Shimizu and Sano first described surgical repair of an atherosclerotic aortic arch branch vessel lesion in 1951. Initially, open surgical repair was performed via a transthoracic approach, but this was replaced by the more popular extraanatomic bypass after Crawford and associates’ report demonstrating a mortality rate of only 5.6% for extraanatomic repair compared with 22% for those patients treated using a transthoracic approach. Their data were reinforced by a more contemporary series by Berguer and colleagues that demonstrated a 10-year primary patency rate of 82% and perioperative stroke and mortality rates of 3.8% and 0.5%, respectively, among 100 consecutive cervical reconstructions for aortic arch vessel (AAV) lesions.
An endoluminal solution to atherosclerotic aortic arch branch vessel lesions is often credited to Mathias and co-workers, who were the first to report a successful percutaneous transluminal angioplasty of an occlusive lesion in a supraaortic vessel in 1980. In a review of 423 subclavian and innominate artery angioplasties, a 92% initial technical success rate was achieved. However, a 19% incidence of restenosis was noted at 5 years. Subsequent reports demonstrated improved results when adjunctive stenting is used, in conjunction with angioplasty, for the treatment of stenotic lesions of branch vessels of the aortic arch.
Atherosclerosis is the most common cause of AAV occlusive disease. Other causes include Takayasu arteritis, giant cell arteritis, and radiation-induced arteritis. As with extracranial carotid artery occlusive disease, many patients with AAV stenotic lesions do not have symptoms. Typically, the atherosclerotic process is localized to the ostium and the proximal portion of the arch vessel. Treatment is generally deemed necessary for patients presenting with symptoms referable to the involved vessel. In these instances, symptoms are due to hypoperfusion or distal embolization, which may occur either in the anterior or posterior cerebral circulation or upper extremity. In the patient with coronary revascularization based on the left internal mammary artery (LIMA), a proximal subclavian artery stenosis may lead to a coronary steal syndrome. Patients with Takayasu arteritis tend to have long, noncompliant fibrotic lesions rather than short, localized, proximal lesions and endoluminal therapy has been less durable. Although firm guidelines for surgery or endoluminal therapy for aortic arch vessel lesions do not exist, most clinicians consider intervention for: (1) asymptomatic patients who present with an innominate or common carotid artery stenosis of at least 80%; or (2) symptomatic patients with an innominate, common carotid, or subclavian artery stenosis of at least 50%.
Cardiovascular status should be assessed and medical management optimized. van Hattum and associates observed that of 18 patients with atherosclerotic lesions of the arch vessels, 78% had coronary artery disease, 33% had carotid artery disease, and 61% were hypertensive. A history of a LIMA-based coronary artery bypass should be noted.
Preoperative physical examination should include bilateral arm pressure measurements. Digital subtraction angiography, magnetic resonance angiography, or computed tomography angiography is advisable to identify the lesion site, length, tandem lesions, arch morphology, and preferred approach to access the lesion.
Patients should receive clopidogrel (75 mg/day) and aspirin (325 mg/day) 5 days before the procedure. Alternatively, patients can receive a loading dose of clopidogrel (300 mg) the day prior to the planned intervention.
Procedures may be performed under general anesthesia, monitored anesthesia care, or local anesthesia. Arterial line monitoring of blood pressure is recommended and prophylactic antibiotics should be considered.
Pitfalls and Danger Points
Access site complications
Inability to “seat” or position the sheath or guiding catheter
Inability to cross the target lesion
Vessel dissection or rupture
“Jailing” the origin of the vertebral artery and internal mammary artery
Late stent failure
Angiographic Anatomy and Common Collateral Pathways
The most common configuration of great vessel arch anatomy is the presence of three separate trunks, with the innominate artery giving rise to the right subclavian and common carotid arteries, the left common carotid artery nearby, and the left subclavian artery originating posterior to and to the left of the left common carotid artery. Common anatomic variants include a bovine arch configuration (16%-24%), as well as a left vertebral artery originating directly off the aortic arch (6%) and an aberrant right subclavian artery (0.5%-1%).
Collateral pathways that compensate for occlusive disease of the left subclavian artery include flow from the right subclavian artery into the right vertebral artery with retrograde flow into the left vertebral artery and subsequently into the left subclavian artery. Additional collateral pathways may arise from the external carotid artery, the ascending cervical artery, and the thyrocervical trunk.
Occlusive disease of the innominate artery will often result in retrograde flow from the right vertebral artery into the right common carotid and subclavian arteries.
Anatomic Considerations for Aortic Arch Vessels
Long, occlusive lesions at the origin of a branch vessel or the presence of steep angulation off the aortic arch may be difficult to cross or maintain sheath access when using a femoral approach. A retrograde approach from the common carotid or brachial artery may help to overcome these problems ( Fig. 13-1 ).
Care should be taken when treating a lesion in the subclavian artery close or innominate bifurcation to avoid jailing a major tributary such as a dominant vertebral artery or left internal mammary artery bypass to the left anterior descending coronary artery.
Unfavorable Anatomic Features
When the left common carotid artery originates from the innominate artery, there is potential for cerebral embolization.
Vessel tortuosity may be sufficiently severe to preclude endovascular intervention.
Access for Common Carotid Artery Lesions
Factors influencing the decision to access a lesion using a retrograde or an antegrade approach include the presence of iliac occlusive disease, aortic arch morphology, angle of takeoff of the target vessel, lesion site and length.
If difficulty is encountered or anticipated via a transfemoral approach because of arch morphology or a tight orifice lesion, a retrograde approach may be more suitable. This approach is recommended for tandem lesions that require simultaneous carotid endarterectomy and stenting of a more proximal common carotid artery lesion.
Access for Subclavian And Innominate Lesions
Lesions of the innominate artery may be treated via an antegrade (transfemoral) or retrograde (transbrachial or transcarotid) approach ( ). A transbrachial approach may be performed percutaneously or via open cutdown. This approach precludes the need for selective catheterization from a remote access site.
Predilation with an undersized balloon is particularly useful in severely diseased lesions and lesions at the orifice in order to allow for safe passage of the stent delivery system. This technique also allows imaging of the distal extent of the lesion to assess the involvement of vertebral artery and internal mammary artery origins.
When feasible, primary stenting has the theoretic benefit of minimizing microembolization. Short lesions close to the origin of the innominate artery or common carotid artery are best treated with a balloon-expandable stent because of their greater accuracy of placement, higher radial force, and good wall apposition. Stents should treat the target lesion and not cover excessive lengths of normal vessel.
Lesions of the mid-common carotid, subclavian, and axillary arteries, are relatively mobile, and frequently the best option is to use a self-expanding nitinol stent. Stents should not be used in the distal subclavian and proximal axillary artery because of the risk of impingement between the clavicle and the first rib. Although uncommon, late stent fracture has been observed after stenting of heavily calcified lesions of arch vessels ( Fig. 13-2 ).