ArticleCureus2026
Multiple Posterior Circulation Infarctions in a Patient With Complex Aortic Atheroma and Left Vertebral Artery Stenosis: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Complex aortic atheroma is a recognized potential source of cerebral embolism, particularly when plaques are thick, protruding, irregular, ulcerated, or mobile. However, establishing a direct causal relationship between aortic atheroma and cerebral infarction remains challenging when competing arterial mechanisms coexist. We describe a 65-year-old man with hypertension, dyslipidemia, and active tobacco use who presented with headache and an acute confusional state. Neurological examination revealed left-sided dysmetria and gait instability. Brain imaging demonstrated multiple ischemic lesions confined to the posterior circulation, involving the left cerebellum, left thalamus, and bilateral occipital regions. Computed tomography angiography revealed subocclusive stenosis of the left V4 vertebral artery, a right vertebral artery terminating as the posterior inferior cerebellar artery, and an irregular atheromatous plaque involving the distal aortic arch and isthmus. Transesophageal echocardiography demonstrated diffuse aortic atheromatosis, including a protruding distal aortic arch plaque measuring 26.03 × 12.79 mm and a descending aortic plaque with a maximum thickness of 12.35 mm. Transthoracic echocardiography, telemetry, and 72-hour Holter monitoring identified no cardiac embolic source or arrhythmia. Given the exclusively posterior infarct distribution and vertebral anatomy, symptomatic left V4 atherosclerotic stenosis, through artery-to-artery embolism, distal hypoperfusion, or both, was considered the more likely mechanism. The patient received dual antiplatelet therapy followed by long-term aspirin, high-intensity statin therapy, and intensive vascular risk-factor management, with favorable neurological improvement. The aortic atheroma may have been contributory, incidental, or a marker of systemic atherosclerosis rather than the direct embolic source. As definitive causal attribution was not possible, the stroke was classified as being of undetermined etiology under the TOAST framework.
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