Abstract Number ‐ 227: Retrograde embolism from a Subclavian Thrombus causing Acute Ischemic Stroke in the Middle Cerebral Artery

Abstract

Introduction Intracranial embolism to the middle cerebral artery usually occurs because of embolization from the heart, carotid artery or the aorta. Here we describe a case of a subclavian thrombus, embolizing to the middle cerebral artery. Retrograde embolism is a rarely described mechanism of acute ischemic stroke. Methods A 49‐year‐old gentleman with a history of hyperlipidemia, peripheral artery disease, smoking, prior stroke, previously treated arteriovenous malformation (AVM) in the left parieto‐occipital region and active methamphetamine use presented with sudden onset dysarthria and left facial weakness (NIH stroke scale–3). CT angiogram (CTA) head and neck demonstrated a right M2 inferior division occlusion and noted nonocclusive thrombus attached to right subclavian artery atherosclerotic plaque, proximal to the origin of the right vertebral artery and otherwise minimal extracranial, and intracranial atherosclerotic disease. He was not a candidate for IV thrombolysis due to his AVM, or mechanical thrombectomy (MT) due to low NIHSS. Apixaban was started. Trans‐esophageal echocardiogram (TEE) demonstrated a grade 2 PFO. Venous doppler ultrasound performed of his upper and lower extremities was negative. On day 2 of hospitalization, his left hemiparesis and dysarthria worsened. Repeat CTA head and neck showed absence of the right subclavian thrombus and new distal M1‐MCA thrombus, suggestive of retrograde embolism from the right subclavian artery. The patient was started on IV heparin and aspirin. A stroke in young work‐up was sent including antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies (ANCA), homocysteine, hexagonal phase phospho proteins, antiphospholipid antibodies, HIV, rheumatoid factor, cryoglobulin, hepatitis B antibodies, hepatitis C antibodies, sickle cell screen, Sjogren’s syndrome antibodies, drug screen, and was negative. Results Embolism (cardioembolism and artery–artery embolism) to the intracranial vasculature is an important cause of acute ischemic stroke. Retrograde embolization is rarely described as a cause of ischemic stroke. Our patient presented initially with distal right M2 occlusion and subocclusive thrombus of the right subclavian artery, associated with focal atherosclerosis but otherwise patent extracranial and intracranial cerebral vessels. Work‐up including transesophageal echocardiogram, and hypercoagulable work‐up was unrevealing. Repeat CT angiogram obtained in view of worsening deficits revealed absence of his right subclavian thrombus and new distal M1‐MCA occlusion presumed retrograde embolism from the right subclavian artery. This is may represent the consequence of local turbulence and retrograde flow during diastole. Conclusions When considering sources of embolic stroke, retrograde embolism should be considered in patients with focal atherosclerosis.