203 Atheroembolization
As recently as the 1950s, nearly half of strokes were thought to result from cerebral vasospasm until Fisher stressed the etiologic importance of emboli from atherosclerotic plaques in the carotid artery.1 Although embolization from the heart and major vessels accounts for a large number of ischemic cerebrovascular accidents, the cause of a significant proportion remains undetermined.2 In those, the source is mainly thought to be embolic in origin. The following account will focus on the pathophysiology, clinical consequences, prevention, and management of atheromatous embolization.
Pathophysiology
Atherosclerosis
Atherosclerosis mainly affects large and medium-sized arteries. Intravascular sites of blood turbulence favor the development of atherosclerotic lesions. Initial changes in arterial wall morphology result in the formation of fatty streaks that consist of lipid-engorged macrophages in the arterial intima. Progression of such precursor lesions occurs secondary to an inflammatory process initiated by endothelial injury and dysfunction.3 Insufficient nitric oxide production results in increased adhesion and aggregation of platelets. Up-regulation in the endothelial expression of adhesion molecules and selectins leads to accumulation of monocytes and T lymphocytes. These cells become activated and produce growth factors, cytokines, and chemokines. Smooth-muscle cells migrate from the media into the intima and proliferate. In time, these lesions develop into raised fibrous plaques consisting of a fibrous cap covering a core containing necrotic material, lipids, and cholesteryl esters. This advanced plaque forms the basis onto which the complicated plaque develops, consisting of fissures, erosions, or ulceration. There has been increased interest in the role of monocytes and macrophages in the pathogenesis of plaque progression and rupture,4 which is related to thrombosis and/or embolism and clinical manifestations.
Atheromatous Embolization
Atheromatous embolization is a descriptive term for embolization of any atheromatous material. Atheroembolization refers to the dislodgement of vascular plaque material that contains cholesterol crystals, red blood cells, and fibrin.5 This “cholesterol emboli” syndrome consists of renal failure, skin lesions, blue toes, and neurologic manifestations. It may develop spontaneously (due to plaque rupture), follow the use of thrombolytics or anticoagulants,6 or result from arterial manipulation (during surgical procedures, cardiac catheterization, or insertion of an intraaortic balloon pump [IABP]).7 Disruption of vascular plaque results in the release of cholesterol crystals. These crystals cause downstream vascular obstruction and initiate an inflammatory process leading to lymphocytic and mononuclear cell infiltration. Biopsy specimens of affected organs such as skin or kidneys are usually diagnostic.
Plaque Morphology and Embolic Risk
Severe atherosclerosis of the ascending aorta appears to be the most important morphologic indicator of an increased risk of atheromatous embolization. The French Aortic Plaque in Stroke group identified a plaque thickness of 4 mm or greater as an independent predictor of recurrent embolization,8,9 with an odds ratio of 13.8. Although ulceration and calcification occurred more frequently in plaques 4 mm or more in thickness, the presence of ulceration did not significantly increase the risk of vascular events. Absence of calcification, however, was associated with a significant increase in risk (relative risk, 10.3 compared with 5.7 for those with calcification). Another study reported an association between the presence of ulceration in aortic plaques and an increased rate of cryptogenic stroke.10 Ulceration and increased size of aortic plaques seem to be markers of severe generalized atherosclerosis and therefore predict a higher risk for thromboembolic complications.
Macroembolization and Microembolization
Emboli can be generally divided into macroemboli and microemboli. The former occlude arteries larger than 200 µm in diameter, whereas the latter result in occlusion of smaller arteries, arterioles, and capillaries.11 The clinical manifestations of each vary. Whereas macroemboli may cause overt clinical presentations (e.g., stroke or peripheral ischemia), microemboli tend to be more occult in their manifestations of end-organ injury or dysfunction (e.g., renal injury, neuropsychological impairment). Their clinical impact depends on the number and nature of microemboli. Embolization may arise spontaneously or be related to vascular interventions and cardiovascular surgery.
Clinical Consequences of Atheromatous Embolization
Cerebral
As the prevalence of aortic atherosclerotic disease increases with age, so does the rate of atheromatous embolization. Postmortem studies indicate that it affects 20% of patients in their fifth decade, increasing to 80% in those in their eighth decade.12 Emboli from the atherosclerotic aorta may result in stroke or transient ischemic attack, and the clinical manifestations of these conditions vary depending on the cerebrovascular territory affected; the middle cerebral artery is the most frequent site of arterial embolism. Stroke has profound effects; outcomes from acute stroke are measured in terms of survival, functional independence, and financial cost. Survival after stroke is significantly poorer than after myocardial infarction (MI) or most cancers and is the leading cause of disability in developed countries.13 When considered separately from other cardiovascular diseases, stroke ranks third among all causes of death, behind diseases of the heart and cancer. Its economic impact is huge, with 2009 estimated direct and indirect costs of stroke in the United States of $68.9 billion.
