Sarah M. Weakley
Peter H. Lin
Presentation
A 73-year-old man presents to the emergency room of a local hospital with a 5-day history of amaurosis fugax of the right eye. The patient reports that his eye symptoms have occurred two to three times daily since the initial onset of symptoms, with each episode lasting for approximately 10 minutes followed by spontaneous symptom resolution. The patient denies any residual ocular deficits or speech impairment after these episodes. The patient reports that he never loses consciousness or experiences any motor weakness or sensory deficits involving his arms or legs. His past medical history was significant for hypertension and coronary artery disease for which he underwent a coronary artery bypass 8 years ago. Regarding his medications, he takes an aspirin daily. On physical examination, a right neck bruit is confirmed, with symmetrical bilateral upper-extremity pulses. The patient does not have any neurologic deficits on physical examination.
Differential Diagnosis
The most likely cause of his transient ischemic attack (TIA) with clinical manifestations of amaurosis fugax is cerebral ischemia due to extracranial carotid artery disease. Other differential diagnoses in this patient with symptomatic cerebral ischemia include carotid aneurysm, carotid dissection, cardiac emboli, paroxysmal emboli, carotid coils or kinks, and fibromuscular dysplasia of the carotid artery. With his prior history of coronary artery atherosclerotic disease requiring coronary revascularization, one must consider carotid artery atherosclerotic disease as the most plausible cause of his symptoms.
Workup
The patient undergoes further evaluation with carotid duplex ultrasound that allows sonographic assessment of the severity of carotid stenosis using grayscale evaluation as well as blood velocity measurement at the level of carotid stenosis. The ultrasound study revealed high-grade right internal carotid artery (ICA) stenosis with greater 70% luminal stenosis, as well as proximal innominate artery stenosis. Due to his hemodynamically significant tandem lesions affecting the origin of the aortic arch vessels and the right ICA, a computed tomography angiography of the neck and the chest with intravenous contrast administration was performed that confirmed the presence of tandem high-grade stenosis involving the innominate artery origin and ipsilateral carotid artery at the level of the carotid bifurcation.
Diagnosis and Treatment
Since the patient’s TIA symptoms can be caused by either the carotid stenosis or the innominate artery stenosis, revascularization of his carotid and innominate artery stenosis should be considered. While current literatures support the role of either carotid stenting or carotid endarterectomy (CEA) for high-grade symptomatic carotid artery stenosis, the presence of a high-grade supra-aortic vessel stenosis adds therapeutic challenges in this patient as it may potentially increase the risk of embolization for carotid stenting via a transfemoral approach. Although a proximal innominate artery stenosis can be treated surgically with aortoinnominate artery bypass via a median sternomy approach, his prior history of coronary artery bypass would make this treatment option a high-risk surgical procedure due to the repeat nature of an open chest operation. An ideal approach for these tandem carotid and supra-aortic trunk stenoses is to correct these two atherosclerotic lesions during one operative setting while minimize potential risk of cerebral embolization. Given these treatment considerations, a combined right CEA with synchronous retrograde innominate artery stenting is recommended.
Surgical Approach
In our patient with tandem lesions involving the carotid and innominate artery origin, a synchronous treatment approach with right CEA and retrograde innominate artery stent placement via the carotid arteriotomy site is planned. While CEA can be performed under various anesthetic options, including general anesthesia, local anesthesia, or cervical nerve block, we elect to perform CEA under local anesthesia without electroencephalic monitoring. A neck incision is made along the lateral border of the sternocleidomastoid muscle, which is followed by the exposure of the common carotid artery (CCA), external carotid artery, and ICA. The patient is given systemic heparin for anticoagulation. The ICA is test-clamped for 1 minute. If the patient does not demonstrate any neurologic changes, carotid shunting is not utilized. Proximal and distal vascular controls are established by placing vascular clamps in the common, external, and internal carotid arteries. A standard CEA is performed in which the carotid plaque is removed in it entirely. We routinely perform prosthetic patch angioplasty using Dacron graft to close the carotid arteriotomy site.
