An Unusual Case of a Vertebrobasilar Transient Ischemic Attack Involving the Subclavian Steal Syndrome

Case Presentation

EOG, aged early 70s, presented to the emergency department with a 2-hour sudden onset of dysarthria followed by weakness in the upper left limb, dizziness, and gait abnormalities. EOG denied symptoms before this event. EOG was right-handed and had a history of cardiovascular risk factors, including type 2 diabetes, hypertension, and rheumatoid arthritis (RA) with joint deformities, mostly in the hands. EOG was taking symptomatic oral medication but no disease-modifying antirheumatic drugs for RA. At admission, a finger-stick glucose test was normal, and blood pressure measurements were 120/70 mm Hg in the right arm and 95/60 mm Hg in the left arm. The left radial pulse was notably diminished compared with the right side.

The neurologic examination showed mild weakness in the left arm, vertigo, and left-sided ataxia, resulting in a baseline National Institutes of Health Stroke Scale score of 6. Given the clinical picture, EOG was treated with intravenous thrombolysis in accordance with American Heart Association/American Stroke Association guidelines for the early management of patients with acute ischemic stroke.¹ EOG had complete symptom remission within 50 minutes.

Diagnostic Process

EOG’s blood test results were unremarkable. Transthoracic echocardiography revealed a left atrium volume index of 46 mL/m², indicating left atrium enlargement, and severe pulmonary artery hypertension, with a pulmonary artery systolic pressure of 60.8 mm Hg. Left ventricular ejection fraction (68%) was preserved. CT angiography showed partial vertebral artery and left subclavian artery stenosis, as well as calcified plaques in the aortic arch. A 24-hour Holter monitor recording was unremarkable.

At 24 hours, noncontrast CT scan of the brain was performed, revealing no signs of ischemic infarct or intracranial hemorrhage. Brain MRI did not demonstrate signs of an acute ischemic stroke. Therefore, although EOG had been admitted with symptoms of a posterior circulation stroke and received prompt treatment for an acute ischemic stroke, the medical evaluation was consistent with a transient ischemic attack (TIA) (Figure 1). Duplex ultrasound indicated total flow reversal in the left vertebral artery because of atherosclerosis of the ipsilateral subclavian artery as well as increased blood flow velocity in the right subclavian artery caused by tortuous anatomic variation (Figure 2).

Case Resolution

After hospital discharge, EOG returned to daily activities, with a modified Rankin Scale score of 0. Antiplatelet therapy and statins were prescribed for secondary prevention.

The testing had revealed that the subclavian steal syndrome (SSS) presented in an atypical manner, with substantial atherosclerosis in both arteries, and the most severe stenosis on the left side. EOG reported no neurologic symptoms of SSS, including presyncope, dizziness, or arm claudication. EOG was referred to a rheumatologist for clinical assessment to address potential RA-related issues. To determine whether interventional therapy would be required, an outpatient visit with a vascular surgeon was scheduled. Follow-up appointments have been scheduled at the neurovascular clinic for medical management of EOG’s comorbidities.

Discussion

In this case of an older individual with multiple cardiovascular risk factors for cerebral ischemia, the diagnostic workup demonstrated vertebrobasilar TIA that involved SSS and a severe burden of atherosclerosis in the vertebral arteries. SSS in this scenario was brought on by proximal left subclavian artery and vertebral artery stenosis, which led to hypoperfusion of the ipsilateral arm and flow reversal from the contralateral vertebral artery to the left ipsilateral artery.² Although most people with the subclavian steal phenomenon are asymptomatic, when symptoms arise, dizziness, syncope, or weakness can develop, which may be exacerbated with exercise or in the presence of underlying illnesses that decrease cardiac output. Deformations or misalignments of the craniocervical junction, such as those seen in RA, could contribute further to the tortuous anatomy and exacerbate blood flow obstruction in vertebral arteries.³

When a steal phenomenon is suspected clinically, duplex ultrasound can support the diagnosis, and angiography is helpful for identifying artery stenosis. The prevalence of steal phenomenon is unknown, but epidemiologic studies have shown that it affects between 0.6% and 6.4% of the general population.⁴ The presence of subclavian steal phenomenon is considered a marker of atherosclerotic disease. When a symptomatic presentation occurs, such as in TIA or symptomatic arm ischemia, revascularization interventions sometimes are necessary.⁵ In a study conducted by Labropoulos et al,⁶ 7881 individuals were assessed using duplex ultrasound; 5.4% of participants had SSS, of whom 2.2% had experienced a stroke. Stroke may occur in as many as 26% of individuals who present with a steal phenomenon.^4,6 Atherosclerosis, the most common cause of vertebral artery stenosis, is reported in up to 90% of cases.^4–6 Treatment options are available for individuals with SSS, ranging from medical management for those with mild symptoms to endovascular stenting and surgical bypass grafting for people with serious clinical or refractory symptoms.^7,8

Although rare, SSS is a vascular condition that may result in vertebrobasilar ischemic stroke, and thus is an important entity to consider during a cardiovascular diagnostic workup. SSS should be considered in the presence of substantial atherosclerotic burden. In addition to secondary prophylaxis with antiplatelet drugs, endovascular therapy may be considered for the treatment of SSS for cases in which symptoms persist despite optimal medical treatment.