Cholesterol emboli are an important and frequently unrecognized cause of stroke.14 Microembolization is a recognized cause of more subtle, sometimes subclinical neurologic injury.15,16 Most frequently this injury is manifested by subtle changes in cognitive function that may only be evident on detailed neuropsychological testing.17,18 This more subtle impairment may appear trivial, but its importance has increased over recent years, particularly in patients undergoing cardiac surgery.19
Cardiac
Atherosclerotic cardiovascular disease is the leading cause of death in developed countries. Every year it results in over 19 million deaths worldwide, and coronary heart disease accounts for the majority of those.20 MI is a consequence of diseased coronary arteries as part of the overall systemic picture of atherosclerosis. Most acute coronary syndromes are due to plaque rupture. Distal embolization of cholesterol and atheromatous material may be important in the pathogenesis of some acute coronary syndromes.21 The occurrence of distal coronary embolization in the setting of acute coronary syndromes has been followed using serum levels of cardiac troponins to detect small degrees of myocardial necrosis. The clinical importance of distal coronary embolization, as defined by serum troponins, is its predictive value for future cardiac events. Embolization following percutaneous coronary interventions is well recognized, and elevations in cardiac troponins are seen in up to 44% of patients undergoing intervention.22,23
Peripheral
Peripheral emboli most frequently lodge in the lower extremities. Cholesterol atheroembolization can be subclinical or can otherwise result in systemic effects. While renal, neurologic, and cutaneous manifestations tend to dominate the clinical picture, involvement of most organs has been previously reported. Atheromatous material can be identified in the pancreas, intestine, and spleen. Symptoms and presentation depend on the site of dislodgement. Embolization into the renal arteries results in renal ischemia and can lead to renal impairment or failure.24,25 In those cases, renal biopsy is diagnostic.26
Involvement of the cutaneous vessels leads to livedo reticularis and the “blue-toe” syndrome, whereas retinal emboli27 result in visual symptoms. Other reported effects include small-bowel bleeding28 and renal transplant failure.29
Diagnosis and Screening
X-Ray Angiography
X-ray angiography is an invasive procedure that allows assessment of the vascular lumen by providing a measure of the degree of stenosis and by identifying plaque disruption, thrombosis, and calcification. However, it provides no information about the vessel wall or the components of the atherosclerotic plaque. Despite that, angiography is still regarded as the gold standard for imaging coronary, carotid, and peripheral arterial disease.30
Surface and Transesophageal Ultrasonography
Measurement of carotid and aortic wall thickness as well as qualitative and quantitative assessment of atherosclerotic plaques can be determined using ultrasonography. The North American Symptomatic Carotid Endarterectomy Trial and the Asymptomatic Carotid Artery Stenosis Study have shown that the degree of stenosis and its hemodynamic consequences are important in the development of stroke.31,32 High-resolution, real-time B-mode ultrasound with Doppler flow imaging is currently considered the modality of choice in imaging the carotid arteries.33
With respect to screening, carotid intima-medial thickness (CIMT) measured by B-mode ultrasound represents a risk factor and a marker for vascular disease risk that most accurately represents subclinical vascular disease but not plaque formation or atherosclerosis per se. Epidemiologic and clinical trial evidence, digitization, and standardization have made CIMT a validated and accepted marker for generalized atherosclerosis burden and vascular disease risk.34 Numerous studies have linked CIMT and CIMT progression with prevalent symptomatic coronary and cerebrovascular disease. Furthermore, CIMT is a predictor of coronary events and stroke as well as all-cause mortality.35,36 The American Society of Echocardiography Carotid Intima-Media Thickness Task Force recommends the use of CIMT measurement by ultrasound in intermediate-risk asymptomatic patients, with a goal of predicting future coronary heart disease events.37
