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Surgical Reconstruction of the Supra-Aortic Trunks and Vertebral Arteries
The supra-aortic trunks (SATs) branch from the aortic arch and ascend through the mediastinum to terminate at the carotid bifurcations and the origins of the vertebral arteries. These trunks carry the entire blood supply to the head and upper extremities. The vertebrobasilar system is composed of the two vertebral arteries, the basilar artery, and their branches to the spinal cord, medulla, pons, cerebellum, and cerebral lobes supplied by the posterior cerebral arteries.
The three most common variants in the anatomy of the SATs have implications when considering their reconstruction. These variants include a shared ostium (16%) or a common origin (8%) for the innominate and left common carotid arteries, a left vertebral artery originating from the aortic arch (6%), and a right retroesophageal subclavian artery (~0.5%) arising as the most distal branch of the aortic arch. When the left vertebral artery originates directly from the aortic arch, its entry into the transverse foramina of the cervical vertebra occurs at a higher level, typically at the C4 or C5 transverse foramen. A retro-esophageal right subclavian artery is associated with a thoracic duct that empties on the right jugulo-subclavian confluent, a nonrecurrent right inferior laryngeal nerve, a common carotid trunk giving origin to both common carotid arteries in approximately half these patients, and in some instances, an anomalous origin of the right vertebral artery from the right common carotid, in which case the recurrent laryngeal nerve will loop around it.
Through the mechanisms of low flow or atheroembolization, occlusive disease of the SATs can cause symptoms in any of the territories they supply, including the hemispheric (carotid) territory, the posterior cerebral (vertebrobasilar) territory, and, in the case of proximal subclavian disease, the upper extremities. Vertebral artery occlusive disease may restrict inflow into the basilar artery, resulting in vertebrobasilar ischemia. This is more likely if compensatory flow from the carotid system is reduced because of an internal carotid occlusion or diminutive or congenitally absent posterior communicating arteries.
The SATs are afflicted by atherosclerosis mostly in the fifth or sixth decade of life. This results in the development of plaques that can obstruct flow or embolize (atheroembolism). Aneurysmal atherosclerotic disease of the SATs is rare. In some regions of the world, the SATs are a common site for Takayasu arteritis, usually in younger individuals, while giant cell arteritis affects mainly older females. Traumatic and mycotic aneurysms of the SATs are uncommon but potentially life-threatening conditions.
The incidence of atherosclerotic disease is lower in the SATs than in the internal carotid and vertebral arteries. Nevertheless, one-third of patients undergoing arch arteriography have a severe lesion involving one or more of the SATs. The morphology of atherosclerotic lesions of the SATs is not defined as well as that of the internal carotid artery, partly because in earlier decades the SATs were not routinely visualized during arteriography of the cerebral vessels. In addition, while ultrasonography provides valuable morphologic information of the cervical segments of the carotid arteries, the proximal SATs cannot be imaged with ultrasonography. Because there is limited knowledge of the natural history of SAT lesions, surgical indications for their treatment are based partly on inferences. In addition, lesions of the SATs are often found in individuals who have concomitant disease of the carotid or vertebral arteries; a situation that confuses the identification of the lesion responsible for the symptoms. Stenotic lesions of the SATs usually appear at their origin from the aortic arch and often involve more than one artery. Plaques located at the ostia of the SATs often present in continuity with atheroma that extends across the dome of the aortic arch.
The high incidence of concomitant carotid and vertebral artery lesions makes it mandatory to outline the extracranial and intracranial cerebrovascular supply when evaluating a patient for cerebrovascular symptoms. Currently, computed tomography angiography has become the most reliable imaging study for the evaluation of the SATs and the vertebral arteries. However, digital subtraction arteriography is still required in complex cases that may require a dynamic evaluation of the cerebral circulation, as is often necessary in patients with vertebrobasilar ischemia.
Vertebrobasilar ischemia can be caused by poor inflow through the carotid and vertebral arteries, reversal of blood flow in a vertebral artery caused by a proximal subclavian artery occlusion (subclavian steal), reversal of right carotid and vertebral artery flow from an innominate artery occlusion, and embolization from the proximal subclavian, the vertebral arteries, and the basilar artery.
