Abstract 114: “Failing” DAPT? Think Again

Abstract

Introduction Bow Hunter’s Syndrome (BHS) is a rare etiology of vertebrobasilar insufficiency that usually occurs with head turn, which causes compression of the vertebral artery by an osteophyte. There is subsequent hypoperfusion of brain tissue, but thromboembolism and ischemic stroke is rare. Timely diagnosis is imperative, as decompressive surgery can be curative. This unique case highlights the diagnostic and therapeutic challenges of a patient with multiple vascular risk factors who suffered from strokes secondary to BHS. Methods A 79‐year‐old man with a past medical history of peripheral artery disease, abdominal aortic aneurysm, myocardial infarction with drug eluding stents (on dual antiplatelet therapy (DAPT)), complete heart block with pacemaker, heart failure with reduced ejection fraction, hypertension, hyperlipidemia, and diabetes mellitus presented to an outside hospital with recurrent episodes of right‐sided weakness every 1‐2 days over the previous 3 weeks. Episodes always occurred after activity and only upon sitting. He had previously undergone non‐contrasted head computed tomography (NCHCT) (magnetic resonance imaging (MRI) was unable to be performed secondary to pacemaker), which did not reveal strokes. His initial computed tomography angiogram (CTA) of the head and neck was unremarkable. However, CTA head and neck 4 days later demonstrated 90 percent stenosis of the mid left V2 at the C3‐4 level and a 75‐90 percent stenosis of the left mid V2 segment at the C5‐6 level (hard and soft plaque in these areas). He was switched from DAPT to aspirin and warfarin because he was considered a “DAPT failure.” He continued to have episodes, so he was transferred to our institution for a second opinion. Results On arrival, the exam was notable for right‐sided hemiparesis and dysmetria. Repeat CTA head and neck demonstrated multifocal intracranial atherosclerosis with marked stenosis of the left V4 segment. However, marked stenosis at V2 appeared to be owed to external compression from facet arthrosis rather than atherosclerosis. He also had moderate stenosis of the right V4 segment. Eventually, he underwent an MRI brain, which demonstrated acute to subacute infarcts in the left pons. He was taken for a cerebral angiogram on the same day, which demonstrated stenosis of the distal V2 segment of the left vertebral artery (at the level of C3‐C4) with interval development of marked stenosis following neck flexion and occlusion of the left vertebral artery following leftward head rotation. Findings were most consistent with rotational occlusion of the left vertebral artery, which is also known as BHS. The patient underwent surgery, but suffered from a gastrointestinal bleed and developed post‐operative atrial fibrillation; after a risks/benefits discussion, he was discharged on anticoagulation only. He had no further strokes. Conclusion This patient suffered from ischemic strokes, which occur in less than 10% of BHS cases. Contralateral vertebral artery stenosis, which is unable to supply retrograde flow during compression, is the likely etiology of this patient's strokes. Recurrent posterior circulation strokes in the setting of optimal medical management should clue clinicians to consider other etiologies of stroke. Dynamic angiography is the gold standard for BHS and decompressive surgery is often curative.