenosis have evolved, thanks to a series of clinical trials over the last 40 years, most notably with the addition of statins and dual-antiplatelet regimens. The ESPS-2 and ESPRIT studies both have shown notable relative risk reduction for stroke when patients received dual-antiplatelet therapy compared to either medication individually (aspirin + clopidogrel: 37% vs. aspirin alone: 18%), although the literature has shown an increase in hemorrhagic complications. Thus, routine dual-antiplatelet therapy is not our standard treatment for carotid disease. The data for statin use in carotid stenosis patients are more impressive, with SPARCL trial showing subgroup analysis of over a thousand patients with carotid stenosis and no clinical coronary disease demonstrating a significant 33% stroke risk reduction for patients randomized to high-dose atorvastatin compared to placebo ( 1 in algorithm ). The literature suggests that maximal conservative therapy may be lowering stroke rates across all treatment modalities. We must look for novel data from SPACE 2, ACST-2, and CREST-2 for guidance in the next several years. Additionally, regardless of whether or not a patient with carotid artery stenosis requires surgical treatment, their comorbid risk of future MIs, strokes, or peripheral vascular syndromes over 5 years exceeds 20%, compelling reason for medication therapy and counseling on cardiovascular monitoring, and for sophisticated primary care.
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