Symptoms of Occlusive Disease of the Supra-Aortic Trunks
Patients with occlusive disease of the SATs may show symptoms of carotid, vertebrobasilar, and upper extremity ischemia. Although there is no pathologic evidence to support this view, it has traditionally been taught that in patients with disease of the SATs, cerebral symptoms are due to low flow rather than atheroembolization. This concept runs contrary to clinical evidence, suggesting that the mechanisms of cerebral ischemia from disease of the SATs are similar to those from atheroma of the carotid bifurcation. In addition, patients with subclavian artery stenosis who have a coronary bypass from the internal mammary artery may present with myocardial ischemia because of a coronary steal phenomenon, as flow may reverse in the mammary artery away from the myocardial bed and towards the arm.
Obliteration of the SATs is suggested by absent pulses in the neck (subclavian, carotid) or arm (axillary, brachial) on one or both sides and by the recording of unequal or abnormally low pressures in the upper extremities. Waveforms recorded by Doppler tracings are dampened in arteries which origins are stenotic or occluded, and if so, bruits may be present. In patients with subclavian steal, a pulse lag may be felt between the radial arteries of the two arms or, more precisely, a pulse wave delay of greater than 30 ms can be measured by simultaneously recording both brachial artery waveforms. Claudication of the arm and digital artery embolization may be present in subclavian artery disease. A computed tomographic scan or MRI of the brain with disease of the SATs may reveal clinically silent cerebral infarctions.
In symptomatic vertebral (or basilar) artery occlusive disease, the patient may have any combination of the following symptoms: dizziness, vertigo, diplopia, perioral numbness, blurred vision, tinnitus, ataxia, bilateral sensory deficits, and drop attacks. The mechanism that triggers the symptom (e.g., standing up, rotating or extending the neck) must be sought when evaluating these patients. Patients with orthostatic hypotension have vertebrobasilar symptoms when they stand abruptly after sitting or lying down. Blood pressure measurements taken immediately after they stand up when experiencing symptoms shows a drop in systolic pressure greater than 20 mm Hg. This mechanism is particularly common in diabetic patients with sympathetic paralysis leading to loss of venomotor tone because a substantial amount of blood is pooled in their legs on standing.
The presence of vertebrobasilar ischemia related to neck rotation or extension suggests compression on the vertebral arteries by the bone and/or muscles that surround them, often by vertebral osteophytes. Patients who develop symptoms by extrinsic compression of the vertebral arteries usually require a few seconds with the neck rotated maximally in a particular direction to develop symptoms, while in patients with vestibular disorders, symptoms appear with brief, head-shaking motions. In addition to orthostatism and osteophytic compression, other conditions are capable of causing vertebrobasilar ischemia and must be ruled out. Dissection of a vertebral artery is accompanied by neck pain. In these patients, the symptoms of brain ischemia may be due to critical compromise of the true lumen of the vertebral artery by an intramural dissecting hematoma or embolization of thrombus formed in the true or false lumens, the latter entering through a distal reentry point of the dissection. A number of medical conditions may also present with symptoms of vertebrobasilar ischemia; among the most common are inappropriate antihypertensive medication, cardiac arrhythmia, anemia, brain tumors, and subclavian steal.
Indications for Surgery
No morphologic database exists for atherosclerotic lesions of the SATs comparable to that available for internal carotid artery disease. It is known from arteriograms and postmortem studies that the SATs are less frequently involved by atherosclerotic disease than is the carotid bifurcation. In general, clinicians do not have the ability to use ultrasonography to study the composition of SAT plaques, and the specimens obtained at operation are few because the interventions to reconstruct the SATs are bypasses rather than endarterectomies. The few specimens available for pathologic study show degenerative features similar to those seen in carotid plaques: surface thrombus, ulceration, and intraplaque hemorrhage. One may reasonably infer that the same pathologic mechanisms operate in both carotid artery plaques and SAT lesions. Until more precise information becomes available, it seems sensible to use criteria similar to those applicable to carotid disease to determine treatment. These criteria, however, must be tempered by the fact that the risk of surgical reconstruction of the SATs is higher than that of carotid endarterectomy, when an endovascular intervention is not applicable.
Currently, perhaps the most common indication for reconstruction of the arch trunks is in combination with proximal thoracic aortic endograft placement. Contemporary vascular surgeons should master the techniques described in this chapter to become comfortable in performing hybrid procedures involving the aortic arch.
