Successful subclavian artery stenting in a patient with subclavian steal syndrome associated with contralateral vertebral artery hypoplasiaMH Ahn1, BD Ku2, MK Kim3
1 Department of Medicine, International St. Mary's Hospital, Catholic Kwandong University College of Medicine, Incheon, South Korea
2 Department of Neurology, International St. Mary's Hospital, Catholic Kwandong University College of Medicine, Incheon, South Korea
3 Department of Cardiology, International St. Mary's Hospital, Catholic Kwandong University College of Medicine, Incheon, South Korea
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/jpgm.jpgm_44_23
Source of Support: None, Conflict of Interest: None
Subclavian steal syndrome (SSS) is characterized by vertebral artery flow reversal caused by hemodynamically severe stenosis or blockade of the proximal subclavian artery. Most patients with subclavian artery stenosis are asymptomatic because of the abundant collateral blood supply in the head and neck area. Symptoms of vertebrobasilar insufficiency (VBI) of the brainstem, such as vertigo, ataxia, drop attacks, or syncope, are uncommon and usually occur in patients with significant compensatory failure of posterior cerebral circulation., Vertebral artery hypoplasia (VAH) is common in healthy individuals without VBI symptoms. However, VAH may lead to regional hypoperfusion and complex neurovascular consequences due to the potential limitation of compensatory posterior cerebral circulation. The compensatory blood flow is easily reversed and results in VBI symptoms if significant stenosis or occlusion is present within the subclavian artery proximal to the origin of the vertebral artery with contralateral VAH. Here, we report a patient with left SSS with right-side VAH that was successfully treated with subclavian stenting.
A 64-year-old male patient with a medical history of hypertension visited the neurology clinic due to frequent paroxysmal vertigo attacks for 6 months. He complained of a sudden unexpected vertigo attack followed by dysarthria, ataxia, or diplopia which developed when walking or exercising. Additionally, these symptoms would improve after a few minutes of stabilization. The patient had no history of coronary or vascular diseases. His blood pressure was 160/90 and 130/70 mmHg on the right and left side, respectively; heart rate was 90 beats/min, respiratory rate was 21 breaths/min, and body temperature was 36°C. Physical and neurological examination was normal. There were no carotid bruits. The patient did not develop any vertigo attack during head turning or upper extremity exercise. Routine blood investigations, chest X-ray and electrocardiogram were normal. Brain computed tomography of the cerebral arteries revealed right VAH with severe stenosis of the left proximal subclavian artery [Figure 1]a and [Figure 1]b. The patient's tentative diagnosis was VBI due to SSS based on the clinical history, neurological examination, and cerebrovascular imaging. The patient subsequently underwent percutaneous transluminal neck angioplasty with stenting. The neck angiogram was performed with a 7 French guiding catheter inserted from the right femoral artery. The neck angiogram showed 75% stenosis of the left subclavian artery, just proximal to the origin of the left vertebral artery, with right VAH having retrograde flow through the left vertebral artery [Figure 2]a and [Figure 2]b. Predialtation balloon inflation was done. A self-expanding left subclavian artery stent was inserted (Epic™ Vascular Self-Expanding Stent diameter 8.0 mm. length 40 mm) to reverse the subclavian steal symptoms of the patient [Figure 2]c and postdilataion balloon inflation was done. The patient was stable during the procedure and underwent successful left subclavian artery angioplasty with stenting [Figure 1]c and [Figure 2]d. Follow-up neck angiogram performed 3 months after the stenting showed that the inserted stent was patent and was functioning properly. After subclavian stenting, the reversed blood flow in the left vertebral artery, the blood pressure differences in both arms, and the paroxysmal vertigo attacks disappeared.
The vertebral artery is hypoplastic in up to 10–15% of the healthy population and makes little contribution to basilar arterial flow. The left vertebral artery is dominant in approximately 50%; the right in 25% and the two vertebral arteries are of similar caliber in the remaining 25% of cases. The clinical significance of unilateral VAH and its relation to VBI is not well understood. Previous studies have revealed that individuals with VAH are at increased risk for posterior circulatory stroke, especially if they have concomitant known risk factors for stroke. In the present patient, right VAH was associated with left subclavian artery stenosis proximal to the origin of the left vertebral artery leading to relatively compromised blood flow compensation to the brainstem and causing paroxysmal vertigo in specific clinical situations.
Previous studies have revealed that the subclavian steal phenomenon and vertebral artery hemodynamics morphologically change the vertebral artery flow spectrum. These hemodynamic changes result in progressive blood flow reversal when the subclavian artery has significant progressive stenosis at the proximal segment of the vertebral artery opening. The change of contralateral vertebral artery flow direction triggers VBI symptom development in most patients with SSS. However, ipsilateral vertebral artery triggered development of VBI symptoms in the present patient. Hence, this case snippet documents one of the clinical variants of SSS.
The combination of subclavian artery stenosis with contralateral VAH can easily cause SSS due to poor compensatory power of the contralateral vertebral artery. To our knowledge, subclavian steal associated with the contralateral VAH artery has not been previously reported. This case suggested that VAH confers an increased probability of SSS in a selected individual aside from its peculiar anatomic pattern, and subclavian stenting should be considered.
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[Figure 1], [Figure 2]