A RARE BUT IMPORTANT CAUSE of SYNCOPE

from Southern Medical Journal
Kirk M. Chan-Tack, MD, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia

Abstract

An elderly woman came to our emergency room for evaluation of a syncopal episode. While climbing a flight of stairs, she had turned her head to the left and abruptly passed out. Positive physical findings included blood pressure of 141/65 mm Hg (right arm) and 80/43 mm Hg (left arm), as well as nonpalpable left radial and brachial pulses that were detectable only by Doppler ultrasonography. Carotid duplex ultrasonography showed reverse flow in the left vertebral artery and an abnormal, stenotic distal left subclavian artery. Magnetic resonance angiography confirmed complete occlusion of the left subclavian artery with classic subclavian steal. The patient had percutaneous transluminal angioplasty with stenting of the left subclavian artery and has remained asymptomatic through 2 years of follow-up with aggressive risk-factor modification.

Introduction

Subclavian steal syndrome is caused by occlusion of the proximal subclavian artery with subsequent retrograde filling of the subclavian artery via the vertebral artery. The decreased blood flow to the brain and upper extremity on the affected side can result in an array of symptoms, classified broadly as due to (1) vertebrobasilar insufficiency or (2) ischemia of the affected extremity. Vertebrobasilar insufficiency may produce light-headedness, dizziness, vertigo, ataxia, visual disturbances, motor deficits, focal seizures, confusion, aphasia, headache, presyncope, or syncope. Symptoms due to ischemia of the affected extremity are less frequent and include weakness, arm claudication, paresthesias, or coldness on the affected side. Risk factors for this syndrome include hypertension, diabetes, hypercholesterolemia, tobacco use, and vigorous exercise of the affected extremity. This report describes a patient with syncope as the presenting symptom of subclavian steal syndrome.

Case Report

A 79-year-old woman was admitted for evaluation of a syncopal episode. The patient was in her usual state of health until the morning of admission when, while climbing a flight of stairs, she turned her head to the left and abruptly passed out. She fell down 12 stairs and sustained a left occipital laceration. The patient denied chest pain, palpitations, prodrome, visual changes or aura, bowel or bladder incontinence, tongue biting, or postictal state. She had had no previous episodes of presyncope or syncope.
Her medical history included longstanding hypertension, type 2 diabetes, hypercholesterolemia, and tobacco use. Medications included fosinopril, repaglinide, and atorvastatin. Family history was notable only for diabetes. She had a 40 pack-year history of tobacco use but never used alcohol or illicit drugs. Review of systems was otherwise negative.

On physical examination, temperature was 37.2°C (98.9°F), blood pressure 141/65 mm Hg (right arm), heart rate 76/min and regular, and respiratory rate 16/min. A 6 cm laceration was present on the left occiput. No carotid bruits were heard. The lungs were clear bilaterally. Cardiac examination showed a regular rate and rhythm, normal S1 and S2, and no murmurs, rubs, or gallops. Findings on abdominal and neurologic examinations were normal. Peripheral pulses were 2+ throughout, with the notable exception of the left radial and brachial pulses, which were detectable only by Doppler ultrasonography. After discovery of the nonpalpable left radial and brachial pulses, the blood pressure was measured in the left arm and found to be markedly low at 80/43 mm Hg.

Admission complete blood count, chemistry panel (including cardiac enzymes and troponin), electrocardiogram, and chest radiograph were all unremarkable. Noncontrast computed tomography of the head was negative for hemorrhage, infarct, or mass effect. Clinical findings were highly suggestive of subclavian steal. Carotid duplex ultrasonography showed reverse flow in the left vertebral artery and abnormal, stenotic distal left subclavian artery. Magnetic resonance angiography confirmed complete occlusion of the left subclavian artery with classic subclavian steal ( scas-Figs 1.jpg, -2.jpg, and -3.jpg).

Scas-Figure 1. Magnetic resonance angiogram of proximal great vessels shows occlusion of left subclavian artery (arrows) with reconstitution proximal to origin of left vertebral artery, as well as stenosis of left vertebral artery origin (curved arrow).

Scas-Figure 2. Magnetic resonance time-of-flight angiogram of mid-neck (depicting superiorly flowing blood) shows absence of superior flow in left vertebral artery (arrow) consistent with occlusion or reversal of flow. (Vertical bright line was artifactual.)

Scas-Figure 3. Magnetic resonance time-of-flight angiogram of mid-neck (displaying inferiorly flowing blood) shows reversal of flow in left vertebral artery (arrow). (Vertical bright line was artifactual.)