Following completion of the endarterectomy and closure of the arteriotomy, retrograde angioplasty and stenting of the proximal innominate artery is performed. The CCA is first clamped just proximal to the bifurcation. Next clamps on the internal and external carotid arteries are released, which allows retrograde flow from the external carotid artery (ECA) to perfuse the ICA during angioplasty and stenting. The placement of a CCA clamp also minimizes cerebral embolus during innominate artery angioplasty and stenting procedure. A Seldinger needle is used to cannulate the common carotid just proximal to the clamp, which is followed by the insertion of a 0.035-in guidewire under fluoroscopic guidance. An 8-F, 12-cm introducer sheath with radiopaque marker at the tip is next inserted over the guidewire whereby the introducer sheath is placed in a retrograde fashion toward the innominate artery origin. A short sheath is important since the endarterectomy is typically in close proximity to the site of angioplasty and stent placement. Following the sheath insertion, retrograde arteriogram of the innominate artery is performed to identify the location of the innominate artery ostial lesion. Next a premounted stainless steel balloon-expandable stent is inserted over the guidewire within the introducer sheath. The sheath should be advanced along with the stent well into the aorta, crossing the lesion first before positioning the stent at the deployment site. This maneuver minimizes the possibility of dislodging the stent from the balloon. The sheath is next retracted proximally to uncover the balloon-expandable stent. A retrograde innominate artery angiogram is performed followed by stent deployment under fluoroscopic guidance. We routinely extend the stent 1 to 2 mm into the aorta to assure ostial plaque coverage by the stent. Once the final angiogram is obtained to demonstrate adequate angioplasty and stent placement, a 5-0 prolene pursestring suture is placed around the introducer sheath site followed by the carotid sheath removal. Back bleeding from the sheath insertion site is allowed in order to flush out any embolic debris during the stenting procedure. Next the CCA clamp is removed, which restores the antegrade blood flow in the innominate and carotid artery.
Postoperative Management
Postoperative management following this combined treatment of CEA and retrograde innominate artery stent placement is similar to post-CEA patient care. Patients are monitored in either surgical intensive care unit or intermediate care unit with careful blood pressure monitoring. Additional attention should be focused on possible neck hematoma formation, which may compromise airway. Neurologic status should be monitored carefully. Any development of neurologic deficit should be assumed to be carotid artery thromboembolism caused by technical error, which should be explored surgically for possible thromboembolectomy. The patient should be given clear liquid diet following the operation. Most patients can tolerate dietary advancement and are discharged home the following day.
The patient should resume oral daily aspirin following the operation. Because of the innominate artery stent placement, postoperative therapy should also include 3 months of oral clopidogrel (Plavix), which has been shown to reduce platelet aggregation and decrease potential stent-related thrombosis.
Discussion
The presence of carotid tandem lesions involving the carotid bulb and its proximal vessel origin, located in either the left CCA or the innominate artery origin, represents a potential therapeutic dilemma and technical challenge. Studies have reported that such combined lesions can occur in 2% to 4% of patients undergoing diagnostic evaluations in preparation for CEA for a carotid bifurcation lesion. When a tandem lesion is detected, several treatment approaches can be considered, which include (a) CEA via neck incision and surgical revascularization of supra-aortic trunk lesion via median sternotomy, (b) endovascular stenting of both carotid and supra-aortic trunk lesion via transfemoral approach, (c) carotid stenting via transfemoral approach and surgical revascularization of supra-aortic trunk lesion via open chest approach, (d) CEA via neck incision and endovascular stenting of supra-aortic trunk lesion via transfemoral approach, or (e) CEA via neck incision and endovascular stenting of supra-aortic trunk lesion via retrograde carotid approach.
In patients with symptomatic carotid artery disease, CEA is effective in preventing future ipsilateral ischemic events, provided that the perioperative combined risk of stroke and death is not higher than 6%. Its effect is marked in patients with high-grade (>70%) stenosis, with eight patients needed to be treated to prevent one ipsilateral stroke in a 2-year period. The stroke-reduction benefit persists, although less significantly, in symptomatic patients with a moderate (50% to 75%) degree of stenosis, with 20 patients needed to be treated to prevent one ipsilateral stroke during a 2-year period.
The ideal treatment strategy for symptomatic carotid artery lesion has been thoroughly investigated in recent years as multiple prospective randomized studies have shown similar efficacy between percutaneous carotid artery stenting (CAS) and CEA. While transfemoral stent placement can be performed for both carotid and innominate lesions, in our patient, the risk of procedural-related embolization would undoubtedly be increased significantly due to the manipulation of endovascular devices across these tandem lesions. It has been shown that procedural-related embolization, caused by vessel plaque breakage due to endovascular device instrumentation, is a major risk factor for cerebral infarction during the carotid stenting procedure.
Considering various recent clinical trials comparing carotid stenting and CEA, it is noteworthy to highlight the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) study, which is the largest trial to date comparing outcomes in patients with symptomatic and asymptomatic carotid artery stenosis. The study enrolled 2,502 patients at 117 centers in the United States and Canada and compared the treatment outcome in prospective randomized fashion between CEA and carotid stenting. The primary end point for the study was any periprocedural stroke, myocardial infarction (MI), death, or postprocedural ipsilateral stroke up to 4 years after intervention. An embolization protection device was successfully used in 96% of carotid stenting patients. A unique outcome measured element in the CREST trial involves a patient of general health status with the use of the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36) at 2 weeks, 1 month, and 1 year after the procedure.
