A 59-year-old Caucasian woman presented for evaluation after a recent right hemispheric stroke. She had residual short-term memory loss but no sensory or motor deficits. She reported previous episodes of dizziness, syncope, and left arm fatigue upon exertion prior to the stroke. Despite a 60 pack-year cigarette smoking history, she had recently quit and was compliant with her statin and antiplatelet therapy. On physical examination she had a right cervical bruit, absent left radial pulse, and her lower extremity vascular examination was unremarkable. There was significant discrepancy in upper extremity pressures.

Computed tomography (CT) and digital subtraction arteriogram (DSA) demonstrated occlusion of the left subclavian and the origin of the left common carotid arteries, but the latter was reconstituted by collaterals at the level of the bifurcation (Figure 9-1A). The right common carotid artery (CCA) had greater than 90% ostial stenosis and the right subclavian artery had significant stenosis, as suggested by the poststenotic dilation (Figure 9-1B). The right vertebral artery was dominant (Figure 9-1C). The innominate artery demonstrated diffuse calcific irregularity with moderate distal stenosis (Figure 9-2). The left vertebral artery was patent with retrograde flow on duplex ultrasonography.

After extensive discussion with the patient regarding the risks and benefits of open versus endovascular management strategies, she proceeded to the operating room for a hybrid procedure. Retrograde open right subclavian artery access was obtained with placement of a balloon expandable stent from the proximal subclavian artery extending into the innominate artery (Figure 9-3A and B). A right subclavian to carotid artery bypass was then constructed with a prosthetic graft, and the proximal common carotid was ligated. She was discharged home on postoperative day 1 (POD1) and had no adverse events. She was doing well with no further neurologic problems at subsequent follow-up.

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  The incidence, and consequence, of atherosclerosis in the aortic arch vessels has been described in few reports. In an autopsy study of patients who suffered a fatal stroke, approximately 50% of subjects had plaque deposition at the origin of the innominate, left common carotid, or left subclavian arteries.¹

  
  
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  Arch multivessel atherosclerotic disease is most common in middle-aged Caucasian females. The majority of them are asymptomatic, even in the presence of flow reversal through the vertebral, and should be managed conservatively. However, more clinically relevant is the 0.6% to 4% incidence of concurrent internal carotid and proximal arch vessel atherosclerotic disease, raising questions regarding preprocedure imaging and indications for treatment of arch vessel disease.²

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  The well-recognized vascular risk factors associated with atherosclerotic disease, including diabetes mellitus, hypertension, hyperlipidemia, obesity, family history of accelerated atherosclerosis, and cigarette smoking, also contribute to the deposition of plaque in the aortic arch vessels.

  
  
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  Differential distribution of atherosclerotic disease is likely related to flow dynamics and is an independent risk factor for stroke.³ In some patients, underlying inflammatory arteritis (eg, Takayasu disease) hastens atherosclerotic degeneration.

Clinical Presentation

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  Patients with disease of the supra-aortic trunk vessels may present with symptoms of global cerebral ischemia, upper extremity fatigue upon exertion, subclavian steal syndrome, or coronary-subclavian steal syndrome.⁴

  
  
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  Transient ischemic attack as well as stroke may result from embolic events from proximal common carotid or innominate artery lesions or acute occlusion.³

  
  
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  Subclavian artery stenosis or occlusion may lead to the sensation of upper extremity cramping or fatigue during heavy activity or repeated use. Alternatively, increased upper extremity workload may precipitate reversal of flow through a patent vertebral artery.⁴ These patients report symptoms corresponding to posterior cerebral ischemia such as dizziness, vision changes, and presyncope (subclavian steal syndrome). Similarly, in patients with prior coronary artery bypass grafting utilizing internal thoracic artery conduit, angina pectoris may be elicited by aggressive upper extremity exercise due to reversal of flow through the bypass segment, a phenomenon known as coronary-subclavian steal syndrome.⁴

  
  
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  Detailed past medical history should be obtained with particular attention to the patient’s atherosclerotic risk factors. A personal history of cigarette smoking is almost always associated with multivessel disease³ and patients should be extensively counseled on cessation. In young patients, a history of fever, malaise, night sweats, weight loss, arthralgias, and fatigue should also be pursued for consideration of large vessel arteritis.

Physical Examination

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  In addition to confirming that the patient’s heart has a regular rate and rhythm without evidence of mitral or aortic murmurs (to rule out secondary cause of embolic event in symptomatic patients), a carotid bruit may be auscultated during evaluation of the neck.

  
  
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  Palpation of carotid and upper extremity pulsation could provide clues to high-grade proximal disease with associated palpable thrill and diminished pulsation distally. Bilateral brachial blood pressure measurements should be performed.

Laboratory Evaluation