Occlusive lesions of the innominate artery are relatively uncommon. They may be asymptomatic or symptomatic. Asymptomatic lesions are usually discovered in the evaluation of asymmetric upper extremity pulses or blood pressures or during aortic arch imaging for unrelated indications. The natural history of asymptomatic innominate artery occlusive lesions is unknown. The treatment of asymptomatic lesions of the innominate artery has typically been indicated by the need for an associated vascular reconstruction dependent on the innominate artery such as the use of the right internal mammary artery for coronary bypass or prior to axillofemoral bypass.

Symptoms may be due to either atheroembolism or globally insufficient blood flow to the two vascular beds supplied by the innominate artery, the right arm and/or the right brain. Typically, atheroembolism is associated with ulcerated, less stenotic lesions, while hypoperfusion is typically due to high-grade stenosis or occlusion of the innominate artery often in combination with obstructive lesions in other arch vessels and reductions in cardiac output.

Cerebral symptoms associated with innominate artery lesions may be due to atheroembolism or global cerebral hypoperfusion. Symptoms may be focal and reproducible, suggesting recurrent microatheroembolism, or may be vague, nonspecific, and poorly lateralized. It may be impossible to determine the precise source of cerebral atheroemboli in the presence of tandem lesions in the innominate artery and the right internal carotid artery. Vague symptoms such as dizziness or sensations of instability or orthostatic weakness may be caused by a variety of metabolic, cardiac, and neurologic conditions other than innominate artery disease. Neurologic consultation may be helpful in the assessment of complex symptoms, and sophisticated imaging of the brain may be appropriate.

Right upper extremity symptoms should be assessed in all patients with innominate artery disease. Insufficient blood flow to the arm may be manifest as easy fatigability, pain with exertion, paresthesias, or a sensation of coolness. Because of its similarity to exercise-induced pain in the legs, pain in the arm with exertion is often, though inaccurately, called arm “claudication” (from the Latin root “to limp”). Atheroembolism from an innominate lesion can present with subungual splinter hemorrhages or bluish discoloration of the fingertips, which can progress to ulceration.

Obstructive lesions at the origin of the common carotid arteries may mimic the presentation of lesions at the carotid bifurcation but occur less frequently. Atherosclerosis, radiation injury, and giant cell arteritis are the most common pathologies in the common carotid arteries. Ipsilateral focal neurologic symptoms due to atheroembolism are often referred to as the four Ss: alterations in speech, sight, strength, or sensation. Cerebral atheroembolic events are more common in the setting of high-grade common carotid stenosis as opposed to complete occlusion. It is important to note that even in the setting of complete common carotid occlusion the internal carotid artery may remain patent through reversed flow in external carotid collaterals and may be the source of ipsilateral cerebral atheroemboli. In one recent case of common carotid occlusion, patency of the left internal carotid artery was maintained through collaterals from the ipsilateral thyrocervical trunk to the inferior thyroid artery to the superior thyroid artery to the carotid bifurcation. If the carotid bifurcation remains patent distal to an occluded common carotid artery, reconstruction may be accomplished with the relatively straightforward subclavian-to-carotid bifurcation bypass. Though synthetic grafts have wide acceptance in this location, we prefer to use an autogenous conduit such as the saphenous vein or (superficial) femoral deep vein in this location because of its resistance to kinking. If the common and internal carotid arteries are occluded, cerebral revascularization may require bypass to the intracranial internal carotid or middle cerebral arteries.

Atherosclerotic obstruction is usually confined to the origin or first few centimeters of the subclavian artery. Arterial disease located in the distal subclavian and axillary arteries is more commonly caused by giant cell arteritis. Proximal subclavian occlusive disease usually presents in one of three clinical patterns: upper extremity pain with use, thromboembolism in the hand and fingers, or rarely vertebrobasilar insufficiency. Symptoms in the arm include early fatigue, pain with exercise, and a sensation of heaviness. Patients often complain of limitations with routine daily activities such as combing their hair. Less commonly, patients present with evidence of microembolism to the hand and fingers. Finally, occasional patients describe a variety of vague neurological symptoms including dizziness, vertigo, unsteadiness or imbalance, drop attacks, lightheadedness, visual disturbances, and hemiparesis or hemisensory dysfunction in association with subclavian disease. The term “subclavian steal” was first used by C.M. Fisher in 1961 in a discussion of two such patients reported in the New England Journal of Medicine. Today, subclavian steal
is used quite commonly to describe the finding of reversed flow in the vertebral artery ipsilateral to proximal subclavian stenosis or occlusion. Based on cerebral blood flow studies, the actual incidence of hemodynamically relevant “steal” is rare. The increased utilization of color flow Doppler in the investigation of cerebrovascular disease has resulted in more frequent detection of unsuspected subclavian steal. Isolated, asymptomatic subclavian steal is usually not clinically relevant, represents a stable and physiologically appropriate collateral pattern of blood flow, and does not warrant invasive diagnostic procedures or treatment. Subclavian steal does not appear to increase the risk of stroke. Carotid artery occlusive disease is present in approximately a quarter of patients with subclavian steal and is probably responsible for most focal hemispheric symptoms. Though described as a classical presentation, the onset of vertebrobasilar symptoms during arm exercise is distinctly uncommon. Due to the rather obscure nature of the symptoms in many patients with subclavian steal, it may be difficult to establish a definite link between the anatomic finding of reversed flow in a vertebral artery and the cerebral symptoms. Other causes of posterior cerebral symptoms include cervical spondylosis or injury, intrinsic vertebral or basilar artery disease, posterior fossa tumors, vestibular dysfunction, and systemic causes of cerebral hypoperfusion such as transient dysrhythmias or hypotension.

The increasing use of the internal mammary artery for coronary bypass grafting has led to the identification of so-called coronary subclavian steal. Coronary subclavian steal syndrome presents as angina due to subclavian stenosis or occlusion proximal to the origin of an internal mammary coronary artery bypass graft. Bilateral brachial blood pressures should be checked in all patients prior to internal mammary bypass and reassessed if angina recurs in follow-up. Percutaneous, endovascular, and direct surgical reconstruction may be appropriate in selected cases of coronary subclavian steal syndrome.

Subclavian obstruction should be suspected in any patient with asymmetric radial pulses on physical examination or a 20 mm Hg difference between brachial systolic blood pressures. Subclavian steal is two to three times more common on the left side than the right, perhaps owing to the short distance between the innominate and right vertebral artery. Symptoms are rare in the setting of isolated single-vessel disease due to the adequacy of cerebellar collateral circulation.