Clinical presentation of subclavian and innominate artery peripheral arterial disease (PAD) varies from hand claudication to cerebral hypoperfusion to distal embolization and digital ischemia. Upper extremity PAD could manifest as coronary steal or lower extremity claudication in patients who have had CABG or extra-anatomic axillary to femoral bypass. Physical examination is significant for weak pulses on an ipsilateral extremity, a systolic blood pressure difference of more than 10mmHg compared to contralateral extremity. Sometimes the affected hand may feel cool to touch, and in severe cases, digital ischemia has also been described. Often patients present during their sixth or seventh decades of life, and they have associated peripheral arterial disease risk factors such as smoking, diabetes mellitus, hyperlipidemia, hypertension, lower-extremity peripheral arterial artery disease, and less common inherited genetic disorders such as inflammatory or Takayasu arteritis.
Subclavian artery stenosis causes notable morbidity because it causes symptomatic ischemic problems that affect the upper extremities, brain, and heart. Atherosclerosis is the most common cause. Other etiologies include arteritis, inflammation due to radiation exposure, compression syndromes, fibromuscular dysplasia, and neurofibromatosis.
PAD of the major vessels is associated with narrowing of the arteries due to atherosclerosis. It is estimated that approximately 2% of the population has subclavian artery PAD. Prevalence of PAD in adults older than 70 years is about 15%. Of these, nearly 25% will require revascularization, and 5% of patients will progress to critical limb ischemia. The majority of the patients are asymptomatic due to slow disease progression. Symptoms usually appear once there is 50% luminal narrowing of the vessel diameter. The prevalence of disease in a brachiocephalic artery in patients with known PAD is about 42%. About half of patients with the known peripheral arterial disease have stenosis of the left subclavian artery (30%). In patients with subclavian artery disease, half of them have coronary artery disease, and one-third have carotid or vertebral disease.
Atherosclerosis risk factors account for atherogenesis in this category of patients. Vascular risk factors including, diabetes, hyperlipidemia, hypertension, and tobacco abuse augment cell adhesion molecules, which promote inflammatory cells to adhere to the arterial wall. This process causes remodeling of the arterial wall and lipid deposition with the tunica media. As this process evolves, narrowing of arterial lumen eventually follows and, in turn, causes calcification of the arterial wall. In addition, brachiocephalic arteries including the innominate and subclavian can be affected by vasculitides like Takayasu arteritis and giant cell arteritis. Brachiocephalic atherosclerosis disease can be unifocal or multifocal. Disease of the brachiocephalic arteries can manifest in several ways including transient ischemic attack (TIA), upper extremity ischemia or claudication and vertebrobasilar insufficiency. Aneurysms of the brachiocephalic arteries occur infrequently and can be related to atherosclerotic post-stenotic dilatation, trauma, inflammation, or infection.
The left subclavian artery is more likely to be affected than the right or innominate arteries. If there is isolated stenosis, the likelihood of symptoms is less than in other vascular beds. However, if the obstructive disease affects other aortic arch vessels, such as the carotid or vertebral arteries, the likelihood of steal or ischemic symptoms increases.
Upper extremity symptoms include arm claudication or muscle fatigue, rest pain, and finger necrosis. Neurologic issues include vertebrobasilar hypoperfusion including visual disturbances, syncope, ataxia, vertigo, dysphasia, dysarthria, and facial sensory deficits.
In patients with internal mammary artery grafts as a result of coronary artery bypass graft surgery, the symptoms of ischemic heart disease, including angina pectoris, due to coronary-subclavian steal, predominate.
While the diagnosis typically rests on imaging, a thorough physical exam is important. On examination, patients can display:
Initial assessment of patients with subclavian artery disease includes blood pressure measurement in both arms to evaluate for discrepancies in the upper extremities and the presence of bruits (carotid, cervical, or supraclavicular). Less frequent physical findings include finger ulcers, necrosis, splinter hemorrhages, or gangrenous skin changes. Auscultation for bruits in the subclavian arteries or carotid arteries will narrow the search for any occult disease.
Duplex ultrasound with color flow imaging is the noninvasive modality of choice in the evaluation of subclavian artery disease. Dampened or monophasic waveforms, turbulent color flow imaging, and increased velocities in the region of stenosis are characteristic findings of obstruction. Reversal of ipsilateral vertebral artery flow is seen in subclavian steal syndrome. CT scan angiography offers an excellent anatomic resolution, determines the length of the lesion as well as location. Its drawback, however, lies in the fact that it does not provide optimal information on the degree of calcification. Digital subtraction angiography and fluoroscopy also do not quantify the degree of calcification. MR angiography can be misinterpreted as the reduced flow can be interpreted as exaggerated disease. The definite test is invasive angiography; nonsubtracted images provide anatomical mapping, while digital subtraction further characterizes the stenosis. There is a small risk of stroke (less than 1%) when manipulating the aortic arch and brachiocephalic arteries.
Treatment is indicated for symptomatic patients with arm claudication, cerebral hypoperfusion, and subclavian steal syndrome. The modality of treating brachiocephalic symptomatic lesions varies and can be accomplished with open, endovascular, or hybrid approaches. Treatment should also be considered for the protection of bypass graft on a patient with previous CABG, axillofemoral, or axilloaxillary.
Initial experience with treatment of the aortic arch arteries was with open surgery. Endovascular therapy of the aortic arch has surpassed open repair in frequency and safety. Its minimally invasive nature, shortened hospital stay and lower complication rates in immediate postoperative period has made it appealing to not only patients but also interventionalists. On the other hand, use of stents in treating brachiocephalic arterial disease with a combination of angioplasty has surpassed angioplasty alone.
Patency rates of endovascular approach are slightly lower compared with open surgery. One-year and 5-year patency for the aortic arch occlusive disease is approximately 80% to 90% and 77% to 89% respectively. Long-term patency rates are better for surgical bypass; however, it carries a higher short-term risk.
Complication rates ranged from 0% to 20% over a 5-year period. They were mostly related to access-entry site type of complications such as pseudoaneurysm, hematoma, and dissection. The incidence of stroke is 1%. Restenosis and stent fracture is described in the literature. Complete occlusion and longer lesions (more than 2 cm) contribute to worse outcomes.
Management is geared towards controlling PAD risk factors (smoking cessation, statins, beta blocker, and aspirin). For those patients who had stent placement dual antiplatelet therapy with aspirin and clopidogrel is highly advocated.
Patient Follow up
Physical examination including bilateral upper extremity blood pressure measurement should be performed every 6 months. Duplex studies of the brachiocephalic arteries including upper extremity segmental pressures and pulse volume recordings should be performed every 6 months for the first 18 to 24 months, and then the interval may be increased to annually. 
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