The standard indications for surgical repair of SAT lesions include lesions with more than 70% of SAT diameter reduction or plaques with ulceration or surface irregularities in patients with appropriate symptoms (ipsilateral carotid or vertebrobasilar); the same lesions plus ipsilateral internal carotid disease for which an endarterectomy is indicated (the operation should correct both); the same lesions plus a nonacute ipsilateral hemispheric infarction (overt or silent); or preocclusive lesions (>90% cross-sectional area loss) in asymptomatic patients who are good surgical risks. The latter indication often occurs in combination with the need for a carotid endarterectomy and can be done using a retrograde transluminal approach. Proximal subclavian artery stenosis or occlusion causing subclavian steal syndrome with symptoms of posterior cerebral ischemia is an indication for left subclavian revascularization. In patients with stenosis of the subclavian artery and a previous coronary artery bypass using the internal mammary artery, flow may reverse in the mammary artery towards the ischemic arm “stealing” blood from the coronary circulation. These cases should also be treated with immediate left subclavian artery revascularization using the most durable reconstruction, which presently is a carotid-to-subclavian bypass. Asymptomatic subclavian artery stenosis should also be treated when a myocardial revascularization using the left internal mammary artery is necessary.
The primary indication for reconstructing a vertebral artery is to treat vertebrobasilar ischemia. Severe occlusive disease of the vertebral artery found in individuals who have no symptoms of vertebrobasilar ischemia does not require any treatment, surgical or otherwise. Conversely, many systemic causes of vertebrobasilar ischemia are not related to vertebral artery disease. Therefore, the decision to reconstruct a vertebral artery must be based on a strong anatomic and clinical presumption that the symptom (vertebrobasilar ischemia) is secondary to the anatomic lesion (occlusive disease or extrinsic compression of the vertebral arteries).
Vertebrobasilar ischemia may be due to stenosis or occlusion of the vertebral or basilar arteries, restricting flow in the territory supplied by these arteries. This is the so-called low-flow (or hemodynamic) mechanism. These patients often have repetitive transient ischemic attacks triggered by positional or postural mechanisms. Although their risk for stroke is lower than that in patients with carotid disease, they may suffer serious traumatic injuries because of loss of balance (such as syncopal attack while driving). In patients with low-flow symptoms of ischemia in the vertebrobasilar territory, the surgical indication rests on the assumption that the basilar artery is not receiving adequate inflow from the vertebral arteries. Ischemia of the vertebrobasilar territory may also be due to microembolization (atheroemboli). Approximately one-third of vertebrobasilar ischemic episodes are caused by atheroembolization from plaques or mural lesions of the vertebral arteries. Patients with embolic symptoms are at high risk for infarctions of the brainstem, cerebellum, and posterior cerebral artery territory. The mechanism here is microembolization from the irregular surface or from the core of a plaque in the proximal subclavian or vertebral arteries or from a lesion in the wall of the vertebral artery secondary to repetitive trauma from an osteophyte or from intramural dissection.
In patients with low-flow symptoms, and because two vertebral arteries usually supply the basilar artery, the presence of a normal vertebral artery contraindicates an operation on the opposite artery, regardless of its anatomic condition. A vertebral artery of normal caliber emptying into a basilar artery is enough to adequately supply the basilar territory. This means that for a lesion in the vertebral arteries to be considered significant, it must be severe (>75% stenosis) and the opposite vertebral artery must be equally diseased, hypoplastic, or absent.
The best approach to a patient with low-flow vertebrobasilar ischemia is first to determine whether any other clinical condition (e.g., orthostatism, arrhythmia) capable of producing these symptoms is present. If so, it should be corrected. If symptoms persist after treatment, an arteriogram is indicated. If the arteriogram shows a lesion that fulfills the anatomic criteria listed previously and the operation appears to be technically feasible, a reconstruction of the vertebral artery is indicated.
In patients with vertebrobasilar ischemic symptoms secondary to embolization, typically suggested by the presence of ischemic infarcts in the vertebrobasilar territory, the indication for surgery rests on demonstration of the emboligenic lesion, regardless of the condition of the opposite vertebral artery. The criteria of bilateralism and degree of severity that apply to low-flow lesions are irrelevant when considering treatment for atheroembolic disease.