Transesophageal echocardiography (TEE) is a quick, safe, and minimally invasive procedure that can be used in different settings ranging from the operating theatre to the bedside.38 It is regarded as the procedure of choice in detection, assessment, and characterization of thoracic aortic atherosclerosis. Imaging using the transthoracic approach is also possible but at the expense of significant loss of resolution when compared to the transesophageal technique. TEE can reliably detect intimal thickening, ulceration, calcification, and the presence of mobile components within the aortic plaque. As outlined earlier, the French Aortic Plaque in Stroke investigators used TEE to assess aortic plaque thickness in patients with stroke and reported that increased plaque thickness imparted a significant increase in stroke risk.8,9 Katz and colleagues used a 5-grade ranking system for the severity of aortic atherosclerosis, assessed using TEE in 130 patients undergoing cardiac surgery with cardiopulmonary bypass: grade 1, normal aorta; grade 2, flat intimal thickening; grade 3, protruding atheroma in the aortic lumen (<5 mm); grade 4, protruding atheroma (>5 mm); and grade 5, atheroma with a mobile thrombus.39 Patients with grade 5 lesions were at highest risk of stroke. Logistic regression identified aortic arch atheroma as the only variable that was predictive of stroke, with an odds ratio of 5.8. Another study of 315 coronary artery bypass graft (CABG) patients undergoing intraoperative TEE also reported a significant increase in the risk of stroke in patients with aortic arch intimal thickening of greater than 5 mm.40
Intraoperative Epiaortic Ultrasound
Epiaortic ultrasonography involves intraoperative imaging of the ascending aorta using a sterile-sheathed transducer. This technique is noninvasive and has been used in the context of cardiac surgery to detect areas of ascending aortic atherosclerosis.41 It allows modification of the surgical technique in an attempt to reduce potential embolic complications.42 The main disadvantage of this technique is suboptimal imaging of the aortic arch. Intraoperative epiaortic ultrasound can therefore be used to complement the information on the aortic arch obtained by TEE.
Transcranial Doppler
Transcranial Doppler (TCD) ultrasonography can be used to detect and quantify cerebral microemboli. Ultrasound probes are placed bilaterally on the temple, overlying the middle cerebral vessels. Emboli cause an increase in the reflected ultrasound, causing high-intensity transient signals (HITS). These HITS are the footprints of microemboli, which may consist of air, fat, atheromatous material, or platelet-fibrin emboli. In addition to detecting cerebral microemboli, TCD can be reliably used to assess cerebral vasomotor reactivity and autoregulation, to document the circle of Willis functional status, and to identify cerebral hypo- and hyperperfusion, recanalization, and re-occlusion.43
TCD can reliably detect HITS intraoperatively and has been used extensively in the context of cardiac and carotid surgery. During cardiac surgery, microemboli can be detected following intraoperative aortic manipulation (aortic cannulation and application and removal of aortic cross-clamp) as well as during cardiopulmonary bypass.44 HITS have also been identified in patients with symptomatic carotid artery stenosis,45 patients with prosthetic heart valves,46 and those with aortic atherosclerosis.47 They are a common phenomenon in patients with acute stroke, and their detection may continue for several days after the acute event. Their presence is a significant independent predictor of early recurrence of stroke.48
TCD is a simple, user-friendly technique that can be used at the patient bedside as well as in the operating room. It can provide valuable information intraoperatively on cerebral blood velocity, which is closely related to flow, and microembolic load, allowing for intraoperative technical modifications. A major limitation is an inadequate acoustic window in 5% to 20% of individuals.49 Another limitation is the ability to reliably reject artifacts (closely resembling microembolic signals and generated by movement) and/or to distinguish between gaseous and particulate microemboli. With multirange, multifrequency Doppler systems, automatic artifact rejection and differentiation between solid and gaseous microemboli has become possible with high sensitivity and specificity.50,51 We have reported a significant reduction in intraoperative cerebral microembolism as well as a reduction in the proportion of solid microemboli, with avoidance of cardiopulmonary bypass and minimizing manipulation of the ascending aorta during cardiac surgery.44,52
An exciting recent development with TCD ultrasonography is its use therapeutically in the treatment of stroke. This involves the use of TCD ultrasound to augment the effect of fibrinolysis and has been shown to at least double the chance of early complete arterial recanalization.53
Computed Tomography
Computed tomography (CT) can be used in imaging the aorta and quantifying aortic wall calcification. Contrast-enhanced CT has been proposed as a valuable method for following the progression and regression of atherosclerotic disease.54 The main advantage over TEE is the ability to completely image the thoracic and abdominal aorta. Other advantages of CT include its minimally invasive nature, its wide availability, and its provision of images of lumens of arteries and of calcium. Disadvantages include radiation and contrast exposure with potential for renal damage, limiting its use in asymptomatic populations.
