Case series reveals acute ischemic stroke linked to bicuspid aortic valve, highlighting challenges in treatment strategies.
Background Spontaneous calcified cerebral emboli (SCCE) are an uncommon cause of acute ischemic stroke, reported in 2.7–5.9% of cases. Bicuspid aortic valve (BAV), the most frequent congenital cardiac malformation, predisposes to accelerated calcification and embolic risk, even in younger patients without conventional vascular risk factors. Recognition is critical, as SCCE can mimic arterial patency on CTA and pose therapeutic challenges. Methods We describe two young male patients with BAV and bulky valve calcification who presented with acute cerebrovascular syndromes. Clinical features, imaging, and management were analyzed. Results Case 1: A 25‐year‐old man with known BAV presented with acute right‐sided weakness. CT/CTA revealed multifocal calcified emboli in the basilar and internal carotid arteries; MRI confirmed acute infarcts. Cardiac CT showed severe valve calcification (score 4186) with patent foramen ovale but no thrombus. He received intravenous thrombolysis with good recovery and later underwent surgical repair. Case 2: A 38‐year‐old man with BAV and ascending aortic aneurysm presented with transient aphasia and visual symptoms. CT/CTA showed calcification in a distal M2 branch; MRI/MRA demonstrated focal narrowing without infarction. Cardiac CT revealed eccentric valve calcification (score 2456). He was treated with dual antiplatelets and subsequently underwent valve replacement. Both remain stable on follow‐up. Conclusion SCCE from calcified BAV should be considered in young stroke patients lacking traditional risk factors. Pitfalls such as “false patency” on CTA and subtle emboli on CT underscore the need for multimodal imaging. Acute therapy is difficult, as calcified emboli respond variably to thrombolysis and complicate thrombectomy. Long‐term prevention is undefined; antithrombotics alone may be inadequate in progressive valve disease. These cases highlight the importance of integrated cardiac–neurovascular evaluation and the need for further study of imaging and treatment strategies in SCCE.
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Sardana et al. (2025) studied this question.
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