Vascular surgery consultation was obtained, and the patient had percutaneous transluminal angioplasty (PTA) with stent placement in the left subclavian artery. She tolerated the procedure well and was discharged on the following day. With close monitoring and support from her primary care physician, the patient has stopped smoking and has also achieved excellent control of her hypertension, diabetes, and hypercholesterolemia. She maintains a moderate level of exercise and activity (including use of her left arm) and has remained asymptomatic through 2 years of follow-up.

Discussion

Subclavian steal syndrome is rare; its incidence and prevalence are unknown. It has a 2:1 male-female ratio, and patients are generally aged 55 years or older.
Subclavian steal syndrome is caused by occlusion of the proximal subclavian artery. Arteriosclerosis is the cause in 95% of cases. Less common causes of occlusion include dissecting aortic arch aneurysm, embolus, and Takayasu's arteritis. The underlying pathophysiology of subclavian steal syndrome is the development of a negative pressure gradient between the vertebral-basilar and vertebral-subclavian artery junctions. Subsequent retrograde filling of the subclavian artery via the vertebral artery causes the subclavian artery to "steal" blood from the vertebrobasilar system. Decreased blood flow to the brain and upper extremity on the affected side results in a variety of symptoms, classified broadly as due to (1) vertebrobasilar insufficiency or (2) ischemia of the affected extremity.Vertebrobasilar insufficiency may produce light-headedness, dizziness, vertigo, ataxia, visual disturbances, motor deficits, focal seizures, confusion, aphasia, headache, presyncope, or syncope. Although rare, strokes and resulting deaths have occurred due to the subclavian steal syndrome. Symptoms due to ischemia of the affected extremity are less frequent and include weakness or arm claudication after exercise, paresthesias, or coldness on the affected side. Both symptom subtypes are classically reproducible by vigorous exercise of the affected arm, often in conjunction with sudden or sharp turning of the head to the affected side.

Risk factors for this syndrome include hypertension, diabetes, hypercholesterolemia, tobacco use, and vigorous exercise of the affected extremity, all of which were present in this patient. Hypertension increases the pressure in the basilar arterial system. Diabetes, hypercholesterolemia, and smoking all worsen endothelial and vascular integrity. Vigorous exercise of the affected extremity also decreases pressure in the subclavian arterial system. This further increases the negative pressure gradient between the vertebral-basilar and vertebral-subclavian artery junctions, causing symptoms as described. If vigorous exercise of the affected arm is combined with sudden or sharp turning of the head to the affected side, as occurred in this patient, the negative pressure gradient is even steeper. Physical findings of subclavian steal syndrome include unilaterally decreased pulses, >20 mm Hg difference in blood pressure between the upper extremities, supraclavicular bruits, and disappearance of the radial pulse with exercise of the affected extremity.

Although subclavian steal is rare, a high index of suspicion is warranted in the presence of a suggestive history, risk factors, and physical findings. Differential diagnosis includes intracranial vascular disease, carotid artery disease, vertebral artery disease, brain tumor, and subdural hematoma. Diagnosis of subclavian steal syndrome confirmed by (1) carotid duplex ultrasonography (which shows reversal of vertebral artery flow and a stenotic distal subclavian artery) and (2) magnetic resonance angiography or arch aortography (which shows subclavian artery occlusion and absence of vertebral artery flow). Risk factor modification (smoking cessation and control of hypertension, diabetes, and hypercholesterolemia) is essential. Patients are also educated about preventing injury to and reducing exercise of the affected arm. Invasive treatment of subclavian steal syndrome is necessary for symptomatic patients. Options include axillo-axillary bypass, carotid-subclavian bypass, and PTA of the stenotic proximal subclavian artery with stent placement. The prognosis is excellent with all three modalities (95% of patients remain asymptomatic after the procedure), but PTA is preferred because of its lower morbidity, shorter hospitalization, and faster recovery. Follow-up includes assessment for recurrence of symptoms, blood pressure measurements in both arms, and risk factor modification.

Conclusion

This case underscores the importance of subclavian steal syndrome, its wide range of clinical manifestations (including syncope), and its morbidity and potential for mortality if undiagnosed or misdiagnosed, Recognition of this syndrome is crucial, since patients can be successfully treated with PTA and stent placement or other bypass graft operations. Aggressive risk factor modification (smoking cessation and control of hypertension, diabetes, and hypercholesterolemia) is also essential in the treatment of subclavian steal syndrome

South Med J 94(4):445-447, 2001. © 2001 Southern Medical Association

 

ILLUSTRATIONS of SUBCLAVIAN ARTERY STEAL

from http://www.vesalius.com/graphics/archive/archtn.asp?VID=514&nrVID=22

 

angoccsca-fig1.jpg

Angiogram of occluded subclavian artery

angoccsca-fig2.jpg

Retrograde filling of left subclavian artery

 

Subclavian steal blood flow

 

 

 

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