Reconstruction of the Supra-Aortic Trunks
Currently, many focal lesions of the proximal SATs can be treated with transluminal angioplasty and or stenting. When a transluminal intervention on the SATs is indicated and technically feasible, most of these procedures are best done using a retrograde approach via the brachial or axillary artery when treating subclavian lesions, or via the common carotid arteries when treating proximal common carotid or innominate artery lesions. The retrograde approach is in general preferable to the transfemoral route because it avoids instrumentation of the arch and proximal SATs without brain protection. Retrograde trans-carotid transluminal interventions are done through a small cervical incision to expose the common carotid artery proximal to the bifurcation. When retrograde access is established in the common carotid, the artery is clamped proximal to the bifurcation to prevent embolization during lesion crossing and stent placement, and to allow external to internal carotid perfusion. Additionally, this hybrid approach permits external flushing of the common carotid before re-establishing flow into the carotid artery, and ideally, the proximal internal carotid is clamped for a few seconds when cephalad flow is resumed, thereby channeling embolic material generated during the intervention into the external carotid territory. These simple technical principles make retrograde stenting of the SATs a safer approach than the transfemoral route. When indicated, trans-carotid retrograde interventions can be done in combination with a carotid endarterectomy. In these cases, after exposure of the carotid vessels, the proximal carotid or innominate stenting is done first, followed by a standard carotid endarterectomy.
In some patients with extensive or heavily calcified lesions of the proximal SATs a transluminal intervention may not be advisable because of the predictable risk of complications or failure. In those cases, the initial decision should be to decide whether to do a trans-cervical or a transthoracic SAT repair. Cervical repairs are typically done by means of a bypass from a suitable donor vessel to the diseased one. Most of these bypasses run transversely either between vessels on the same side of the neck (carotid to subclavian or subclavian to carotid) or across the neck (carotid to carotid and subclavian to contralateral carotid). Cervical reconstructions include bypass procedures between the ipsilateral carotid and subclavian arteries and transposition procedures that provide the advantage of a single arterial anastomosis without the need for a saphenous vein graft or a prosthetic graft. Transthoracic repairs require a partial or total sternotomy for a direct approach to these vessels. The lesions are corrected with a bypass from the ascending aorta to the innominate, common carotids or right subclavian artery.
Transthoracic repairs are preferred in younger patients who have innominate artery lesions or multiple severe lesions not amenable to endovascular repair (usually innominate and left common carotid). They are also a good choice for patients in whom a simultaneous coronary bypass operation is indicated.
Cervical repairs are preferred in older patients, in those who are at high risk of thoracotomy, in those who have had previous trans-sternal procedures, and in those with calcified plaque in the ascending aorta that makes partial aortic clamping contraindicated. A cervical repair is the choice for all single arterial lesions (other than those of the innominate artery).
Currently, one of the most common indications for reconstruction of the SATs is in conjunction with placement of endografts in the proximal thoracic aorta. These operations are also known as arch “debranching” procedures. The intent of this surgery is to revascularize the supra-aortic trunks whose origins will be covered by a thoracic aortic endograft requiring a proximal landing zone in the arch. Contemporary vascular surgeons should be very familiar with these principles and surgical techniques. When the left subclavian artery origin requires coverage, a left common carotid to left subclavian artery bypass or a subclavian to carotid transposition is indicated. If there is a left vertebral artery arising from the arch, the vertebral artery should be transposed to the left common carotid artery, a critical intervention in patients who have an occluded or hypoplastic right vertebral artery that may prevent a devastating stroke involving the posterior brain. When the left common carotid origin also requires coverage, a retropharyngeal right common carotid to left common carotid is added to the “debranching.” Finally, when the innominate artery requires coverage, a transthoracic bypass from the ascending aorta to the innominate, and to the left common carotid is done in addition to a left common carotid to left subclavian bypass done transcervically.
Cervical Repairs
The bypass between the carotid and the subclavian artery is constructed between the proximal cervical segment of the common carotid artery and the retro-scalene segment of the subclavian artery. In some cases, the carotid artery is the donor vessel, to bypass a stenosis of the most proximal portion of the subclavian artery. In others, the subclavian artery is the donor vessel to bypass a proximal common carotid artery lesion. In subclavian-carotid bypasses, an end-to-end anastomosis to the common carotid artery is recommended because with an end-to-side anastomosis there is a possibility of embolization (from the diseased proximal common carotid artery) or of extension of the proximal thrombus across the end-to-side anastomosis.
Carotid-subclavian bypass is the standard operation for the correction of subclavian steal syndrome affecting the vertebrobasilar or coronary territories. However, proximal subclavian artery stenting has become a very acceptable alternative when performed in favorable lesions. In rare cases, when a transluminal intervention or a carotid-to-subclavian bypass are not possible, correction of subclavian steal can be achieved with bypasses between both subclavian arteries or both axillary arteries, albeit with predictably lower patency rates. These remote bypasses are constructed with the graft crossing the neck in front of the sternum, giving a poor cosmetic result, and are subject to external compression. In addition, bypasses coursing the anterior, low-neck may interfere with an eventual tracheostomy or midsternotomy if so required later.