Coronary multidetector CT angiography (MDCTA) can be used in identifying patients at a particularly high risk of dying suddenly or suffering a nonfatal MI. It provides information on coronary artery stenosis as well as an estimate of calcification, coronary artery calcium (CAC). The latter is related to multiple risk factors of coronary artery disease. The importance of CAC screening lies in its potential ability to increase predictive power for future events.36,55
Magnetic Resonance Imaging Techniques
Magnetic resonance imaging (MRI) has emerged as a leading noninvasive imaging modality for atherosclerotic disease. It can be used to image atherosclerotic plaques in aortic, carotid, peripheral, and coronary arterial disease.56,57 Its major strengths rest in its ability to determine plaque morphology. Using a range of techniques, MRI can provide valuable information on the composition of the atherosclerotic plaque by identifying the three main factors that determine plaque stability: (1) presence of a lipid core, (2) thickness of the fibrous cap, and (3) inflammation within the cap. MRI allows identification of high-risk unstable plaques and thus guides intervention and therapy.58 Some studies have documented regression of atherosclerotic lesions on MRI in patients treated with statins.59 Magnetic resonance angiography has a high sensitivity and specificity and can be used to image the aorta, carotid, renal, and other peripheral vessels. Evolving magnetic resonance techniques include intravascular60 and transesophageal61 MRI. MRI is therefore a noninvasive, powerful tool with high spatial resolution that can be used clinically without exposing the patient to the risks of ionizing radiation.
Vascular Manipulation and Embolic Events
Cardiac Surgery
Stroke, transient ischemic attack, and peripheral embolization are potential complications following cardiac surgery. Atheroembolism results in a variety of clinical manifestations and can be fatal in about 20% of patients.62 Stroke affects less than 2% of CABG patients, and this is further increased in those undergoing open-heart procedures.63 The risk of perioperative stroke increases with advancing age, and those with concomitant cardiovascular risk factors are at highest risk.64 In addition, it has been shown that the female gender is independently associated with a significantly higher risk of perioperative stroke.65 Embolization from the atheromatous aorta is the single most important etiologic factor for stroke. This risk arises during intraoperative manipulation of the aorta, including cannulation for cardiopulmonary bypass, application and removal of aortic cross-clamp for administration of cardioplegia, and the use of side-clamps for anastomosis of the proximal end of the graft to the aorta.66 Roach et al. showed that atherosclerosis of the ascending aorta is the strongest independent predictor of perioperative stroke, with an odds ratio of 4.5.67
Cardiac Catheterization and Peripheral Vascular Intervention
Aortic manipulation during cardiac catheterization procedures or IABP may cause embolization from aortic atheroma. In a report comparing 59 patients with atherosclerotic aortic debris undergoing transfemoral cardiac catheterization, with 71 control patients, an embolic event occurred in 17% of the patients with atherosclerotic aortas compared to 3% of controls.68 In the proportion of patients requiring IABP, 5 out of 10 patients with atherosclerotic aortas had an embolic event, compared with none of the 12 patients with IABP in the control group. When a transbrachial approach was used in patients with atherosclerotic aortas, none of 11 patients suffered an embolic event. Patients with mobile aortic atheromas, identified using TEE, are at highest risk of catheter-related embolization.68
Microembolic events have also been identified in patients undergoing peripheral arterial intervention. A recent study reported the rate of clinically significant distal embolization in 2.4% of patients undergoing peripheral arterial intervention.69 Logistic regression identified patients with more advanced arterial lesions, angiographic thrombus, and prior history of amputation as those at highest risk.
Cholesterol embolization can complicate cardiac catheterization. Because it is commonly asymptomatic, the exact incidence is uncertain and mainly depends on the detection criteria used (clinical or pathologic). Cholesterol can be identified in the lumen of affected arterioles in up to 12% of patients following cardiac catheterization.70 A prospective multicenter study reported cholesterol embolization in 1.4% of patients following cardiac catheterization. The diagnostic criteria used in this study was based on evidence of peripheral cutaneous involvement or renal dysfunction.71 The syndrome occurred more frequently in patients with generalized atherosclerosis. Interestingly, they identified preprocedural elevation of C-reactive protein as an independent predictor of cholesterol embolization, suggesting involvement of an inflammatory process.
