Upper Extremity Intervention

Introduction

Atherosclerotic upper extremity obstructive disease is predominantly secondary to subclavian or innominate artery stenosis (SAS or IAS). The diagnosis is usually suspected when a significant (often ≥15 mm Hg) systolic brachial blood pressure discrepancy (SBBP) is detected between the two arms. Applying this threshold, the prevalence of SAS in the general population is estimated at approximately 2% and increases with advancing age. In a high-risk population with known or suspected vascular disease, including individuals referred for coronary artery bypass surgery, the prevalence is estimated at about 7%. Involvement of the left subclavian artery (L-SCA) is three to four times more common than the right brachiocephalic and subclavian arteries. This may be explained by increased flow turbulence in the L-SCA due to its acute angle of origin. Moreover, one third of the stenotic lesions on the right side are found in the innominate trunk, proximal to the subclavian origin.

The presence of SAS correlates well with known atherosclerotic risk factors and is a strong indicator of the presence of PAD, defined as ABI ≤0.90. The incidence is much higher in patients with symptomatic PAD. In one study of 48 subjects with PAD who underwent aortic arch angiography, 19% had more than 50% stenosis of at least one brachiocephalic artery. Furthermore, SAS predicts total and cardiovascular mortality (independent of both risk factors and existent cardiac disease at baseline) and all-cause mortality. On the other hand, SAS is present in 11.5% of patients with known PAD. Therefore, we routinely recommend bilateral blood pressure measurements in high-risk patients.

Nonatherosclerotic conditions that can result in SBPD and SAS include Takayasu's arteritis, giant cell arteritis, coarctation of the aorta, thoracic outlet syndrome causing compression from an overlying rib, radiation-induced vascular disease, and, rarely, fibromuscular dysplasia (FMD), arterial thrombosis ( Figure 19-1 ), and neurofibromatosis. Therefore, routine evaluation for these disorders is not warranted. FMD is more likely to affect small and medium size arteries, notably the brachial artery, and can occasionally lead to upper extremity ischemia and bilateral pulse discrepancy. Importantly, the presence of a BBPD with associated acute chest pain should alert the clinician for the possibility of aortic dissection.

Diagnosis and Clinical Syndromes

Isolated SAS rarely leads to symptoms, perhaps due to the lower muscular mass it supplies (compared to that supplied by the lower extremity inflow arteries) and the high degree of collaterals that develop. Symptoms related to vertebrobasilar insufficiency (also referred to as vertebral subclavian steal syndrome, or vSSS) remain uncommon with isolated SAS and most likely occur when multiple craniocervical arteries are stenotic or occluded. The clinical manifestations of SAS are listed in Table 19-1 .

Lord et al. showed that the discontinuity of the circle of Willis due to the vertebral-vertebral shunt (from the patent vertebral artery [VA] to the occluded one, across the circle of Willis) is responsible for symptoms experienced during repetitive use of the affected upper extremity. Occasionally, the blood is routed from the anterior circulation through the descending cervical branches of the ipsilateral external carotid artery, providing collateral pathways to the occluded subclavian artery. In these case, symptoms of anterior circulation ischemia, such as transient hemiparesis paresis, speech disturbances, and sensory loss, may be reported. On the other hand, ischemic syndromes attributable to the anterior circulation are common in symptomatic patients presenting with occlusive lesions of the right innominate trunk. Fifty percent of such patients express anterior ischemia, while 40% present with posterior symptoms, and up to 10% manifest global (anterior and posterior) symptoms.

Javid test is a highly reliable clinical maneuver in demonstrating flow reversal via the circle of Willis. In this test, the examiner compresses the ipsilateral carotid artery, thereby decreasing intracranial pressure and flow and abolishing retrograde flow into the arm. This leads to an abrupt change in the quality of the ipsilateral radial pulse.

Acute symptoms of arm or cerebral ischemia usually result from acute injury to the subclavian artery, as seen with sharp and blunt trauma, inadvertent misplacement of a large venous catheter into an SCA, and coverage by a stent graft during TEVAR.

Most cases of SAS are asymptomatic and diagnosed either incidentally on imaging studies or during routine physical exam. In addition to BBPD ≥15 mm Hg, careful physical examination can yield absent or markedly diminished distal pulses and a systolic supraclavicular bruit. The bruit is best auscultated by lightly applying the stethoscope bell in each supraclavicular fossa while the patient sits looking forward with the shoulders relaxed and hands resting on the lap. Once detected, firm compression of the patient's ipsilateral radial artery decreases the SCA outflow and should shorten or obliterate the bruit. Arm exercises that can be carefully performed in the office (with the patient in a supine position to avoid provoking syncope) will induce peripheral vasodilation, thus augmenting the SCA outflow, which increases the turbulence across the stenotic lesion, rendering the bruit louder and longer.

Duplex ultrasound (DUS) with color flow is the diagnostic first test of choice. This modality provides excellent information of the lesion, identifies disease in the rest of the aortic arch vessels, and adequately assesses flow direction in the vertebral artery. Once the diagnosis is made and the symptoms are considered significant enough to warrant intervention, we routinely obtain a CTA or MRA to confirm the diagnosis, exclude proximal VA stenosis or occlusion (difficult to visualize by DUS and when present can manifest as retrograde vertebral flow, mimicking vSSS), and clearly define the anatomic relationships between the SCA lesion, the aortic arch (since ostial lesions represent an extension of atherosclerosis arising in the aortic arch), and the origins of the ipsilateral vertebral and internal mammary arteries. This information can be very useful in planning the treatment modality. Angiography is reserved for patients who were determined to undergo endovascular therapy.

We advise all patients referred to CABG with BBPD ≥15 mm Hg or history of a nonatherosclerotic condition that is known to be associated with SAS (see above) and those with known vascular disease to undergo screening for SAS prior to their open heart surgery. This can be done in the outpatient setting by DUS or angiography during the index cardiac catheterization procedure.