Cervical bypasses are preferably done with prosthetic conduit. Either polytetrafluoroethylene (PTFE) or Dacron grafts provide a good-caliber match, and their patency rates are higher than those of transluminal interventions, probably as a result of the high flow rates usually measured in these arteries.
Anatomic Indications
Innominate artery occlusion or stenosis.
A variety of cervical techniques are available to correct flow deficits caused by innominate artery stenosis or occlusion. Subclavian-subclavian and axilloaxillary bypasses can supply the right carotid artery through retrograde flow into the proximal right subclavian or axillary arteries. Carotid-carotid bypasses are technically feasible, but for the correction of severe innominate artery disease they represent an unnecessary risk because both carotid systems will likely be severely hypotensive during the proximal anastomosis of the bypass to the donor left common carotid artery, unless shunted.
If the innominate artery lesion is suspected to be embolizing—or if it exhibits a grossly irregular surface or large ulcerations—the distal innominate artery should be ligated (excluded) at the completion of the remote bypass procedure. This may not be possible using a supraclavicular approach. A complex solution is an end-to-end anastomosis between the proximal subclavian artery and the proximal right common carotid artery, with ligation of the proximal carotid stump, and then revascularization of the middle or distal third of the right subclavian through a remote bypass from the other side of the neck.
Common carotid artery occlusion or stenosis.
The common carotid artery can be revascularized by means of a subclavian-carotid bypass from the ipsilateral subclavian artery, with the distal anastomosis being performed end to end to avoid embolization from the diseased proximal common carotid artery. In some cases, the entire common carotid is occluded, with a patent carotid bifurcation maintaining retrograde flow from the external carotid into the internal carotid artery antegradely. Most of these patients necessitate a carotid endarterectomy in conjunction with a subclavian to carotid bypass. This reconstruction can be done placing the distal anastomosis for a graft at the level of the carotid bifurcation in an end-to-side junction (an onlay patch), with or without a concomitant endarterectomy of the carotid bulb ( Fig. 20.1 ). A preferable technique for the distal anastomosis ( Fig. 20.2 ) is to transect the distal common carotid artery at the carotid bulb, doing then a type 2 eversion endarterectomy. The ample cross section of the endarterectomized carotid bifurcation allows a simple end-to-end anastomosis to the bypass arising from the subclavian artery.
If the stenosing lesion of the common carotid artery is located at its origin and its distal two-thirds are free of disease, transposing the midportion of the common carotid artery to the subclavian artery is a better solution than a subclavian-carotid bypass. It requires only one anastomosis and no prosthesis. At times, a thrombosed common carotid artery with a patent bifurcation can be thrombectomized after dividing it low in the neck and doing an eversion endarterectomy up to the bifurcation. The distal portion of the endarterectomy is terminated under direct vision through the standard arteriotomy used for a conventional carotid endarterectomy. After endarterectomy, the common carotid artery is reimplanted into the second portion of the subclavian artery. Subclavian-carotid bypass and transposition of the carotid into the subclavian are easier on the right side, where the subclavian artery is more accessible.
In cases in which the ipsilateral subclavian artery is not a suitable donor vessel, a common carotid artery lesion can be corrected by means of a carotid-carotid bypass. This operation is traditionally done by placing a bypass between both carotids in front of the airway, or preferably using the shorter retropharyngeal route (see later in this chapter).
Subclavian artery occlusion.
Reconstruction of the proximal subclavian artery is done (1) to correct symptomatic subclavian steal from the vertebral or the coronary territories, (2) to correct an emboligenic lesion of the proximal subclavian, (3) to revascularize the subclavian before an internal mammary transposition to the coronary arteries, or (4) to revascularize the left subclavian from the left common carotid artery before implanting a thoracic aorta stent-graft across its origin. When not occluded, the subclavian artery must be ligated proximal to the origin of the vertebral artery at the time of the bypass. A direct transposition of the subclavian artery (prevertebral portion) to the common carotid artery is a more complex procedure than the bypass, but it involves only one anastomosis, excludes the diseased proximal subclavian artery when necessary, and does not require a prosthetic graft.
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