Prevention and Management
Antiplatelet Agents and Anticoagulants
Thrombi can develop on and embolize from atherosclerotic plaques, so it may seem logical to use antiplatelet agents or anticoagulants to prevent these thromboembolic complications. However, there have been reports linking the atheroemboli syndrome with anticoagulation in patients with atherosclerosis. Three studies have reported a reduction in the risk of stroke with anticoagulation.72–74 These studies, however, were not randomized and did not include long-term follow-up. It is over the long term that the potential risks of warfarin therapy may become evident. A randomized trial reported that in patients with stroke, large aortic plaques remain associated with an increased risk of recurrent stroke and death at 2 years despite treatment with warfarin or aspirin.75
The current ARCH (Aortic Arch Related Cerebral Hazard) trial is an open-label trial where patients with aortic arch atheroma (4 mm or greater) and nondisabling stroke are being assigned to oral anticoagulation (target INR 2.0-3.0) versus aspirin (75 mg/d) plus clopidogrel (75 mg/d) and followed longitudinally for recurrence of vascular events. Results of this trial are still awaited. The main concern with anticoagulation is the risk of plaque hemorrhage and atheroembolization.76 However, the risk of clinical atheroemboli syndrome during warfarin therapy in such patients appears to be low (only 1 episode in 134 patients according to the SPAF [Stroke Prevention in Atrial Fibrillation] trial).72
In patients with atherosclerosis, acute ischemic events are usually precipitated by thrombosis, and antiplatelet agents play a fundamental role in thrombosis prevention. The beneficial effects of long-term antiplatelet therapy have been firmly established in patients with a wide range of atherosclerotic diseases. Routine use of aspirin in high-risk patients is universally recommended.77 The Antithrombotic Trialists’ Collaboration published a major meta-analysis with over 200,000 patients, assessing the effect of antiplatelet therapy in patients with various manifestations of atherosclerosis. This reported a significant reduction in the rate of stroke, MI, or vascular death in those on antiplatelet therapy.78
Aspirin is the most commonly used antiplatelet agent. It inhibits thromboxane-dependent platelet activation. Thienopyridines, including clopidogrel and ticlopidine, act by blocking adenosine diphosphate (ADP)-dependent activation of platelets. There is evidence that thienopyridine derivatives are modestly but significantly more effective than aspirin in preventing serious vascular events in patients at high risk, but there is uncertainty about the size of the additional benefit.78 The thienopyridines are also associated with less gastrointestinal hemorrhage and upper gastrointestinal upset compared to aspirin, but with an excess of rash and diarrhea.79 The risk of the latter is greater with ticlopidine than with clopidogrel.13 Ticlopidine, but not clopidogrel, is associated with an excess of neutropenia and thrombotic thrombocytopenic purpura.13,79 In the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial, a long-term benefit was observed with the use of clopidogrel in addition to aspirin in high-risk patients (unstable angina and non-Q-wave MI).80
Dextran has antiplatelet and intravascular volume expansion effects. Lennard and colleagues observed that postoperative or perioperative administration of 10% dextran 40 reduces the rate of TCD-detected microembolic signals after carotid endarterectomy.81,82 Dextran, however, may interfere with cross-matching blood and cause bleeding, renal failure, or (occasionally) acute allergic reactions.
The Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease have been recently published. Oral anticoagulation therapy with warfarin (INR 2.0-3.0) or antiplatelet therapy in stroke patients with aortic arch atheroma 4.0 mm or greater to prevent recurrent stroke was a class IIb recommendation (level of evidence: C).83
Statins
There is a clear association between elevated levels of plasma cholesterol and atherosclerotic disease. Statins or 3-hydroxy-3-methylglutaryl coenzyme-A (HMG Co-A) reductase inhibitors reduce the hepatocyte cholesterol content and increase expression of LDL-cholesterol receptors, resulting in a drop in serum low-density lipoprotein (LDL) cholesterol. In addition, it has become evident in recent years that statins possess cholesterol-independent or pleiotropic effects. These include improvement of endothelial function by improving the bioavailability of nitric oxide, decreasing vascular inflammation, and plaque stabilization.84 Statins are widely used in primary and secondary prevention of ischemic heart disease. A meta-analysis of randomized placebo-controlled double-blind trials with statins reported a 30% reduction in stroke risk with statin therapy.85 Another meta-analysis of data pooled from over 49,000 patients treated with statins in 28 trials reported a relative risk of stroke of 0.76 in statin-treated patients.86 Tunick et al. showed that statin therapy was independently and significantly protective against the occurrence of embolic events (risk ratio, 0.39) in patients with severe thoracic aortic plaque.87
Plaque size reduction, stabilization, and prevention of plaque thrombosis may be the mechanisms leading to a reduction in atheromatous embolization. Two randomized studies of low-dose and higher-dose statins in patients with aortic and/or carotid plaques showed significant regression in plaque seen on MRI.88,89
Minimal Aortic Manipulation
The use of smaller arterial catheters during cardiac catheterization may help reduce the risk of embolization.90 Reduction of embolization during cardiac surgery is possible with modifications to the operative technique. Avoidance of aortic manipulation intraoperatively is most important.66 This can be achieved in patients undergoing CABG by avoidance of cardiopulmonary bypass, which obviates the need for aortic cannulation and cross-clamping.91,92 The use of composite arterial grafts (bilateral internal thoracic artery grafts with the radial artery anastomosed to the internal thoracic artery) avoids the need for proximal aortic anastomosis requiring a side-clamp.93 In addition, there is a potential survival advantage with arterial grafts. Off-pump surgery has been shown to result in a significant reduction in the risk of stroke in patients with atheromatous aortas.94 We have reported a significant reduction in cerebral microembolization by avoiding cardiopulmonary bypass and aortic manipulation.44,52 A strategy for potential prevention of embolization in cardiac surgery is summarized in Box 203-1.
Screening with Transesophageal Echocardiography and Epiaortic Ultrasound
As previously outlined, patients with mobile atheroma in the aortic lumen have the highest incidence of perioperative stroke compared to patients with lesser degrees of atherosclerosis.39 TEE has confirmed the association between aortic atherosclerosis and perioperative stroke and thus provided a mechanism of identifying patients at highest risk,39,95,96 as well as allowing for modification of surgical techniques to minimize embolic complications.
There is an association between atherosclerosis of the ascending aorta, as detected using epiaortic ultrasound, and increased postoperative neurologic morbidity.41,97 In a study of more than 1900 patients undergoing cardiac surgery, detection of atherosclerosis of the ascending aorta using epiaortic ultrasound was identified as an independent predictor of long-term neurologic events and mortality.41 Comparison between intraoperative TEE and epiaortic ultrasound demonstrated that the former underestimates the presence and severity of aortic atherosclerosis.98,99 Modification of surgical technique based on intraoperative epiaortic ultrasonography may reduce the frequency of stroke and neurobehavioral changes related to atheromatous embolization.100
Surgical Treatment
Treatment of patients with symptomatic carotid atherosclerosis is well established. The European Carotid Surgery Trial (ECST) and North American Symptomatic Carotid Endarterectomy Trial (NASCET) investigators reported a clear benefit of carotid endarterectomy (CEA) in the prevention of stroke in patients with high-grade, recently symptomatic carotid stenosis.31,101 This benefit is offset by the surgical risk of the procedure. Perioperative stroke and death rate for patients with high-grade stenosis was 8% at 30 days in ECST and 6% in NASCET. These rates are acceptable, given the absolute risk reduction from surgery of 10% and 17%, respectively. However, for patients with asymptomatic carotid disease, the risk-to-benefit ratio is narrower, and carotid endarterectomy is currently only recommended for high-grade carotid stenosis (70%-99%).
Over recent years, there has been increasing interest in endovascular intervention for carotid stenosis with angioplasty and stenting. The international carotid stenting study has recently reported higher rates of stroke and mortality with carotid stenting compared to endarterectomy. It was therefore recommended that carotid endarterectomy should remain the treatment of choice until the long-term efficacy of stenting is established.102
Management of patients with recurrent embolic events due to aortic atherosclerotic disease can be problematic. Aortic arch endarterectomy in patients with severe aortic atherosclerosis has been reported.103–105 This procedure is performed using deep hypothermic circulatory arrest and is associated with significant perioperative morbidity and mortality. When performed during cardiac surgical procedures using cardiopulmonary bypass, it resulted in a significantly higher rate of stroke and mortality. Therefore, there is insufficient evidence to recommend this mode of treatment for stroke prevention. In the context of cardiac surgery, replacement of the ascending aorta can be performed with acceptable mortality and morbidity,106 particularly in the intraoperative management of patients with so-called porcelain aorta107 (severe diffuse atherosclerosis and calcification of the ascending aorta that causes an eggshell appearance on x-ray or CT).
SummaryKey Points
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