The study reported similar primary end point at a mean follow-up of 2.5 years between the two groups. However, the 30-day incidence of stroke or death was 4.4% and 2.3% for CAS- and CEA-treated symptomatic and asymptomatic patients, respectively, a difference that was significant. The incidence of MI was significantly higher in CEA-than in CAS-treated patients (2.3% vs. 1.1%). Interestingly, the SF-36 data indicate that the impact on quality of life by MI was not significant, whereas the impact of major or minor stroke was significant. No significant differences (CAS vs. CEA) in results were noted when the outcomes were examined by symptomatic status. A 4-year Kaplan-Meier curve examining freedom from the primary end point demonstrated no significant difference in the curves for CAS versus CEA treatment out to 4 years (risk reduction, <1% per year), showing that both methods result in durable benefit. The SF-36 subscale data at 1 year indicate that the increased incidence of cranial nerve palsy in CEA-treated patients has no significant impact on quality of life.
Regarding treatment approach for supra-aortic trunk lesions, direct aortic reconstructions via transthoracic approach have been reported as a durable treatment option. However, complication rates for these procedures can be as high as 23% which chylothorax, graft thrombosis, pneumothorax, phrenic nerve palsy, and Horner’s syndrome being the most serious. Over the past decades, endovascular treatment with transluminal balloon angioplasty and stent placement of the brachiocephalic vessels has shown acceptable results with outcomes equal to surgery. These endovascular treatment strategy offers the advantages of reduced morbidity and mortality and decreased length of stay compared to the traditional open transthoracic aortic bypass procedures. In our patient who had undergone a prior coronary artery operation, endovascular treatment of his innominate artery stenosis offers significant advantage of reduced operative morbidities and expeditious recovery due to the avoidance of a redo open chest incision.
Taken together these various treatment considerations for tandem lesion involving carotid artery and supra-aortic trunk ostial lesion, it is our assessment that the best treatment strategy for this patient is to perform synchronous CEA and retrograde innominate artery stenting (Table 1). We postulate that synchronous treatment strategy offers several advantages. The innominate stenting procedure is performed using a retrograde approach and employed temporary occlusion of the CCA to prevent distal embolization. Because CEA has already been completed prior to innominate stent placement, the placement of a CCA clamp during the innominate stenting procedure allows continual ICA perfusion via retrograde ECA circulation. Additionally, the retrograde approach allows a short distance access to the origin of the supra-aortic arch occlusive lesion, which reduces the hazards of guidewire manipulation through a diseased or tortuous aortic arch typically associated with a transfemoral approach. The short working distance between the supra-aortic trunk lesion and the carotid entry site permits precise fluoroscopic control for lesion location, guidewire manipulation, and stent deployment. Once the endovascular procedure is completed, back bleeding from the sheath insertion site prior to arteriotomy closure was performed, which permits flushing away of procedural-related embolic debris.
TABLE 1. Key Technical Steps and Potential Pitfalls to Performing CEA and Innominate Artery Stenting
Several studies have reported the technical feasibility and the clinical efficacy of this synchronous treatment approach in patients with tandem lesion involving the carotid and the supra-aortic arch ostial lesions. Length of hospital stay was decreased substantially when compared to transthoracic bypass procedures for treatment of similar aortic arch occlusive lesions. The majority of patients were discharged after 23 hours of observation. This decreased length of stay resulted in decreased care costs because extensive bypass surgery was avoided and return to full activity occurred more quickly. Performing the endovascular portion of the procedure using a retrograde approach from the neck avoided potential vessel entry site complications that can be associated with a retrograde femoral approach.
TAKE HOME POINTS
· The most likely cause of TIA with clinical manifestations of amaurosis fugax is cerebral ischemia due to extracranial carotid artery disease.
· Carotid duplex ultrasound allows sonographic assessment of the severity of carotid stenosis using grayscale evaluation, as well as blood velocity measurement at the level of carotid stenosis.
· In patients with symptomatic carotid artery disease, CEA is effective in preventing future ipsilateral ischemic events, provided that the perioperative combined risk of stroke and death is not higher than 6%.
· CREST comparing CAS and CEA reported similar primary end point at a mean follow-up of 2.5 years between the two groups. However, the 30-day incidence of stroke or death was 4.4% and 2.3% for CAS- and CEA-treated symptomatic and asymptomatic patients, respectively, a difference that was significant.
· While there are various treatment considerations for tandem lesion involving carotid artery and supra-aortic trunk ostial lesions, it is our assessment that the best treatment strategy for most patients is to perform synchronous CEA and retrograde proximal CCA or innominate artery stenting.
SUGGESTED READINGS
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