Extraanatomic Repair of Aortic Arch Vessels

Historical Background

Savory was the first to describe a patient with signs and symptoms suggesting occlusive disease involving the aortic arch vessels. Nearly 20 years later, in 1875, Broadbent chronicled a patient who while living had no radial pulses and at postmortem examination was found to have brachiocephalic and left subclavian artery occlusion. In 1908 Takayasu reported a patient with an ischemic retinopathy on ophthalmologic examination who later was found to have occlusive lesions in all three aortic arch vessels from a chronic inflammatory process that was later termed “pulseless disease” by Shimizu and Sano. The inflammatory arteritis involving the arch branches now bears Takayasu’s name. In 1960 Contorni was the first to describe the anatomy of subclavian artery steal.

The first surgical procedures were performed for aneurysmal changes of the arch vessels, mostly syphilitic subclavian lesions. The first attempt at surgical correction of a proximal subclavian aneurysm, by innominate ligation, was carried out by Mott of New York City in 1818, but the patient did not survive. Bahnson was the first to perform a bypass from the ascending aorta to the innominate artery using an aortic homograft in a patient with occlusive lesions from syphilitic arteritis. One year later, in 1956, Davis and associates described endarterectomy of an innominate artery through a right anterior thoracotomy for a symptomatic atherosclerotic occlusive lesion. Endarterectomy to reestablish flow through obliterated subclavian vessels was described by Cate and Scott in 1957.

In 1956 Lyons first reported a series of four subclavian to carotid artery bypasses from a cervical approach. In 1964 Parrott reported two subclavian-to-carotid transpositions through a similar exposure. In 1994 Berguer and Gonzalez described transcervical extraanatomic revascularization of the aortic arch vessels via a retropharyngeal route.

Indications

Atherosclerosis is, by far, the most common disease affecting the aortic arch vessels. Occlusive lesions less commonly result from inflammatory diseases such as Takayasu arteritis, or they can be the result of exposure to therapeutic radiation.

Severe disease is defined as stenosis with a diameter of more than 75%. In addition, in symptomatic patients, a deep ulcerated plaque or a thrombus within the arterial lumen is also considered a severe lesion even though the defect may be less than 75% of the diameter. When the disease is seen in multiple trunks, the occlusive process is likely an extension of disease originating within the aortic arch that has “spilled over” into the vessel ostia. Accordingly, the pathophysiology of vertebrobasilar ischemia is typically from low flow. Single trunk disease manifests more commonly as symptoms from hemispheric or upper extremity emboli. Isolated proximal disease can lead to symptomatic steal phenomenon.

Symptomatic atherosclerotic trunk disease may manifest as ocular, hemispheric, or vertebrobasilar transient ischemic attack or stroke. Patients commonly present with a combination of both anterior and posterior cerebrovascular ischemic symptoms. Cerebrovascular symptoms can be the result of emboli or low flow. Patients with subclavian steal syndrome present with posterior cerebrovascular symptoms as blood is siphoned from the basilar artery ( Fig. 12-1 ). A similar but less common steal phenomenon can occur when the innominate artery is occluded and flow in the common carotid artery and ipsilateral vertebral artery is reversed to supply the right arm. Another rare problem is that of myocardial ischemia from the phenomenon of coronary steal, which can develop in patients with innominate or subclavian disease proximal to an internal mammary revascularization of the coronary arteries. Such patients can also present with symptoms of upper extremity ischemia. Patients may develop varying degrees of arm ischemia, ranging from the claudication observed in patients with subclavian steal to limb-threatening ischemia resulting from extensive arterial occlusion or emboli.

Over the last decade the most common indication for surgical manipulation of the aortic arch vessels has been to prepare patients with thoracic and thoracoabdominal aortic aneurysms, dissections, or traumatic tears for an endovascular stent-graft repair. Left subclavian artery and even left common carotid artery transpositions are not infrequently performed to preserve vertebral and left upper extremity flow while extending the proximal neck “landing zone” before endograft deployment ( Fig. 12-2 ).

Preoperative Preparation

• Once a diagnosis has been established, multiplanar views of the aortic arch using digital subtraction angiography, computed tomography (CT) angiography, or magnetic resonance angiography are necessary for planning arch branch revascularization. A complete arch and four-vessel study can be performed with emphasis placed upon the vessel’s origins and late views to show vascular reconstitution from steal. Magnetic resonance and CT angiography are noninvasive modalities with imaging capabilities that may equal those for invasive angiography.

• It is often useful to obtain a transesophageal echocardiogram (TEE) to assess myocardial function and rule out a cardioembolic source. In addition, like CT, TEE allows for the identification of significant calcific lesions or atheromata within the arch that would preclude aortic clamping during direct repair or contraindicate passage of wires and catheters for antegrade endolumenal therapy.

• Patients with recent brain infarcts (symptomatic or silent) should have surgery delayed, especially if multiple vessel revascularization is considered to decrease the risk of reperfusion injury.

• If a cervical approach to trunk revascularization is planned, preoperative cardiac evaluation should follow guidelines similar to those for carotid bifurcation surgery.

• Preoperative aspirin is administered before surgery based upon recommendations for carotid surgery.

• Vocal cord function should be evaluated if patients have a history of prior carotid surgery.

• A single dose of prophylactic antibiotics are administered within 1 hour of incision.

• Blood pressure monitoring by the intraoperative arterial line is advisable.